Av. Blasco Ibáñez 17. Servicio de CardiologÃa. Hospital Clinic Universitari Valencia-Spain CP 46010
yulnunez@gmail.com
Medical School was completed in 1998 at the University of Valencia (Spain). Specialist in Cardiology. Hospital Clinic Universitari Valencia, Spain (2004). Fellowship Interventional Cardiology . Hospital Clinic Universitari Valencia (2004-2005) PhD, University of Valencia (2006). Medical staff of Cardiology Departament Hospital Clinic Universitari (2005...) Supervisor of residents in Cardiology (2006...) Profesor University of Valencia (2010...)
Abstract: To evaluate remote myocardial function after ST-elevation myocardial infarction (STEMI) and the impact of infarct size (IS) using cardiovascular magnetic resonance (CMR). 161 patients and 15 controls underwent CMR at 1st week and 6th month after STEMI. Using the 17-segments model, segments were categorized into infarcted, adjacent and remote myocardium. Relative systolic wall thickening (SWT, %) was assessed using the centerline method. IS (% of left ventricular mass) was determined in late enhancement imaging. Overall, in remote myocardium, SWT was comparable (83 ± 32) to controls (77 ± 25, P = .5) and did not increase significantly (P = .2) at the 6th month (88 ± 35, P = .3 vs. control). When IS was categorized into tertiles (<13.6%, (n = 49), 13.7-28.2%, (n = 60), >28.2%, (n = 52)), SWT in the remote area at the 1st week was not different from controls, regardless of infarct size (p between .2 and .8 for all tertiles). At 6 months, SWT was larger compared to controls only in small infarctions (98 ± 34 vs. 77 ± 25, P = .03). In medium and large infarctions there was no difference in SWT of the remote area compared to controls (87 ± 33 and 79 ± 34, P = .3 and P = .09) and there was no significant increase at 6 months (P between .2 and .9). In remote myocardium there was no difference in contractility compared to controls after STEMI. After 6 month a slight hypercontractility can only be observed in small infarctions. In medium and large infarctions no difference of SWT in remote myocardium compared to controls can be observed.
Abstract: Continuous ambulatory peritoneal dialysis (CAPD) has been proposed as an additional therapeutic resource for patients with advanced congestive heart failure (CHF). The objective of this study was to determine the therapeutic role of CAPD, in terms of surrogate endpoints, in the management of patients with advanced CHF and renal dysfunction.
Abstract: The aim of this study was to investigate the metabolomic profile of acute myocardial ischemia (MIS) using nuclear magnetic resonance spectroscopy of peripheral blood serum of swine and patients undergoing angioplasty balloon-induced transient coronary occlusion.
Abstract: Heart failure (Killip>I) in patients with acute coronary syndrome (ACS) is a recognized risk factor for death. However, its relationship with the risk of new acute ischemic events has not been well established.
Abstract: FUNDAMENT AND OBJECTIVES: The early readmission after a hospitalization for acute heart failure (AHF) is frequent; however, factors associated are not clearly established. Plasma levels of carbohydrate antigen 125 (CA125) have shown to be associated with the presence of systemic congestion and increased risk of death in patients with AHF. The aim of this study was to assess the relationship between CA125 levels (during hospitalization, at the first outpatient visit or their changes) and readmission for AHF at 6 months follow up. PATIENTS AND METHOD: We analyzed 293 consecutive patients hospitalized for AHF in which CA125 was determined during the index hospitalization (T1) and the first outpatient visit after discharge (T2) (median 31 days). We examined the relationship between CA125 levels, both isolated determinations as their serial changes (absolute, relative or categorical) and readmission for AHF by Cox regression analysis adjusted for competing events. The reclassification technique integrated discrimination improvement (IDI) index was used to assess the additional discriminative power of this biomarker over the final multivariate model. RESULTS: At 6 months follow up, we identified 32 (10.9%) and 54 (18.4%) deaths and readmissions for AHF, respectively. CA125 categorical changes [decrease and normalization (C1, n=153), decrease but no normalization at T2 (C2, n=72) and increase, with high levels at T2 (>35 U/ml) (C3, n=68)], followed by the isolated determination of CA125 at T2, showed the best discriminative accuracy. Thus, with respect to patients in the C1 category, patients in categories C2 and C3 showed a higher risk of readmission for AHF: C2 vs. C1: HR=3.48, 95% CI:1.84-6.59, p<0.001; C3 vs. C1: HR=3.18, 95% CI:1.62-6.21, p=0.001. On the other hand, patients with elevated levels of CA125 in T2 (>35 U/ml) (41%) tripled the risk of readmission for AHF at 6 months compared with those with normal levels of CA125 at T2: HR=3.06, 95% CI:1.79-5.23, p<0.001. The addition of the categories of serial measurements of CA125 and the presence of elevated levels of CA125 at T2 showed a significant increase in the discriminating power of 6.27% and 6.17% in the IDI index, respectively. CONCLUSIONS: After an episode of AHF, the elevation of CA125 levels (>35 U/ml) after the first weeks of admission is associated with an increased risk of readmission for AHF.
Abstract: The prognostic benefit of statins in patients with heart failure is a topic of controversy. Under the hypothesis that statins may provide greater benefit in a subgroup of patients with heightened inflammatory activity, we sought to explore whether statins are associated with a decreased risk of long-term mortality in patients with acute heart failure based on elevated levels of carbohydrate antigen 125, a biomarker related to systemic congestion and proinflammatory status.
Abstract: The prognostic value of arterial blood gases (ABG) in patients with acute decompensated heart failure (ADHF) is not well-established. We therefore conducted the present study to determine the relationship between ABG on admission and long-term mortality in patients with ADHF.
Abstract: BACKGROUND: Early stratification of patients according to the risk for developing microvascular obstruction (MVO) after ST-segment elevation myocardial infarction (STEMI) is desirable. We aimed to identify predictors of cardiovascular magnetic resonance (CMR)-derived MVO from clinical+ECG, laboratory and angiographic parameters available on admission. METHODS: Characteristics available on admission were documented in 97 STEMI patients referred for primary angioplasty. MVO was determined using contrast-enhanced CMR. RESULTS: MVO was present in 44 patients (45%). The C-statistic for predicting MVO was: clinical+ECG (.832), laboratory (.743), and angiographic parameters (.669). Adding laboratory to clinical+ECG information did not improve the C-statistic (.873 vs. .832, p=.2). Further addition of angiographic data (.904) improved the C-statistic of clinical+ECG (p=.04) but not of clinical+ECG and laboratory (p=.2). Independent predictors of MVO using clinical and ECG parameters were: Killip class >1 (OR 15.97 95%CI [1.37-186.76], p=.03), diabetes (OR 6.15 95%CI [1.49-25.39], p=.01), age <55years (OR 4.70 95%CI [1.56-14.17], p=.006), sum of ST-segment elevation >10mm (OR 4.5 95%CI [1.58-12.69], p=.005) and delayed presentation >3h (OR 3.80 95%CI [1.19-12.1], p=.02). A score was constructed assigning Killip class >1 2 points and the remaining indexes 1 point. The incidence of MVO increased with the score: 0 point: 8.7%; 1 point: 28.1%; 2 points: 71.4%; and 3+ points: 93% (p<.0001). CONCLUSIONS: MVO can be predicted using parameters already available on patient admission. We developed a clinical-ECG score allowing for early and reliable classification of STEMI patients according to the risk of MVO.
Abstract: The aim of this study was to evaluate the impact of glucose levels on admission and High Risk Ventricular Tachyarrhythmia (HRVT) in hospital mortality in patients with Acute Myocardial Infarction (AMI).
Abstract: BACKGROUND: The prognostic utility of combining serial measurements of brain natriuretic peptide (BNP) and antigen carbohydrate 125 (CA125) is largely unknown. The aim of this work is to assess the prognostic utility of serial measurements of BNP, CA125, and their optimal combination for predicting long-term mortality, following a hospitalization for acute heart failure (AHF). METHODS AND RESULTS: We analyzed 293 consecutive patients admitted with AHF where CA125 and BNP were measured at discharge (T1) and at the first ambulatory visit (T2: median 31days after discharge). Biomarkers were evaluated as snapshot determinations or as serial changes in absolute, relative or categorical changes and related to subsequent mortality with Cox regression analysis. The incremental prognostic value added by each biomarker was evaluated by the integrated discrimination improvement (IDI) index. During a median follow-up of 18months, 91 deaths (31.1%) were identified. From the different metrics tested, the categorical changes in CA125 (Normalization: decreasing to≤35U/ml at T2; Decreasing but not normalization: decreasing but T2>35U/ml; small-increase: increasing but T2≤35U/ml and; high-increase: increasing and T2>35U/ml) showed the best discriminative accuracy. For BNP none of the serial changes metrics tested were superior to a single determination at T2 (BNP≥100pg/ml). Adding these two biomarkers characterization to the clinical model, resulted in a 9.21% (p<0.001) gain in IDI index. CONCLUSIONS: In patients discharged for AHF, CA125 modeled as a pre-post categorical change, and BNP as a single determination at T2, resulted in the best marker combination for predicting all-cause mortality.
Abstract: In patients with acute myocardial infarction, elevation of plasma glucose levels is associated with worse outcomes. The aim of this study was to evaluate the association between stress hyperglycemia and in-hospital mortality in patients with acute myocardial infarction with ST-segment elevation (STEMI).
Abstract: Several works have endorsed a significant role of the immune system and inflammation in the pathogenesis of heart failure. As indirect evidence, an association between a low relative lymphocyte count (RLC%) and worse outcomes found in this population has been suggested. Nevertheless, the role of RLC% for risk stratification in a large and nonselected population of patients with acute heart failure (AHF) has not yet been determined. Thus, the aim of this study was to determine the association between low RLC% and 1-year mortality in patients with AHF and consequently to define whether it has any role for early risk stratification. A total of 1,192 consecutive patients admitted for AHF were analyzed. Total white blood cell and differential counts were measured on admission. RLC% (calculated as absolute lymphocyte count/total white blood cell count) was categorized in quintiles and its association with all-cause mortality at 1 year assessed using Cox regression. At 1 year, 286 deaths (24%) were identified. A negative trend was observed between 1-year mortality rates and quintiles of RLC%: 31.5%, 27.2%, 23.1%, 23%, and 15.5% in quintiles 1 to 5, respectively (p for trend <0.001). After thorough covariate adjustment, only patients in the lowest quintile (<9.7%) showed an increased risk for mortality (hazard ratio 1.76, 95% confidence interval 1.17 to 2.65, p = 0.006). When RLC% was modeled with restricted cubic splines, a stepped increase in risk was observed patients in quintile 1: those with RLC% values <7.5% and <5% showed 1.95- and 2.66-fold increased risk for death compared to those in the top quintile. In conclusion, in patients with AHF, RLC% is a simple, widely available, and inexpensive biomarker, with potential for identifying patients at increased risk for 1-year mortality.
Abstract: Inflammation plays a crucial pathophysiological role in the entire continuum of the atherosclerotic process, from its initiation, progression, and plaque destabilization leading ultimately to an acute coronary event. Furthermore, once the clinical event has occurred, inflammation also influences the left ventricular remodelling process. Under the same paradigm, there is evidence that lymphocytes play an important role in the modulation of the inflammatory response at every level of the atherosclerotic process. Low lymphocyte count (LLC) is a common finding during the systemic inflammatory response, and clinical and animal studies suggest that LCC plays a putative role in accelerated atherosclerosis. For instance, there is recent evidence that LLC is associated with worse outcomes in patients with heart failure, chronic ischemic heart disease and acute coronary syndromes. Further indirect evidence supports the pathologic role of LLC related to the fact that 1) lymphopenia - due to a decreased count of lymphocyte T cells - normally occurs as a part of the human ageing process, and 2) increased incidence of cardiovascular events has been reported in conditions where lymphopenia is common, such as renal transplant recipients, human immunodeficiency virus infection, survivors of nuclear disasters and autoimmune diseases. The aim of the present article is to review: a) the pathophysiological mechanisms that have been proposed for the observed association between LLC and cardiovascular diseases (CVD), b) the available evidence regarding the diagnostic and prognostic role attributable to LLC in patients with CVD, and; c) the potential therapeutic implications of these findings.
Abstract: Pharmacoinvasive strategy represents an attractive alternative to primary angioplasty. Using cardiovascular magnetic resonance imaging we compared the left ventricular outcome of the pharmacoinvasive strategy and primary angioplasty for the reperfusion of ST-segment elevation myocardial infarction.
Abstract: BACKGROUND AND OBJECTIVES: There are few cases described in the literature in which depigmentation of melanocytic nevi occurs without the appearance of halos. The aim of this study was to analyze the correlation between clinical and dermoscopic findings and to assess the usefulness of dermoscopy to identify possible markers of complete regression in melanocytic lesions. MATERIALS AND METHODS: A prospective, observational, descriptive study of 77 melanocytic lesions in 52 patients was undertaken over a 5-year period. Melanocytic lesions from patients who underwent periodic follow-up in the digital dermoscopy unit were analyzed if they had exhibited partial or total, permanent depigmentation without a clinically apparent halo. RESULTS: We observed substantial variation in the time taken for pigmentation to disappear and the morphological characteristics of the nevi during the depigmentation process. Female sex and dermoscopic evidence of melanophage activity or of a halo were all associated with more rapid involution of pigmented lesions. The only variable which displayed a statistically significant association with complete depigmentation of melanocytic nevi was the presence of vascular proliferation. Fibrosis was the only variable that displayed a statistically significant association with heterogeneous depigmentation of melanocytic nevi. CONCLUSIONS: In this study, we have identified patterns of depigmentation in melanocytic lesions that differ from the classic halo nevus.
Abstract: Multivariable regression models are widely used in health science research, mainly for two purposes: prediction and effect estimation. Various strategies have been recommended when building a regression model: a) use the right statistical method that matches the structure of the data; b) ensure an appropriate sample size by limiting the number of variables according to the number of events; c) prevent or correct for model overfitting; d) be aware of the problems associated with automatic variable selection procedures (such as stepwise), and e) always assess the performance of the final model in regard to calibration and discrimination measures. If resources allow, validate the prediction model on external data. Full English text available from: www.revespcardiol.org.
Abstract: Aims: We seek to assess the factors associated with the anticoagulation prescription in a cohort of patients with atrial fibrillation (AF) collected from out-patient clinics. Methods: A total of 1524 patients with a history of AF were collected from out-patients clinics. CHADS(2), CHA(2)DS(2)-VASc and HAS-BLED scores were calculated in every patient. Variables associated with anticoagulant treatment prescription were analyzed in univariant and multivariant models. Results: Most patients received either anticoagulant (62%) or antiplatelet treatment (37%). Anticoagulation rates increased among higher CHADS(2) and CHA(2)DS(2)-VASc score values. A logistic regression model was performed to assess the variables associated with the prescription of anticoagulant treatment; the variables with stronger association were the presence of arrhythmia at the current visit (odds ratio (OR) 33, 95% CI 27 - 40, p < 0.001) and lack of concomitant antiplatelet treatment (OR 0.17, 95% CI 0.14 - 0.21, p < 0.001). Conclusions: Although prognosis of patients with AF is mainly determined by the long-term thrombotic risk, the prescription of antithrombotic therapy depends more on the bleeding risk and the immediate thrombotic risk perception.
Abstract: INTRODUCTION AND OBJECTIVES: Hypertension is one of the most prevalent and poorly controlled risk factors, especially in patients with established cardiovascular disease (CVD). The aim of this study was to describe the rate of blood pressure (BP) control and related risk factors. METHODS: Multicenter, cross-sectional and observational registry of patients with hypertension recruited from cardiology and primary care outpatient clinics. Controlled BP defined as <140/90mmHg. RESULTS: 55.4% of the 10 743 patients included had controlled BP and these had a slightly higher mean age. Patients with uncontrolled BP were more frequently male, with a higher prevalence of active smokers, obese patients, and patients with diabetes. The rate of controlled BP was similar in patients with or without CVD. Patients with uncontrolled BP had higher levels of blood glucose, total cholesterol, low density lipoproteins and uric acid. Patients with uncontrolled BP were receiving a slightly higher mean number of antihypertensive drugs compared to patients with controlled BP. Patients with CVD were more frequently receiving a renin-angiotensin-aldosterone axis inhibitor: 83.5% vs. 73.2% (P<.01). Multivariate analysis identified obesity and current smoking as independently associated with uncontrolled BP, both in patients with or without CVD, as well as relevant differences between the two groups on other factors. CONCLUSIONS: Regardless of the presence of CVD, 55% of hypertensive patients had controlled BP. Lifestyle and diet, especially smoking and obesity, are independently associated with lack of BP control. Full English text available from: www.revespcardiol.org.
Abstract: To evaluate the relationship between systolic blood pressure (SBP) and long-term mortality in patients with acute heart failure (AHF) stratified by ejection fraction (LVEF): reduced (< or =40%) vs. preserved (> or =50%).
Abstract: BACKGROUND: Exercise testing constitutes the usual tool for decision making in chest pain units. This policy implies logistical constrains. Our aim was to evaluate a new strategy, combining a clinical risk score and N-terminal pro-B-type natriuretic peptide (NT-proBNP), in patients presenting to the emergency department with chest pain, without ischemic electrocardiogram changes or troponin elevation. METHODS: A total of 320 patients were randomized to either usual management, involving exercise testing, or a new strategy combining a clinical risk score and NT-proBNP without exercise testing. In the usual management, discharge decision was guided by the result of exercise test. In the new strategy, those patients with low clinical risk score and NT-proBNP were directly discharged. The primary outcome was hospitalization at the index episode. Secondary outcomes were cardiac events at 1 year. RESULTS: A total of 110 patients (69%) were hospitalized using usual management in comparison with 90 (56%) in the new strategy (P = .03). There were no differences in death or myocardial infarction (n = 11, 6.9% vs n = 6, 3.8%, P = .3) or cardiac events (n = 38, 24% vs n = 28, 18%, P = .2). Revascularizations at the index episode were more frequent under usual management (18% vs 8%, P = .01), although the new strategy was associated with higher rate of planned postdischarge revascularizations (0.6% vs 5%, P = .04). CONCLUSIONS: A strategy combining clinical history and NT-proBNP is simpler and reduced initial emergency hospitalizations in patients with chest pain, in comparison with the usual strategy involving exercise testing. Larger studies to assess its impact on long-term hard end points are needed.
Abstract: To compare a quantitative assessment of contrast cardiovascular magnetic resonance (CMR) after ST-segment elevation myocardial infarction (STEMI) with visual analysis for predicting depressed ejection fraction (dEF) and major adverse cardiac events (MACE). 192 patients underwent CMR at 1 week and 6 months after STEMI. Three quantitative (initial slope, maximal signal intensity and contrast delay in first-pass imaging) and 2 visual perfusion indexes (hypoenhancement in first-pass and microvascular obstruction in late enhancement imaging (LE)) were determined. Quantification of infarct mass and visual assessment of the extent of transmural necrosis (ETN) were also performed. At 6 months, 69 patients displayed dEF. During follow-up (mean 655 days) 20 MACE (death, re-infarction, re-admission for heart failure) occurred. Perfusion quantification took longer (P < 0.001) and, in ROC curve analyses and the C-statistic, was not superior to visual perfusion analysis for predicting late EF or MACE (P = ns). Similarly, infarct size quantification was not superior to visual assessment of ETN (P = ns). In multivariate analyses, only visual assessment of ETN (per segment) predicted dEF (OR 1.30 95%CI [1.04-1.61], P = 0.02) and MACE (HR 1.38 95%CI [1.19-1.60], P < 0.001). Visual analysis of CMR after STEMI is not time consuming and predicts dEF and MACE comparable to quantification. ETN was the strongest parameter.
Abstract: OBJECTIVE: We sought to determine the relationship between the lowest lymphocyte count (lymphocyte(min))obtained within the first 96 h of symptoms onset and the risk of postdischarge recurrent spontaneous myocardial infarction (re-MI) in patients admitted with ST-segment elevation MI (STEMI). METHODS: We analyzed 549 consecutive patients admitted with STEMI from a single academic hospital. Lymphocyte counts were determined at admission and routinely during the first 96 h. Lymphocyte(min) was selected as the main exposure. Patients with inflammatory or infectious diseases, in-hospital death, or reinfarction were excluded from the analysis (final sample= 426 patients). Lymphocyte(min) was divided into quartiles (Q) and their association with re-MI was assessed by competing risk analysis. Postdischarge death and coronary revascularization were considered competing events. RESULTS: During a median follow-up of 36 months, 53 re-MI (12.4%) were registered. The re-MI crude rate was significantly higher in patients in the lowest lymphocyte(min) quartile (Q1r1045 cells/ml) compared with Q2-Q4: 22.4, 9.4, 8.4, 9.4%, respectively; P =0.005. In a multivariate setting, Q1 was also associated with a significant increased risk of re-MI compared with Q2-Q4 (hazard ratio: 2.04, 95% confidence interval: 1.11-3.76; P = 0.021). CONCLUSION: Low lymphocyte count obtained within the first 96 h of a STEMI predicts the risk of re-MI.
Abstract: INTRODUCTION AND OBJECTIVES: The usefulness of ST-segment elevation resolution (STR) for predicting epicardial reperfusion is well established. However, it is still not clear how ST-segment changes are related to microvascular obstruction (MVO) observed by cardiovascular magnetic resonance (CMR) after primary percutaneous coronary intervention (pPCI) for ST-segment elevation myocardial infarction (STEMI). METHODS: The study involved 85 consecutive patients admitted for a first STEMI and treated by pPCI who had a patent infarct-related artery. An ECG was recorded on admission and 90 min and 6, 24, 48 and 96 h after pPCI. Thereafter, STR and the sum of ST-segment elevation (sumSTE) in all leads were determined. RESULTS: Overall, CMR revealed MVO in 37 patients. In infarcts with MVO, sumSTE was greater both before and after revascularization than in infarcts without MVO (P≤.001 at all times). In contrast, there was no significant difference in the magnitude of STR between infarcts with and without MVO 90 min after revascularization (P=.1), though there was after 6 h (P< .05 at all times). The area under the receiver operating characteristic curve for detecting MVO was greater for sumSTE than STR (P< .05 for all measurements). On multivariate analysis, after adjusting for clinical, angiographic and ECG characteristics, a sumSTE >3 mm 90 min after pPCI was an independent predictor of MVO on CMR, while an STR ≥70% was not (odds ratio=3.1; 95% confidence interval, 1.2-8.4; P=.02). CONCLUSIONS: MVO was associated with a significantly increased sumSTE at all times after revascularization. The difference in the magnitude of STR between infarcts with and without MVO was significant only >6 h after revascularization. The best predictor of MVO was a sumSTE >3 mm 90 min after pPCI.
Abstract: The aim of the present study was to evaluate the involvement of the right ventricle (RV) in reperfused anterior ST-elevation myocardial infarction (STEMI).
Abstract: To perform a comparison of cardiac magnetic resonance (MR) imaging-derived ejection fraction (EF) during low-dose dobutamine infusion (EF(D)) with the extent of segments with transmural necrosis in more than 50% of their wall thickness (ETN) for the prediction of major adverse cardiac events (MACEs) and late systolic recovery soon after a first ST-segment elevation myocardial infarction (STEMI).
Abstract: Few data are available on the use of invasive treatment in patients with non-ST-segment elevation acute coronary syndrome (NSTEACS) and systolic dysfunction. The aim of this study was to determine the effect of invasive treatment on the prognosis of patients with NSTEACS, with or without systolic dysfunction.
Abstract: Aim Elevated brain natriuretic peptide (BNP) and tumour marker antigen carbohydrate 125 (CA125) levels have shown to be associated with higher risk for adverse outcomes in patients with acute heart failure (AHF). Nevertheless, no attempt has been made to explore the utility of combining these two biomarkers. We sought to assess whether CA125 adds prognostic value to BNP in predicting 6-month all-cause mortality in patients with AHF. Methods and results We analysed 1111 consecutive patients admitted for AHF. Antigen carbohydrate 125 (U/mL) and BNP (pg/mL) were measured at a median of 72 +/- 12 h after instauration of treatment. Antigen carbohydrate 125 and BNP were dichotomized based on proposed prognostic cutpoints, and a variable with four categories was formed (BNP-CA125): C1 = BNP < 350 and CA125 < 60 (n = 394); C2 = BNP >/= 350 and CA125 < 60 (n = 165); C3 = BNP < 350 and CA125 >/= 60 (n = 331); and C4 = BNP >/= 350 and CA125 >/= 60 (n = 221). The independent association between BNP-CA125 and mortality was assessed with the Cox regression analysis, and their added predictive ability tested by the integrated discrimination improvement (IDI) index. At 6 months, 181 deaths (16.3%) were identified. The cumulative rate of mortality was lower for patients in C1 (7.8%), intermediate for C2 and C3 (17.8% and 16.9%, respectively), and higher for C4 (37.2%), and P-value for trend <0.001. After adjusting for established risk factors, the highest risk was observed when both biomarkers were elevated (C4 vs. C1: HR = 4.05, 95% CI = 2.54-6.45; P < 0.001) and intermediate when only one of them was elevated: (C2 vs. C1: HR = 1.71, 95% CI = 1.00-2.93; P = 0.050) and (C3 vs. C1: HR = 2.10, 95% CI = 1.30-3.39; P = 0.002). Moreover, when CA125 was added to the clinical model + BNP, a 10.4% (P < 0.0001) improvement in the IDI (on the relative scale) was found. Conclusion In patients admitted with AHF, CA125 added prognostic value beyond the information provided by BNP, and thus, their combination enables better 6-month risk stratification.
Abstract: AHF (acute heart failure) causes significant morbidity and mortality. Recent studies have postulated that the expression of inflammatory mediators, such as cytokines and chemokines, plays an important role in the development and progression of heart failure. A pro-inflammatory state has been postulated as a key factor in triggering CMV (cytomegalovirus) reactivation. Therefore we sought to determine the prevalence of active CMV infection in immunocompetent patients admitted for AHF and to quantify the association with the risk of the combined end point of death or AHF readmission. A total of 132 consecutive patients admitted for AHF were enrolled in the present study. Plasma CMV DNAaemia was assessed by qRT-PCR (quantitative real-time PCR), and cytokine measurements in plasma were performed by ELISA. Clinical data were evaluated by personnel blinded to CMV results. The independent association between active CMV infection and the end point was determined by Cox regression analysis. During a median follow-up of 120 [IQR (interquartile range), 60-240] days, 23 (17.4%) deaths, 34 (24.2%) readmissions for AHF and 45 (34.1%) deaths/readmissions for AHF were identified. Plasma CMV DNAaemia occurred in 11 (8.3%) patients, albeit at a low level (<100 copies/ml). The cumulative rate of the composite end point was higher in patients with CMV DNAaemia (81.8 compared with 29.8%; P<0.001). After adjusting for established risk factors, the occurrence of CMV DNAaemia was strongly associated with the clinical end point [hazard ratio = 4.39 (95% confidence interval, 2.02-9.52); P<0.001]. In conclusion, active CMV infection occurs, although uncommonly, in patients with AHF, and may be a marker of disease severity.
Abstract: The evolution of white blood cells after ST elevation myocardial infarction (STEMI) and their association with infarct size and major adverse cardiac events (MACE) remains unclear. Two hundred eleven patients underwent CMR after STEMI. Infarct mass (grams) was determined. Neutrophil, lymphocyte, and monocyte counts (x1,000 cells/ml) were measured upon arrival and at 12, 24, 48, 72, and 96 h. Patients with large infarctions (3rd tertile >/= 28.5 g vs. 1st and 2nd tertiles < 28.5 g) showed a larger neutrophil count at 12 h (14.8 +/- 4.8 vs. 11.4 +/- 3.3, p < 0.0001) and an increased monocyte count (maximum at 24 h (0.65[0.50-0.91] vs. 0.55[0.42-0.71], p = 0.004)) but no difference in lymphocyte count. Neutrophil count at 12 h independently predicted large infarctions (OR 1.14, 95%CI [1.04-1.26], p = 0.008). During follow-up (median 504 days), 25 MACE occurred. Neutrophil count at 96 h independently predicted MACE (HR 1.2, 95%CI [1.1-1.4], p = 0.003). Large infarctions show a marked neutrophil peak and an increasing monocyte count. Neutrophil count independently predicts large infarctions and MACE.
Abstract: BACKGROUND: Evaluation of chest pain of uncertain origin in the emergency department is a challenge. Chest pain units, involving non-invasive stress testing, have logistic constraints. Our aim was to identify very low risk patients for early discharge using clinical data. METHODS: A total of 772 patients were studied. Ischemia in the electrocardiogram, troponin elevation or history of ischemic heart disease, were exclusion criteria. The primary end point was 30day cardiac events (death, myocardial infarction or revascularization). The secondary end point was 1year major events (death or myocardial infarction). RESULTS: The primary and secondary end point rates were 123 (18%) and 31 (4%). Predictive variables for the primary end point were typical chest pain (OR=1.8, p=0.007), >/=2 pain episodes in last 24h (OR=3.4, p=0.0001), age>/=55years (OR=1.8, p=0.03), male (OR=2.2, p=0.001), diabetes (OR=1.8, p=0.01) and family history of ischemic heart disease (OR=2.0, p=0.02). A very low risk category could be distinguished (<2 predictors, n=114) that showed only 3 (2.6%) events at 30days (all 3 revascularizations), compared with 120 (18%) in the remaining patients (p=0.0001). The very low risk criteria had 97% negative predictive for 30day cardiac events. No very low risk patient presented major events at 1year compared with 31 (4.7%) in the remaining patients (p=0.009). CONCLUSION: In patients presenting to the emergency department with chest pain of uncertain origin and without prior ischemic heart disease, very low risk patients can be identified using clinical data. These patients could be quickly discharged without further non-invasive stress testing.
Abstract: INTRODUCTION AND OBJECTIVES: Little is known about how prognosis is influenced by readmission for acute heart failure (AHF) following non-ST-segment elevation acute coronary syndrome (NSTEACS). The aim of this study was to determine the prognostic effect of a first admission for AHF on the risk of acute myocardial infarction (AMI) or death in patients who survived an episode of high-risk NSTEACS. METHODS: The study involved 972 consecutive patients with high-risk NSTEACS who survived after hospital admission. Readmission for AHF was selected as the main exposure variable, and its association with subsequent AMI or all-cause death was assessed using Cox proportional hazards models for time-dependent covariates that also included adjustment for competing risks. RESULTS: After a median follow-up period of 30 [interquartile range, 12-48] months, 82 patients (8.4%) were admitted for AHF, 146 (15%) had an AMI, and 202 (20.8%) died. The median time to readmission for AHF was 203 [56-336] days after NSTEACS. Patients readmitted for AHF had an increased risk of subsequent death (hazard ratio [HR]=1.67; 95% confidence interval [CI], 1.13-2.45; P=.009) or AMI (HR=2.15; 95% CI, 1.41-3.27; P< .001), which was independent of baseline prognostic and time-dependent variables. CONCLUSIONS: Readmission for AHF after high-risk NSTEACS was associated with an increased risk of subsequent death or AMI.
Abstract: Background Decision making in chest pain of uncertain origin is challenging. Objectives To evaluate the predictive value of simple characteristics of pain presentation in patients coming to the emergency department with chest pain and without electrocardiogram ischaemia or raised troponin. Methods 789 patients were studied. The following categorical pain characteristics were collected: effort related pain, pressing character, radiation, associated symptoms, and ≥2 episodes in 24 h. Additionally, a predefined semi-quantitative pain score including seven items (Geleijnse score) was completed. Risk factors and co-morbidities were also recorded. The primary and secondary endpoints were cardiac events at 30 days and at 1 year. Results After adjusting for risk factors and co-morbidites, the pain characteristics associated with the primary and secondary endpoints were effort related pain (HR=2.1, 95% CI 1.5 to 3.0, p=0.0001; HR=1.8, 95% CI 1.3 to 2.5, p=0.0003) and ≥2 episodes in 24 h (HR=2.4, 95% CI 1.7 to 3.5, p=0.0001; HR=2.3, 95% CI 1.7 to 3.2, p=0.0001). Both variables retained their predictive value in women, diabetics and elderly (>70 years) patients. The discriminatory capacity of the predictive models including these two pain characteristics for the primary and secondary endpoints (C-statistic 0.76 and 0.76) was better than using the complex semi-quantitative pain score (C-statistic 0.69 and 0.71). Conclusion In patients presenting to the emergency department with chest pain and without electrocardiogram ischaemia or raised troponin, effort related pain and ≥2 episodes in 24 h are the main characteristics to be considered for decision making.
Abstract: INTRODUCTION AND OBJECTIVES: The right radial (RR) approach has been incorporated into daily clinical practice as a valid alternative to the femoral (F) approach. The left radial (LR) approach is seldom used and few data are available from randomized studies comparing this approach with F and RR approaches. METHODS: We randomized 1005 consecutive patients referred to a tertiary-care hospital for cardiac catheterization to different approaches. Procedures were performed by three interventional cardiologists experienced in transradial catheterization. There were no exclusion criteria. The primary end-point was the percentage of procedures completed using the assigned approach. Secondary endpoints were the percentage completed in the absence of contraindications to any approach, the duration of the procedure, and the incidence of vascular complications. RESULTS: More procedures were completed with the F approach (LR, 71%; F, 92%; RR, 68%; P< .001). The success rate in the absence of contraindications to any approach (n=907) was greater with the F approach, with no difference between LR and RR approaches (LR, 80%; F, 96%; RR, 82%; P< .001). The canalization time was greater with the LR approach (P< .001), the time required for diagnosis was shorter with the F approach (P< .001) and compression was faster with the radial approach (P< .001). There was no difference in the total duration of diagnostic procedures (P=.22) or interventions (P=.9). The incidence of vascular complications was lower with the radial approach (P=.03). CONCLUSIONS: The left radial approach is as valid an alternative to the femoral approach as the right radial approach.
Abstract: INTRODUCTION AND OBJECTIVES: Dipyridamole stress perfusion cardiovascular magnetic resonance (CMR) is used to detect coronary artery disease (CAD). However, few data are available on the diagnostic value of the systolic dysfunction induced by dipyridamole. This study investigated whether the induction of systolic dysfunction supplements the diagnostic information provided by perfusion imaging in the detection of CAD. METHODS: Overall, 166 patients underwent dipyridamole CMR and quantitative coronary angiography, with CAD being defined as a stenosis > or =70%. Systolic dysfunction at rest, systolic dysfunction with dipyridamole, induced systolic dysfunction, and stress first-pass perfussion deficit (PD) and delayed enhancement were quantified. RESULTS: In the multivariate analysis, PD (hazard ratio [HR]=1.6; 95% confidence interval [CI], 1.33-1.91;P< .0001) and induced systolic dysfunction (OR=1.8; 95% CI, 1.18-2.28; P< .007) were independently associated with CAD and had a sensitivity and specificity of 92% and 62% and 43% and 96%, respectively. Patients were categorized as having no ischemia (Group 1), PD but no induced systolic dysfunction (Group 2), or induced systolic dysfunction irrespective of PD (Group 3). In Group 3, the prevalence of CAD was higher than in Group 1 or 2 (96% vs. 22% and 79%, respectively; P=.001) and the risk of CAD was two-fold higher than in Group 2 (OR=2.34; 95% CI, 1.07-5.13; P=.034). Compared with Group 2, more hypoperfused segments were observed in Group 3 (6.2+/-2.6 vs. 7.4+/-3.4; P=.044), and more diseased vessels (1.4+/-1.0 vs. 1.8+/-0.9; P=.036). Adding induced systolic dysfunction to perfusion and clinical data improved the multivariate model's C-statistic for predicting CAD (0.81 vs. 0.87; P=.02). CONCLUSIONS: Combining induced systolic dysfunction with perfusion imaging increases the diagnostic accuracy of detecting CAD and enables patients with severe ischemia and a high probability of CAD to be identified.
Abstract: OBJECTIVE: To investigate the safety of discharge of patients deemed at low risk of cardiac events after evaluation in a chest pain unit and to determine the prognostic effect of revascularization of patients deemed at high risk. PATIENTS AND METHODS: The study population consisted of 1088 patients presenting at the emergency department from January 15, 2001, to September 1, 2006, with chest pain but without ischemia on electrocardiography or troponin elevation. Patients were managed by a chest pain unit protocol that included early exercise testing. Three groups of patients were distinguished: (1) those discharged after exercise testing (424 [39%]); (2) those in whom unstable angina was ruled out after in-hospital evaluation (208 [19%]); and (3) those in whom unstable angina was confirmed or not ruled out (456 [42%]). Of the 456 patients in group 3, 183 (40%) were revascularized at the index episode. The primary end point was the occurrence of myocardial infarction or death within 1 year. Adjustments were made for patient characteristics and a propensity score for revascularization (c statistic [0.83]). RESULTS: Groups 1 and 2 showed lower rates of the primary end point than group 3 (group 1: 7 [1.7%]; group 2: 1 [0.5%]; group 3: 62 [13.6%]; P=.001). In group 3, revascularization at the index episode did not reduce the primary end point in the univariate (22 [12%] vs 29 [11%]; P=.80) and multivariate (hazard ratio, 1.4; 95% confidence interval, 0.7-2.5; P=.40) analyses. In-hospital revascularization decreased the need for postdischarge revascularization (hazard ratio, 0.3; 95% confidence interval, 0.1-0.7; P=.01). CONCLUSION: Chest pain unit protocols are associated with safe patient discharge. Although early revascularizations may decrease the need for postdischarge revascularizations, they may not improve 1-year outcomes by reducing the number of myocardial infarctions or deaths.
Abstract: Risk stratification of patients with acute chest pain, non-diagnostic electrocardiogram and normal troponin (ACPneg) remains a challenge, partly because no standardized set of biomarkers with prognostic ability has been identified in this population. Lymphopenia has been associated with atherosclerosis progression and adverse outcomes in cardiovascular diseases; although its prognostic value in ACPneg is unknown. We sought to determine the relationship between the lymphocyte count obtained in the Emergency Department (ED) and the risk of the long-term all-cause mortality or myocardial infarction (MI) in patients with ACPneg.
Abstract: BACKGROUND: Hyperuricemia is a prevalent condition in chronic heart failure (CHF), describing increased oxidative stress and inflammation. Although there is evidence that serum uric acid (UA) predicts mortality in CHF, its role as a prognostic biomarker in acute heart failure (AHF) has not yet been well assessed. The aim of this study was to determine if UA levels predict all-cause mortality. Additionally, as a secondary endpoint we sought the clinical predictors of UA serum level in this population. METHODS: We analyzed 560 consecutive patients with AHF admitted in a single university center. UA (mg/dl) was measured during early hospitalization. Patient survival status was followed up after discharge (median follow-up: 330 days). The independent association of UA level with all-cause mortality was analyzed using Cox regression analysis. RESULTS: During follow-up 165 (29.5%) deaths were identified. Patients with UA levels above the median value (>or=7.7 mg/dl) exhibited higher mortality rates (21.1 vs. 37.9%; p<0.001). In multivariable analysis, after adjusting for recognized prognostic factors and potential confounders, UA>or=7.7 mg/dl and per change in 1 mg/dl of UA was associated with an increased risk of mortality (HR 1.45, CI 95%=1.03-2.44; p=0.03 and HR 1.08, CI 95%=1.01-1.15; p=0.03, respectively). CONCLUSION: UA serum levels is an independent predictor of all-cause mortality in an unselected patients admitted with AHF.
Abstract: The association of the temporal evolution of cardiac necrosis marker release with cardiovascular magnetic resonance-derived microvascular perfusion after ST-elevation myocardial infarction is unknown.
Abstract: OBJECTIVES: To evaluate the prognostic value of a comprehensive cardiac magnetic resonance (CMR) assessment soon after a first ST-segment elevation myocardial infarction (STEMI). BACKGROUND: CMR allows for a simultaneous assessment of wall motion abnormalities (WMA), WMA with low-dose dobutamine (WMA-dobutamine), microvascular obstruction, and transmural necrosis. This approach has been proven to be useful to predict late systolic recovery soon after STEMI. Its prognostic value and the relative prognostic weight of these indexes are not well-defined. METHODS: We studied 214 consecutive patients with a first STEMI treated with thrombolytic therapy or primary angioplasty discharged from hospital. In the first week (7 +/- 1 day after infarction), with CMR we determined the extent (number of segments) of WMA, WMA-dobutamine, microvascular obstruction, and transmural necrosis. RESULTS: During a median follow-up of 553 days, 21 major adverse cardiac events (MACE) including 4 cardiac deaths, 6 nonfatal myocardial infarctions, and 11 readmissions for heart failure were documented. The MACE was associated with a larger extent of WMA (8 +/- 4 segments vs. 5 +/- 3 segments, p < 0.001), WMA-dobutamine (6 +/- 4 segments vs. 4 +/- 3 segments, p = 0.004), microvascular obstruction (3 +/- 3 segments vs. 1 +/- 2 segments p <0.001), and transmural necrosis (7 +/- 3 segments vs. 3 +/- 3 segments, p < 0.001). In a complete multivariate analysis that included baseline characteristics, electrocardiogram, biomarkers, angiography, ejection fraction, left ventricular volumes, and all CMR indexes, WMA/segment (hazard ratio: 1.29 [95% confidence interval: 1.11 to 1.49], p = 0.001) and the extent of transmural necrosis/segment (hazard ratio: 1.30 [95% confidence interval: 1.12 to 1.51], p < 0.001) were the only independent prognostic variables. CONCLUSIONS: A comprehensive CMR assessment is useful for stratifying risk soon after STEMI, but only the extent of systolic dysfunction and of transmural necrosis provide independent prognostic information.
Abstract: Low lymphocyte count (LLC), a surrogate for inflammation, has emerged as a potential risk factor for cardiovascular outcomes, especially new ischemic events. To identify patients with non-ST segment elevation acute coronary syndromes (NSTEACS) who benefit from an invasive revascularization strategy remains a challenge. We sought to determine if patients with high-risk NSTEACS who exhibited LLC have a greater reduction in long-term post-discharge myocardial infarction (MI) when managed under a revascularization invasive strategy (RIS) as compared with conservative strategy (CS).
Abstract: INTRODUCTION AND OBJECTIVES: Occasionally, coronary arteries without significant stenosis are observed during invasive treatment of acute non-ST-elevation myocardial infarction (NSTEMI). The aim was to investigate predictive factors and prognosis in these patients. METHODS: The study involved 504 patients admitted for NSTEMI who underwent cardiac catheterization. The primary end-point was the observation of coronary arteries without significant stenosis, and the secondary end-point was death or myocardial infarction within a median of 3 years. In evaluating the secondary end-point, a control group of 160 patients with a normal troponin level and no significant coronary artery stenosis who were admitted for chest pain during the same period was included. RESULTS: Overall, 64 patients (13%) had coronary arteries without significant lesions. The predictors were: female sex (odds ratio [OR]=6.6; P=.0001), age <55 years (OR=3.0; P=.001), and the absence of diabetes (OR=2.4, P=.02), previous antiplatelet treatment (OR=3.9, P=.007) or ST-segment depression (OR=2.4, P=.008). The composite variable of female sex plus at least two additional predictive factors had a specificity of 85% and a sensitivity of 53% for coronary angiography showing no significant stenosis. The absence of coronary artery stenosis decreased the probability of death or myocardial infarction during follow-up (hazard ratio=0.3, 95% confidence interval, 0.2-0.9; P=.03). Among all patients without significant stenosis (n=224), there was no difference in the event rate between those with elevated and normal troponin levels. CONCLUSIONS: In NSTEMI, female sex, age <55 years and the absence of diabetes, previous antiplatelet treatment or ST-segment depression were all associated with coronary angiography showing no significant stenosis. The long-term prognosis in these patients was good.
Abstract: INTRODUCTION AND OBJECTIVES: The presence of microvascular obstruction after ST-segment elevation acute myocardial infarction is associated with a poor outcome. The pathophysiology of this process has not been fully defined. The aim of this study was to investigate the relationship between post-reperfusion lymphopenia and microvascular obstruction. METHODS: This prospective study involved 212 patients with a first ST-segment elevation acute myocardial infarction who underwent reperfusion with thrombolytic agents or primary angioplasty and who had an open infarct-related artery. Serial measurements of lymphocyte, neutrophil and monocyte counts were taken. Cardiac magnetic resonance was used to detect microvascular obstruction during the first week after the infarction. Imaging was repeated 6 months after infarction. RESULTS: Microvascular obstruction was observed in 67 patients (32%). A post-reperfusion lymphocyte count <1800 cells/ml was associated with a higher risk of microvascular obstruction (44% versus 20%; P< .001) as well as with a low left ventricular ejection fraction and large left ventricular volumes (P< .05). After adjustment for baseline characteristics, ECG findings, necrosis marker levels and angiographic variables, multivariate analysis showed that a post-reperfusion lymphocyte count <1800 cells/ml was independently associated with an increased risk of microvascular obstruction (odds ratio=3.2; 95% confidence interval 1.6-6.3; P< .001). CONCLUSIONS: In ST-segment elevation myocardial infarction, post-reperfusion lymphopenia is an early and powerful predictor of the presence of microvascular obstruction. The pathophysiological and therapeutic implications of this association require further study.
Abstract: The role of the angiotensin converting enzyme (ACE) gene on the result of thrombolysis at the microvascular level has not been addressed so far. We analyzed the implications of the insertion/deletion (I/D) polymorphism of the ACE gene on the presence of abnormal cardiovascular magnetic resonance (CMR)-derived microvascular perfusion after ST-segment elevation myocardial infarction (STEMI).
Abstract: INTRODUCTION AND OBJECTIVES: The aims of the study were to characterize myocardial edema after ST-elevation acute myocardial infarction using cardiac magnetic resonance imaging and to investigate its impact on ventricular function and its subsequent evolution. METHODS: In total, 134 patients admitted to hospital for a first ST-elevation myocardial infarction who had a patent infarct-related artery underwent cardiac magnetic resonance imaging. Cine images (at rest and with low-dose dobutamine) and edema, perfusion and viability images were acquired. Imaging was repeated after 6 months. RESULTS: In the first week after infarction, edema was detected in at least one segment in 96.6% of patients (4+/-2.1 segments per patient). Extensive edema (>/=4 segments) was associated with large ventricular enddiastolic and end-systolic volumes (P< .0001), a small left ventricular ejection fraction at rest (P=.001) and with low-dose dobutamine (P=.006), a large number of segments showing hypoperfusion (P=.001) or microvascular obstruction (P=.009), a more extensive infarct (P=.017) and greater transmural extent of the infarct (P=.003). The association between the presence and extent of edema during the first week and functional, perfusion and viability variables was still observable after 6 months. No patient exhibited edema at 6 months. CONCLUSIONS: Cardiac magnetic resonance imaging was useful for characterizing the myocardial edema that occurred after ST-elevation acute myocardial infarction. Extensive edema was associated with poor left ventricular characteristics. Edema was a transitory phenomenon that vanished within 6 months.
Abstract: OBJECTIVE: To determine the prognostic and therapeutic implications of stress perfusion cardiovascular magnetic resonance (CMR) on the basis of the ischaemic cascade. SETTING: Single centre study in a teaching hospital in Spain. PATIENTS: Dipyridamole stress CMR was performed on 601 patients with ischaemic chest pain and known or suspected coronary artery disease. On the basis of the ischaemic cascade, patients were categorised in C1 (no evidence of ischaemia, n = 354), C2 (isolated perfusion deficit at stress first-pass perfusion imaging, n = 181) and C3 (simultaneous perfusion deficit and inducible wall motion abnormalities, n = 66). CMR-related revascularisation (n = 102, 17%) was defined as the procedure prompted by the CMR results and carried out within the next three months. RESULTS: During a median follow-up of 553 days, 69 major adverse cardiac events (MACE), including 21 cardiac deaths, 14 non-fatal myocardial infarctions and 34 admissions for unstable angina with documented abnormal angiography were detected. In non-revascularised patients (n = 499), the MACE rate was 4% (14/340) in C1, 20% (26/128) in C2 and 39% (12/31) in C3 (adjusted p value = 0.004 vs C2 and <0.001 vs C1). CMR-related revascularisation had neutral effects in C2 (20% vs 19%, 1.1 (0.5 to 2.4), p = 0.7) but independently reduced the risk of MACE in C3 (39% vs 11%, 0.2 (0.1 to 0.7), p = 0.01). CONCLUSIONS: Dypiridamole stress CMR is able to stratify risk on the basis of the ischaemic cascade. A small group of patients with severe ischaemia-simultaneous perfusion deficit and inducible wall motion abnormalities-are at the highest risk and benefit most from MACE reduction due to revascularisation.
Abstract: Revascularization strategy in the setting of non-ST-segment acute coronary syndromes remains a controversy. Evidence obtained from clinical trials, generally performed in selected patients, reveals heterogeneous and insufficient results when a routine invasive revascularization strategy and a conservative one are compared. The conflicting results among trials are due to differences in: a) baseline characteristics; b) methodology and protocols applied and; c) objectives and outcomes definitions. Although present guidelines recommend that a routine invasive strategy should be used in high risk non-ST-segment elevation acute coronary syndromes, there is no consistent evidence that supports this approach. In order to reach definitive conclusions, further randomized studies should: a) expand inclusion criteria to highest risk populations and; b) standardize the methodology, objectives and outcome definitions.
Abstract: BACKGROUND AND OBJECTIVE: The relation between left ventricular ejection fraction (LVEF) and prognosis in patients with heart failure is controversial. The aim of this study was to determine the relation of LVEF in long-term mortality and readmissions for acute heart failure in a non-selected population of patients admitted with acute heart failure (AHF). PATIENTS AND METHOD: We included 507 patients admitted consecutively for AHF in a cardiology department of a single-centre. LVEF was assessed with transthoracic echocardiography during hospitalization. All-cause mortality and readmission for AHF were selected as primary and secondary endpoints, respectively. The independent association between LVEF and endpoints was assessed with traditional Cox regression analysis for all-cause mortality and Cox regression for competing risks for readmission for AHF. RESULTS: 47% of patients exhibited LVEF > or = 50%. During a median follow-up of one year, 151 (30%) deaths and 139 (27%) readmissions for AHF were observed. Mortality rates were higher in patients with LVEF < 50% (34 vs 25%; p = 0.028) and no differences were observed for readmissions for AHF (26 vs 29%, p = 0.510). In multivariate analysis, after adjustment for traditional risk factors, patients with LVEF < 50% did not show higher risk of mortality (hazard ratio [HR] = 1.08; 95% confidence interval [CI], 0.76-1.57; p = 0.645) or readmissions for AHF (HR = 1.00; 95% CI, 0.68-1.47; p = 1). CONCLUSIONS: Patients with preserved LVEF constitute a substantial proportion of patients with AHF, exhibiting similar mortality and readmissions risks compared with patients with depressed LVEF.
Abstract: OBJECTIVE: To investigate the combination of clinical data, exercise testing and biomarkers for the evaluation of patients with chest pain without ST-segment deviation or troponin elevation. DESIGN: Prospective cohort design. SETTTING: Two teaching hospitals in Spain. PATIENTS: 422 patients presenting to the emergency department were studied. Leukocyte count, C-reactive protein (CRP), pregnancy-associated plasma protein A (PAPP-A) and N-terminal pro-brain natriuretic peptide (NT-proBNP) were determined. A validated clinical risk score (number of points according to pain characteristics and risk factors) was used for clinical evaluation and early exercise testing was performed. MAIN OUTCOME MEASURES: Adverse events (death, myocardial infarction or revascularisation) during a median 60 weeks follow-up. RESULTS: By receiver operating characteristic curve analysis, the association between death or myocardial infarction and adverse events was not significant with leukocyte count (p = 0.3, p = 0.3) or CRP (p = 0.5, p = 0.8), was borderline significant with PAPP-A (p = 0.07, p = 0.04) and strongly significant with NT-pro-BNP (p = 0.0001, p = 0.0001). By Cox regression including clinical risk score, exercise testing result and biomarkers, exercise testing was the independent predictor of revascularisation (p = 0.0001), whereas risk score (p = 0.03) and NT-proBNP (p = 0.0004) predicted death or myocardial infarction. The inclusion of NT-proBNP improved the accuracy of the model for death or myocardial infarction (C-statistic 0.84 versus 0.76, p = 0.01). The combination of clinical score and NT-proBNP afforded the stratification in high (17.2%, p = 0.0001), intermediate (5.3%) and low (1.1%) risk categories of death or myocardial infarction. CONCLUSIONS: NT-proBNP provides incremental prognostic information above that given by clinical history and exercise testing in patients with chest pain without ST-segment deviation and negative troponin.
Abstract: The prognostic value of brain natriuretic peptide (BNP) measurement in patients with acute heart failure is not well understood. The aim of this study was to investigate the relationship between the BNP level and mortality and readmission for acute heart failure. We studied 569 consecutive patients who were admitted with a diagnosis of acute heart failure. The BNP level was measured after the patient became clinically stable. The relationship between the BNP level and mortality was assessed by Cox regression analysis, and the relationship with readmission, by competing risks regression analysis. During a median follow-up period of 9 (range, 3-18) months, 156 deaths (27.4%) and 140 readmissions (24.6%) occurred. Multivariate analysis demonstrated a positive linear association between the risk of death and the BNP quintile. In contrast, the BNP level did not predict readmission for acute heart failure, mainly because of the effect of death as a competing outcome.
Abstract: Neutrophil to lymphocyte ratio (N/L) has been associated with poor outcomes in patients who underwent cardiac angiography. Nevertheless, its role for risk stratification in acute coronary syndromes, specifically in patients with ST-segment elevation myocardial infarction (STEMI), has not been elucidated. We sought to determine the association of N/L maximum value (N/L max) with mortality in the setting of STEMI and to compare its predictive ability with total white blood cell maximum count (WBC max). We analyzed 515 consecutive patients admitted with STEMI to a single university center. White blood cells (WBC) and differential count were measured at admission and daily for the first 96 hours afterward. Patients with cancer, inflammatory diseases, or premature death were excluded, and 470 patients were included in the final analysis. The association between N/L max and WBC max with mortality was assessed by Cox regression analysis. During follow-up, we registered 106 deaths (22.6%). A positive trend between mortality and N/L max quintiles was observed; 6.4%, 12.4%, 11.7%, 34%, and 47.9% of deaths occurred from quintiles 1 to 5 (p <0.001), respectively. In a multivariable setting, after adjusting for standard risk factors, patients in the fourth (Q4 vs Q1) and fifth quintile (Q5 vs Q1) showed the highest mortality risk (hazard ratio 2.58, 95% confidence interal 1.06 to 6.32, p = 0.038 and hazard ratio 4.20, 95% confidence interal 1.73 to 10.21, p = 0.001, respectively). When WBC max and cells subtypes were entered together, N/L max remained as the only WBC parameter; furthermore, the model with N/L max showed the most discriminative ability. In conclusion, N/L max is a useful marker to predict subsequent mortality in patients admitted for STEMI, with a superior discriminative ability than total WBC max.
Abstract: Decision making and risk stratification for patients with acute chest pain, nondiagnostic electrocardiogram results, and normal troponin levels are challenging. The aim of this study was to optimize the clinical history for the evaluation of these patients. A total of 1,011 patients presenting to an emergency department were included. The following data were collected: clinical presentation (pain characteristics and number of pain episodes), coronary risk factors, previous ischemic heart disease, and extracardiac vascular disease (peripheral artery disease, stroke, or creatinine >1.4 mg/dl). Two different predictive models were calculated according to the end points: model 1 for 1-year major events (death or myocardial infarction) and model 2 for 30-day cardiac events (major events or revascularization). For 1-year major events, model 1 showed optimal discrimination capacity (C statistic = 0.80), which was significantly better than that of model 2 (C statistic = 0.77, p = 0.04). With respect to 30-day cardiac events, however, discrimination was lower in the 2 models, without differences between them (C statistic = 0.74 vs 0.75, p = NS). Using model 1, a large low-risk subgroup with <3 predictive variables could be defined, including 442 patients (44% of the total population) with a 1.4% rate of 1-year major events; however, the incidence of 30-day cardiac events (8%) was not negligible, mainly because of revascularizations. In conclusion, in patients with acute chest pain of uncertain coronary origin, clinical predictive models afford good risk stratification for long-term major events. Short-term outcomes, including revascularization, however, are not predicted as well. Therefore, ancillary tools, such as noninvasive stress tests, should be implemented for decision making at initial hospitalization or discharge.
Abstract: Recently, the theory that hyperinflammation is the body's primary response to potent stimulus has been challenged. Indeed, a deregulation of the immune system could be the cause of multiple organ failure. So far, clinicians have focused on the last steps of the inflammatory cascade. However, little attention has been paid to lymphocytes, which play an important role as strategists of the inflammatory response. Experimental evidence suggests a crucial role of T lymphocytes in the pathophysiology of atherosclerosis and acute myocardial infarction (AMI). In summary, from the bottom of an imaginary inverted pyramid, a few regulatory T-cells control the upper parts represented by the wide spectrum of the inflammatory cascade. In AMI, a loss of regulation of the inflammatory system occurs in patients with a decreased activity of regulatory T-cells. As a consequence, aggressive T-cells boost and anti-inflammatory T-cells drop. A pleiotropic proinflammatory imbalance with damaging effects in terms of left ventricular performance and patient outcome is the result of this uncontrolled immune response. It is needed to unravel the thread of the inflammatory cells to better understand the pathophysiology as well as to open innovative therapeutic options in AMI.
Abstract: BACKGROUND: The objective of this study was to evaluate the simultaneous evolution of 5 cardiovascular magnetic resonance-derived myocardial viability indexes. METHODS: We studied 72 patients with a first ST-elevation myocardial infarction and sustained TIMI 3 flow. In the first week and in the sixth month of the study, using cardiovascular magnetic resonance imaging, we determined wall thickening (WT) and the following viability indexes: wall thickness, WT with low-dose dobutamine, microvascular perfusion in first-pass imaging, microvascular obstruction in late-enhancement imaging, and transmural extent of necrosis. RESULTS: In 250 dysfunctional segments, the evolution outcomes for the viability indexes were as follows: (1) wall thickness thinned (8.6 +/- 2.9 versus 7.7 +/- 3 mm, P < .001), (2) WT with low-dose dobutamine improved (1.5 +/- 1.9 versus 2.6 +/- 3 mm, P < .001), (3) the number of segments showing abnormal microvascular perfusion in first-pass imaging decreased (22% versus 7%, P < .001), (4) the number of segments showing microvascular obstruction in late-enhancement imaging decreased (14% versus 2%, P < .001), and (5) the transmural extent of necrosis remained stable throughout follow-up (56% +/- 40% versus 54% +/- 39%, P = .3). CONCLUSIONS: After reperfused myocardial infarction, dynamic changes in wall thickness, contractile reserve, microvascular perfusion, and microvascular obstruction take place. These changes may affect their accuracy as viability indexes early after myocardial infarction. The transmural extent of necrosis does not vary, however.
Abstract: Antiphospholipid syndrome (APS) is a cause of infertility and fetal loss. Ovarian stimulation can induce previously unknown APS. Ovarian hyperstimulation syndrome (OHS) is uncommon but potentially life-threatening, as well as catastrophic APS. A woman that simultaneously developed a severe OHS and a catastrophic APS is described in this paper. Both entities produced thrombotic cardiac and brain thrombosis. A peculiar mechanism of cardiac ischemia is also described. In spite of the life-threatening risk of this situation, the indication for preventive anti-aggregation and/or anticoagulation is not clear.
Abstract: BACKGROUND: Studies evaluating the role of N-acetylcysteine in patients undergoing coronary angiography have yielded inconsistent data. Less is known about patients with normal renal function at baseline. METHODS: Prospective, double-blind, placebo-controlled trial to determine the benefits of intravenous N-acetylcysteine as an adjunct to hydration in this kind of population. Patients were randomly assigned to receive either N-acetylcysteine (600 mg twice daily) or placebo, in addition to 0.45% intravenous saline. The primary end point was development of contrast-induced nephropathy, defined as an acute increase in the serum creatinine concentration > or = 0.5 mg/dl and/or > 25% increase above baseline level at 48 h after contrast dosing. RESULTS: A total of 216 patients were studied: N-acetylcysteine = 107 and placebo = 109. Treatment groups were similar with respect to baseline clinical characteristics. Overall incidence of contrast-induced nephropathy was 10.2%, 10.3% in the N-acetylcysteine group and 10.1% in the placebo group. Furthermore, no significant differences were observed when considering the non-diabetic population, although there was a trend towards a protective effect of N-acetylcysteine in the subgroup of 47 patients with both hypertension and diabetes. There were no significant changes in serum urea nitrogen concentrations. The incidence of in-hospital adverse clinical events was low: no patient with contrast-induced nephropathy required dialysis, the median Coronary Unit stay was 4.5 vs. 4 days, and the mortality rate was 2.8% vs. 4.6% in the N-acetylcysteine and placebo groups, respectively (p=NS). CONCLUSIONS: The prophylactic administration of intravenous N-acetylcysteine provides no additional benefit to saline hydration in high-risk coronary patients with normal renal function.
Abstract: Patients with non-ST-elevation chest pain constitute a heterogeneous population. Our aim is to compare the outcome of patients with chest pain, non-ST-segment deviation, and normal troponin, categorized using a risk score, with that of patients with ST depression or troponin increase. A total of 1,449 patients with non-ST-elevation chest pain were evaluated. A validated risk score (using pain characteristics and risk factors) was applied to patients without ST depression or troponin increase. Accordingly, 4 risk categories were defined: group 1, no troponin increase, no ST depression, and risk score <3 points (n = 633); group 2, no troponin increase, no ST depression, but risk score > or = 3 points (n = 158); group 3, no troponin increase, ST depression (n = 106); and group 4, troponin increase (n = 552). Median follow-up was 26 months, and the end point was death or myocardial infarction. Group 1 experienced fewer events at 30 days (1.7%, p = 0.0001) and long-term follow-up (9.4%, p = 0.0001) than groups 2 (10.8% and 26%), 3 (6.6% and 30%), and 4 (9.5% and 25%). Kaplan-Meier curves overlapped among groups 2, 3, and 4, whereas group 1 showed a flatter curve (p = 0.0001). Using multivariate analysis, risk group (group 1 vs remaining groups) predicted 30-day (p = 0.0003) and long-term (p = 0.0001) outcome. There were no differences among groups 2, 3, and 4. In conclusion, application of a risk score to patients without troponin increase or ST deviation identified a high-risk group with prognosis similar to that of patients with troponin increase or ST depression and affords a practical classification for the full spectrum of non-ST-elevation chest pain.
Abstract: BACKGROUND: The optimal revascularization strategy for non-ST elevation acute coronary syndromes (NSTE-ACS) remains controversial, especially in a real world context. The objective of this work was to assess differences at 1 year in all-cause mortality and the composite endpoint of mortality or acute myocardial infarction (MI) between two management strategies for NSTE-ACS: a conservative strategy (CS) versus a routine invasive strategy (RIS). METHODS: Of 799 consecutive patients admitted to our institution, 369 were treated with CS (from January 2001 to October 2002); 430 patients admitted with the same diagnosis were treated with RIS (from November 2002 to November 2004). A propensity score (PS) matched sample was created and included 694 patients (87% of the original population). The event rate was compared between each paired member of the PS-matched sample, one receiving RIS and the other CS, and their differences were tested by Cox proportional analysis. RESULTS: No significant differences in baseline characteristics were noted between the two management cohorts. By design, the rate of in-hospital catheterization and revascularization procedures increased in RIS compared with CS. The mortality rate was lower, but not significant, in RIS (HR: 0.76, 95% CI=0.51-1.11; p=0.155). For the composite of death or MI, RIS showed a relative risk reduction of 29% (HR: 0.71, 95% CI=0.53-0.94); p=0.018) compared with CS, differences that become non-significant (p=0.680) if we adjust for differences in rate of revascularization procedures and changes in medication prescription. CONCLUSIONS: RIS was associated with a 1-year lower risk of the combined endpoint of all-cause death and MI in patients with NSTE-ACS, attributable to changes in frequency of revascularization procedures and in medical treatment.
Abstract: INTRODUCTION AND OBJECTIVES: It has been suggested that abnormal perfusion as derived from cardiovascular magnetic resonance imaging (CMR) is a transient dysfunction of microcirculation after myocardial infarction (MI) with TIMI 3 flow. We hypothesized that defects of myocardial perfusion may persist during the following months. METHODS: Forty-seven patients with MI and sustained TIMI 3 flow underwent intracoronary myocardial contrast echocardiography (MCE) 1 week and 6 months after infarction. Abnormal perfusion by MCE was regarded as > 1 hypoperfused segment. RESULTS: At the first week, 20 patients showed abnormal perfusion as derived from MCE. At the sixth month 10 patients displayed chronic abnormal perfusion. These patients had greater left ventricular volumes and lower ejection fraction at the sixth month by CMR (P< .01). CONCLUSIONS: MCE detects perfusion defects which can persist in chronic phase--this relates to more severe systolic dysfunction and increased left ventricular volumes.
Abstract: OBJECTIVES: We evaluated the prognostic value of dipyridamole stress cardiovascular magnetic resonance imaging (CMR) in patients with chest pain and known or suspected coronary artery disease. BACKGROUND: Stress perfusion CMR has been incorporated in daily practice. Data on its prognostic value are preliminary. METHODS: Dipyridamole stress CMR was performed in 420 patients with chest pain and known or suspected coronary artery disease. The extent (number of segments according to the 17-segment model) of abnormal wall motion at rest (AWM-rest), abnormal wall motion with dipyridamole (AWM-D), perfusion deficit (at stress first-pass perfusion imaging), and delayed enhancement (at late enhancement imaging) were analyzed. RESULTS: During a median follow-up of 420 days, 41 major adverse cardiac events (MACE), including 9 cardiac deaths, 14 nonfatal myocardial infarctions, and 18 readmissions for unstable angina with documented abnormal angiography, were documented. The MACE were more frequent in patients with significant (>1 segment) AWM-rest (22% vs. 5%), AWM-D (21% vs. 4%), perfusion deficit (17% vs. 5%), and delayed enhancement (20% vs. 6%; p <0.0001 in all cases). In a multivariate analysis adjusted for baseline characteristics, the extent of AWM-D was independently related to MACE (hazard ratio [HR] 1.15 [95% confidence interval (CI) 1.06 to 1.24] per segment; p = 0.0006) and to major events (cardiac death or nonfatal myocardial infarction; HR 1.15 [95% CI 1.05 to 1.26] per segment; p = 0.002). CONCLUSIONS: Dipyridamole stress CMR is useful for predicting the outcome of patients with known or suspected coronary artery disease.
Abstract: OBJECTIVE: To assess whether circulating levels of carbohydrate antigen 125 (CA125) predict subsequent 6-month all-cause mortality in patients after the index hospitalisation for acute heart failure (HF). DESIGN AND SETTING: Prospective cohort study at a single teaching centre in Spain. METHODS: 529 consecutive patients with acute HF admitted in a single university centre were analysed. In addition to the traditional clinical information, CA125 (U/ml) was measured during the early course of hospitalisation. The independent association between baseline CA125 and mortality was assessed with Cox regression analysis. The follow-up was limited to 6 months. RESULTS: 349 (66%) patients showed serum levels of CA125 >35 U/ml (established cut-off point value). At a 6-month follow-up, 89 (16.8%) deaths were identified. A positive trend between mortality and CA125 quartiles was observed; 3.8%, 15.2%, 22% and 26.5% of deaths occurred from quartile 1 to 4 of CA125 (p<0.001). Likewise, a monotonic, ascending trend in the risk ratios was estimated from the multivariable Cox model. Compared with the first quartile of CA125, the HRs (95% CI) for the second, third and fourth quartiles were 3.25 (1.20 to 8.79), 4.91 (1.88 to 12.85) and 8.41 (3.24 to 21.79), respectively. CONCLUSIONS: Serum levels of CA125 obtained in patients admitted with a diagnosis of acute HF was shown to be an independent predictor of mortality up to the 6-month follow-up.
Abstract: INTRODUCTION AND OBJECTIVES: Advanced diabetes can be associated with diffuse coronary artery disease that is difficult to treat by revascularization. We studied angiographic findings and disease progression in patients with advanced diabetes (either insulin-dependent or taking antidiabetic drugs for >5 years) and non-ST-elevation acute coronary syndrome who were being treated using an invasive strategy. METHODS: The study included 141 patients. The extent of the coronary artery disease was quantified using a score derived from a 29-segment coronary angiogram. The composite endpoint was death, myocardial infarction, or readmission for unstable angina within one year of follow-up. RESULTS: The extent of coronary disease was associated with Killip class >1 at admission (P=.02), previous coronary surgery (P=.003), ST-segment depression (P=.01), and a poor ejection fraction (P=.0001). The more of these factors present (i.e., 0, 1, 2 or 3 factors), the greater the extent of the coronary disease (i.e., 12 [7], 15 [7], 21 [6] and 23 [7] points, respectively; P=.0001). There was a significant difference between patients with > or =2 factors and those with P=.02), even after adjustment using a revascularization propensity score (C-index 0.80). CONCLUSIONS: In patients with non-ST-elevation acute coronary syndrome and advanced diabetes being managed using an invasive strategy, a history of coronary surgery, ST-segment depression and poor left ventricular function were all associated with the presence of diffuse coronary artery disease. Clinical follow-up indicated that revascularization during hospital admission improved prognosis.
Abstract: INTRODUCTION AND OBJECTIVES: Quantification of intravascular ultrasound (IVUS) images is essential in ischemic heart disease and interventional cardiology. Manual analysis is very slow and expensive. We describe an automated computerized method of analysis that requires only minimal initial input from a specialist. METHODS: This study was carried out by interventional cardiologists and biomedical engineers working in close collaboration. We developed software in which it was necessary only to identify the media-adventitia boundary in a few images taken from the whole sequence. A three-dimensional reconstruction was then generated from each sequence, from which measurements of areas and volumes could be derived automatically. In total, 2300 randomly selected images from video sequences of 11 patients were analyzed. RESULTS: Results obtained using the proposed method differed only minimally from those obtained with the manual method: for vessel area measurements, the variability was 0.08 (0.07) (mean absolute error [standard deviation] normalized to the actual value; this corresponds to an error of 0.08 mm(2) per mm(2) of vessel area); for lumen area, 0.11 (0.11) (normalized), and for plaque volume, 0.5 (0.3) (normalized). Regions with severe lesions (<4 mm(2)) were correctly identified in more than 90% of cases. Specialist time needed for each reconstruction was 10 (8) minutes (vs 60 [10] minutes for manual analysis; P< .0001). CONCLUSIONS: The computerized method used dramatically reduced the time and effort needed for IVUS sequence analysis, and the automated measurements obtained were very promising.
Abstract: We investigated whether the result of early exercise testing yields prognostic information in addition to that afforded by a clinical risk score in patients who present with chest pain in the emergency department. The study group consisted of 340 patients without preexisting evidence of myocardial ischemia. A clinical risk score was calculated. Primary (mortality or myocardial infarction) and secondary (mortality, myocardial infarction, or rehospitalization due to unstable angina) end points at 1 year were defined. Patients with a positive exercise test result underwent invasive management. Frequencies of primary (7.4% vs 2.1%, p = 0.06) and secondary (9.3% vs 2.8%, p = 0.04) end points and risk score (1.6 +/- 1.0 vs 1.0 +/- 0.9 points, p = 0.0001) were higher in patients with a positive exercise test result. However, in multivariate analysis, clinical risk score was the only independent predictor for the primary (hazard ratio 2.0, 95% confidence interval 1.2 to 3.2, p = 0.004) and secondary (hazard ratio 1.9, 95% confidence interval 1.2 to 2.9, p = 0.003) end points. In conclusion, if a policy of invasive management is implemented for patients with positive exercise test results, the clinical risk score constitutes the main prognostic predictor of 1-year outcome.
Abstract: PURPOSE: The present study was designed to assess, 1) the independent prognostic effect of renal dysfunction on all-cause mortality in the setting of acute myocardial infarction with ST-segment elevation (STEMI), and 2) to determine if such effect varies based upon the presence of heart failure (HF) on admission. METHODS: 549 consecutive patients admitted with the diagnosis of STEMI were prospectively recruited in a teaching hospital in Spain. Serum creatinine (sCr) and glomerular filtration rate (GFR) were obtained on admission, together with other relevant information used for risk stratification. The independent effect of sCr and GFR on long-term mortality was determined by Cox regression analysis. Main outcome was all-cause mortality, with a median follow-up of 1 year. RESULTS: In a multivariate analysis the degree of renal impairment was a strong predictor of mortality in patients without clinical evidence of HF at admission (HR=1.15; 95% CI 1.10 to 1.19 and HR=1.58; 95% CI 1.30 to 1.81) for sCr (per 0.1 mg/dl) and GFR (per decreasing 10 ml/min/1.73 m2), respectively. In the group with HF, the effect was less pronounced (HR=1.03; 95% CI 1.01 to 1.04 and HR=1.17; 95% CI 1.02 to 1.37) for sCr and GFR, respectively. CONCLUSIONS: In the setting of STEMI, renal dysfunction estimates showed a differential prognostic effect depending on HF status, with a greater impact seen in patients without clinical evidence of HF.
Abstract: INTRODUCTION AND OBJECTIVES: Cardiovascular disease is the main cause of death in patients with kidney failure. Moreover, the presence of impaired renal function is an important prognostic factor in patients with heart disease, and is a determinant of outcome during follow-up. The main aim was to investigate the relationship between kidney failure at admission and one-year mortality in patients with non-ST-elevation acute coronary syndrome. PATIENTS AND METHOD: We studied 1029 consecutive patients admitted to our institution. The serum creatinine level and glomerular filtration rate were determined at admission, and classical risk factors and biochemical markers were assessed. The primary endpoint was all-cause mortality at one year. RESULTS: Patients who died were older, more frequently had a history of diabetes or coronary artery disease, were more likely to have heart failure at admission, had higher troponin-I, myoglobin and creatinine levels, and were less likely to have dyslipidemia or to be a smoker. Multivariate analysis showed that the independent predictors of all-cause mortality at one year were age, diabetes, troponin-I level, Killip class > 1, male gender, creatinine level, and glomerular filtration rate. There was a linear correlation between increased risk and creatinine level. CONCLUSIONS: Creatinine level at admission is one of the most important covariates in early prognostic stratification in these patients. A high serum creatinine level (or a low glomerular filtration rate) increases the probability of death due to all causes. The serum creatinine level is, moreover, an inexpensive, easy-to-use, and widely available prognostic marker.
Abstract: AIMS: We aimed to characterize the extension of Q-waves after a first ST-segment elevation myocardial infarction using body surface map (BSM) and its relationship with infarct size quantified with cardiovascular magnetic resonance imaging (CMR). METHODS AND RESULTS: Thirty-five patients were studied 6 months after a first ST-segment elevation myocardial infarction (23 anterior, 12 inferior). All cases had single-vessel disease and an open artery. The extension of Q-waves was analyzed by means of a 64-lead BSM. Infarct size was quantified with CMR. Absence of Q-waves in BSM was observed in 5 patients (14%), 2 of whom (40%) had >1 segment with transmural necrosis. Absence of Q-waves in 12-lead ECG was observed in 8 patients (23%), 7 of whom (87%) had >1 segment with transmural necrosis. Patients with inferior infarctions (n=12, 34%) showed a larger number of Q-waves in BSM (18+/-7.1 leads) than patients with anterior infarctions (n=23, 66%; 3.7+/-3.6 leads; p<0.0001). When the study group was analysed as a whole, the total number of Q-waves detected in BSM did not correlate with the number of necrotic segments (r=0.15; p=0.4). In anterior infarctions, a number of Q-waves >median (2 leads) was related to a higher number of necrotic segments (5.1+/-2.4 vs. 2+/-2.2 segments; p=0.004). The same was observed in inferior infarctions (median 20 leads: 3.5+/-1.9 vs. 1.2+/-1.2 segments; p=0.03). CONCLUSION: In a stable phase after a first ST-segment elevation myocardial infarction, absence of Q-waves does not mean non-transmural necrosis. Using BSM, extension of Q-waves is much higher in inferior infarctions; a separate analysis depending on infarct location is necessary. A major BSM-derived extension of Q-waves is related to larger infarct size both in anterior and in inferior infarctions.
Abstract: INTRODUCTION AND OBJECTIVES: An analysis was made of variability in the measurement of the angiographic index blush between a university hospital and an independent core laboratory, as well as its correlation with perfusion analyzed by intracoronary myocardial contrast echocardiography (MCE) and the ventricular function at the sixth month. METHODS: The study comprised 40 patients with a first ST-segment elevation myocardial infarction, single-vessel disease and open infarct-related artery. Perfusion was quantified by angiography (median fifth day, range 3-7) with blush in our laboratory and in an independent core laboratory. MCE was performed. Ejection fraction at the sixth month was determined with magnetic resonance imaging. RESULTS: We found a weak correlation (r=0.38) between both laboratories. In the comparison of blush measurements concordance was 80%, kappa=0.43 if normality was defined by blush 2-3; and concordance 55%, kappa=0.1 for blush 3. Neither perfusion analyzed by MCE (r= 0.23, P=.2) nor ejection fraction by resonance (r=0.20, P=.3) did correlate to blush. CONCLUSIONS: After infarction in patients with TIMI 3, variability is observed in blush measurements between a university hospital and an independent core laboratory, therefore it seems advisable to centralize blush measures in highly specialized core laboratories. A weak correlation was detected with perfusion analyzed by MCE and with late systolic function.
Abstract: BACKGROUND AND AIM: Studies performed on selected patients in other countries have shown that anemia is frequently associated with heart failure and results in a worse prognosis. We sought to determine the prognosis significance of hemoglobin/anemia in patients with acute heart failure which required management with hospital admission. MATERIAL AND METHODS: We analysed 412 patients diagnosed with acute heart failure as outlined in the criteria of the European Society of Cardiology (ESC). We measured hemoglobin within the first 24 hours and obtained demographic, clinical and biochemical variables. Anemia was defined in accordance with OMS criteria. The main variable was all-cause mortality. The association between all-cause mortality and hemoglobin/anemia was determined using the multiple regression Cox model. RESULTS: During follow-up (median six months) we observed 101 all-cause mortality events. In the multivariate analysis, hemoglobin was an independent predictive variable adjusted by covariates (HR 1.15, IC 95% [1.04-1.25], p = 0.014). Anemia (hemoglobin < 13 g/dL) was also found to be an independent predictive variable adjusted by covariates (HR 2.06, IC al 95% [1.28-3.33], p = 0.003). CONCLUSIONS: Hemoglobin and anemia (hemoglobin < 13 g/dL) are consistently associated with short-term, poorer survival in patients with acute heart failure.
Abstract: Little is known about the prognostic value of leukocyte count on admission for patients with chest pain. In total, 1,461 patients who presented to the emergency department with non-ST-segment elevation chest pain were studied by clinical history, electrocardiography, serial troponin I determination, and leukocyte count on admission. End points were 1-year mortality and major events (mortality or infarction). Overall patient distribution by quartiles of leukocyte count showed increased mortality (6%, 7%, 6%, and 17%, p = 0.0001) and major events (13%, 13%, 15%, and 24%, p = 0.0001) in the fourth quartile. After adjustment for other risk factors, the fourth quartile cut-off value (>10,000 cells/ml) predicted mortality (hazard ratio 2.0, 95% confidence interval 1.4 to 2.8, p = 0.0001) but not major events (p = 0.07). When analysis was performed to assess troponin status, in the subgroup with increased troponin (n = 634, 16% mortality), a leukocyte count >10,000 cells/ml was related to mortality (hazard ratio 2.2, 95% confidence interval 1.5 to 3.4, p = 0.0001). However, in the subgroup with normal troponin levels (n = 827, 4.2% mortality), there were no differences in mortality between patients with or without a leukocyte count >10,000 cells/ml (4.4% vs 4.2%, p = 0.8), with survival curves showing a tight overlap (p = 0.9). Further, in the subgroup with normal troponin levels, leukocyte count was not significantly different between patients with or without ST depression (7,969 +/- 2,171 vs 8,108 +/- 2,356 cells/ml, p = 0.6) and was not associated with mortality in patients with ST depression (p = 0.7). In conclusion, leukocyte count on admission is predictive of mortality in patients with chest pain and non-ST-segment elevation myocardial infarction. However, in the absence of myocardial necrosis, leukocyte count lacks prognostic value.
Abstract: BACKGROUND AND OBJECTIVE: There are few studies evaluating the effect of a previous history of hypertension on long term prognosis after an acute coronary syndrome, using the new definitions and incorporating new risk markers in the analysis. The aim of our study was to determinate if hypertensive patients differ from non-hypertensives in the epidemiological profile, clinical presentation, treatment prescribed at discharge and prognosis after admission with non ST segment elevation acute coronary syndrome. PATIENTS AND METHOD: A total of 1,029 consecutive patients admitted with high suspicion of non ST segment elevation acute coronary syndrome were evaluated. Prognostic variables were determined during admission (epidemiological and biochemical), as it was the discharge treatment. The primary endpoint was defined as all cause mortality at one year follow up. RESULTS: 65.8% (n = 677) of patients had hypertension. Hypertensive patients displayed a worst epidemiological and biochemical profile, and different discharge treatment. There were 139 (13.5%) deaths at one year follow up. The all cause mortality for non-hypertensive patients was 12.5% and for hypertensives 14.6% (p = NS). In the multivariate analysis (Cox regression) there were no differences in mortality between these groups. CONCLUSIONS: A previous history of hypertension is an important factor to explain differences in the presence of other risk factors or the treatment, but is not a mortality predictor.
Abstract: In recent years, numerous studies have validated the role of inflammation in the pathogenesis of atherosclerosis. Several of such studies have produced compelling evidence that inflammation participates in both, the initiation and perpetuation of the atherosclerotic process. Furthermore, epidemiological observations have found basal white blood cell (WBC) count is strongly associated with future cardiovascular disease (CVD), highlighting the participation of leukocytes in the pathogenesis of the ischemic damage that occurred during an acute coronary event, in particularly during the acute myocardial infarction (MI). Fundamentally, an acute MI triggers a systemic response to a necrotic insult characterized by leukocytosis and acute-phase protein synthesis. In this setting, elevated WBC count plays a central role in the reparative process that takes place to replace the necrotic tissue for collagen. In addition to be a proxy for the intensity of the peri-infarction inflammatory response, recent evidence has also shown that an elevated WBC counts, measured during the acute phase of MI, to be associated with adverse outcomes. This relationship holds true even when adjusting for classical prognostic variables some of which are surrogates for the extension of the infarcted-area. WBC count prognostic value in absence of necrosis marker elevation (like unstable angina), however, remains unclear and controversial. Additionally, and essentially due to its simplicity, cost-effectiveness and wide availability, WBC count has drawn the attention of researchers as a potential stratification tool in acute coronary syndromes (ACS). However, a formal comparison is needed between WBC count with other inflammatory markers such high-sensitive C-reactive protein to fully characterize its diagnostic accuracy.
Abstract: OBJECTIVE: To characterise the evolution of myocardial perfusion during the first 6 months after myocardial infarction by first-pass perfusion cardiovascular magnetic resonance imaging (CMR) and determine its significance. DESIGN: Prospective cohort design. SETTING: Single-centre study in a teaching hospital in Spain. PATIENTS: 40 patients with a first ST-elevation myocardial infarction, single-vessel disease and thrombolysis in myocardial infarction (TIMI) grade 3 flow (stent in 33 patients) underwent rest and low-dose dobutamine CMR 7 (SD 1) and 184 (SD 11) days after infarction. Microvascular perfusion was assessed at rest by visual assessment and quantitative analysis of first-pass perfusion CMR. Of the 640 segments, 290 segments subtended by the infarct-related artery (IRA) were focused on. RESULTS: Both 1 week and 6 months after infarction, segments with normal perfusion showed more wall thickening, contractile reserve and wall thickness, and less transmural necrosis, p <0.05 in all cases. Of 76 hypoperfused segments at the first week, 47 (62%) normalised perfusion at the sixth month. However, 42 segments (14% of the whole group) showed chronic abnormal perfusion; these segments showed worse CMR indices in the late phase (p<0.05 in all cases). CONCLUSIONS: In patients with an open IRA, more than half of the segments with abnormal perfusion at the first week are normally perfused after six months. First-pass perfusion CMR shows that in a small percentage of segments, abnormal perfusion may become a chronic phenomenon-these areas have a more severe deterioration of systolic function, wall thickness, contractile reserve and the transmural extent of necrosis.
Abstract: BACKGROUND AND OBJECTIVE: We analyzed the diagnostic utility of a chest pain score in patients evaluated for chest pain of possible coronary origin. PATIENTS AND METHOD: We studied 1,068 consecutive patients coming to the emergency room with acute chest pain of possible coronary origin without ST-segment elevation, using a chest pain unit protocol. Chest pain was quantified by validated score (0-20 points). The diagnostic value of the chest pain score was analyzed for the diagnosis of acute myocardial infarction (AMI), unstable angina (UA) and acute coronary syndrome (ACS; AMI or UA). RESULTS: The diagnosis of ACS was established in 651 patients (61%), AMI in 439 (41%) and UA in 212 (20%). In the multivariate analysis a chest pain score > or = 10 was an independent predictor of ACS (odds ratio [OR] = 2.9; 95% confidence interval [CI] 2.1-4; p = 0.0001), along with an age older than 70 years (OR = 2.6; 95% CI,1.8-3.7; p = 0.0001), male gender (OR = 2; 95% CI, 1.4-2.8; p = 0.0001); insulin-dependent diabetes (OR = 2.3; 95% CI, 1.2-4.6; p = 0.016); previous myocardial infarction (OR = 1.6; 95% CI, 1.1-2.4; p = 0.022), ST depression (OR = 9.3; 95% CI, 5.2-16.7; p = 0.0001) and T wave inversion (OR = 2.5; 95% CI, 1.4-4.3; p = 0.0001). The chest pain score was associated with the diagnosis of both AMI (OR = 1.4; 95% CI, 1.1-1.9; p < 0.02) and UA (OR = 2.8; 95% CI, 1.8-4.2; p < 0.0001). CONCLUSIONS: The chest pain score allows independent information for the early diagnosis of patients coming to the emergency department with acute chest pain of possible coronary origin.
Abstract: INTRODUCTION: The role of glucose elevation above levels considered normal in non- diabetic patients with acute coronary syndromes (ACS) is not adequately defined. The aim of this study was to determine the association between serum glucose at admission and 1-year mortality in this type of patients. METHODS: We studied 648 non diabetic patients admitted consecutively with ACS. Serum glucose was determined at admission, together with classical risk factors, biochemical and inflammatory markers. The primary endpoint was all cause mortality at one year follow-up. RESULTS: Patients with normal glucose had lower mortality than patients with impaired fasting glucose (14.1% vs 5.7% 1-year mortality) or with glucose levels in diabetic range (24.7% vs 5.7% 1-year mortality). CONCLUSIONS: In non-ST elevation acute coronary syndromes, elevated levels of glucose in non-diabetic patients are strong predictors of all cause death at one year follow-up. This prognostic value is independent of other risk factors biochemical and inflammatory markers.
Abstract: BACKGROUND AND OBJECTIVE: The management of cardiac ischemic patients differs depending on their comorbidity. The Charlson Index (ChI) and its adaptations are well established and widely used tools to quantify a patient comorbidity. The aim of this study is to evaluate the influence of comorbidity quantified by the ChI in the treatment administered at admission and in the pharmacological treatment prescribed at discharge in the setting of an acute myocardial infarction with and without ST segment elevation. PATIENTS AND METHOD: We studied a total of 955 patients consecutively admitted in our hospital with the diagnosis of acute myocardial infarction. Comorbidity was obtained at the first day of admission applying the ChI. According to this value patients were classified from minor to major in 2 subgroups (ChI <or= 2, ChI >or= 2) and differences in the admission and discharge treatments between both groups were analyzed. RESULTS: Patients admitted with acute myocardial infarction without ST segment elevation and ChI > 2 received less frequently betablockers at discharge, but there were no significant differences in the use of ACE inhibitors, calcium channel blockers or statins. In addition they were submitted less frequently to revascularization procedures or treadmills, and no differences were found in the use of echocardiograms. Patients with ST segment elevation and ChI > 2 were less frequently treated with betablockers or statins at discharge, and were submitted to less treadmills or echocardiograms; furthermore, in these patients, there were no significant differences in the use of ACE inhibitors, calcium channel blockers, thrombolytics or revascularization procedures. CONCLUSIONS: Comorbidity quantified on admission by the ChI is an independent factor that modifies in-hospital and ambulatory management of patients with acute myocardial infarction. There is a lower use of invasive techniques as well as a lower prescription of betablockers at discharge in patients with greater comorbidity.
Abstract: BACKGROUND: The aim of this study was to define the utility of the combined measurement of troponin I, myoglobin, C-reactive protein, fibrinogen, and homocysteine to predict risk in non-ST elevation acute coronary syndromes. METHODS: Troponin I, myoglobin, high-sensitivity C-reactive protein, fibrinogen, and homocysteine were measured in 557 consecutive patients admitted to our institution for non-ST elevation acute coronary syndrome. The risk for major events (death or nonfatal myocardial infarction) at first month and at first year follow-up was analyzed. RESULTS: In a multivariate model adjusting for baseline characteristics and electrocardiographic changes, the only biomarkers related to major events at first month were C-reactive protein (P = .007) and myoglobin (P = .02), and at first year troponin I (P = .02), C-reactive protein (P = .03), and homocysteine (P = .04). The rate of major events depending on the number (0-5) of elevated biomarkers were at first month: 4.1%, 3.7%, 5.7%, 6.1%, 6.5%, and 30.8% (P < .0001), and at first year: 8.2%, 11.1%, 12.3%, 16.2%, 23.7%, and 50% (P < .0001). A simple score including the number of elevated biomarkers showed an adjusted risk of major events of 1.6 [1.3-1.9] at first month and of 1.4 [1.2-1.7] at first year. CONCLUSIONS: Markers of myocardial damage, inflammation, and homocysteine analyzed separately provide prognostic information. The number of elevated biomarkers is an independent risk predictor of major events.
Abstract: INTRODUCTION: Increased concentrations of homocysteine (tHcy) are considered a potentially modifiable risk factor for coronary heart disease. The relationship between plasma homocysteine and prognosis has been less well studied. The aim of this study was to examine a possible relationship between the homocysteine levels in admission and all cause mortality in subjects presenting with non-ST segment elevation (NSTE) acute coronary syndrome. METHODS: We studied 854 patients with suspected NSTE acute coronary syndrome admitted consecutively to our institution, tHcy was determined at a median of 3 days from enrolment and was analyzed in tertiles together with classical risk factors and other biochemical markers. The primary end point was all cause mortality at 1 year follow-up. RESULTS: There were 86 deaths in the upper 2 tertiles (> or =10.1 mmol/L). The events registered in the lower tertile of admission homocysteine concentration were 12 deaths. Therefore, tHcy values over 10 mumol/l increases the posibility of long term all cause mortality after an NSTE acute coronary syndromes (HR 2.5). This is independent of other prognostic factors as important as age, cardiovascular risk factors, congestive heart failure or creatinine levels at arrival. This is the first study that shows the tHcy prognostic value with independece of the acute phase reactants. CONCLUSION: Determination of plasmatic levels of tHcy in the acute phase of a NSTE acute coronary syndrome is a useful tool in the prognostic stratification, independently of classical risk markers (age, cardiovascular risk factors, heart failure, troponin peak) of acute phase reactants and of creatinine obtained at arrival.
Abstract: INTRODUCTION AND OBJECTIVES: After a myocardial infarction, damage to the microcirculation indicates a worse prognosis. We compared the usefulness of the quantitative analysis of myocardial contrast echocardiography with intravenous injection of contrast (MCE-iv) with intracoronary injection (MCE-ic) for analyzing coronary perfusion. PATIENTS AND METHOD: We studied 42 patients with a first ST-elevation myocardial infarction, single-vessel disease and a patent artery (TIMI 3, stenosis < 50%). Myocardial perfusion in segments in the infarct-related area was quantified (normalized scale 0-1) with MCE-ic (bolus of Levovist, real-time imaging, perfusion considered normal if > 0.75) and MCE-iv (perfusion of SonoVue, single-image capture in 1 out of each 6 cycles with trigger set at end-systole, perfusion considered normal if > 0.9). Perfusion was considered abnormal if 2 or more segments showed altered perfusion. RESULTS: Quantification with MCE-iv took 5 +/- 1 minutes. No side effects were observed. MCE-ic was normal in 141 segments (80%) out of 176 segments included in the infarcted area, whereas 35 segments (20%) showed abnormal perfusion. MCE-ic was normal in 31 patients (74%) and was altered in 11 cases (26%). Normal perfusion with MCE-iv had a sensitivity of 91%, a specificity of 84% and a kappa index of 0.67 for predicting normal perfusion with MCE-ic (r = 0.86; P < .0001 between the two techniques). CONCLUSIONS: In comparison with MCE-ic, quantitative analysis of single images captured during intravenous perfusion of contrast is an easy, rapid and valid method for analyzing postinfarction coronary perfusion.
Abstract: INTRODUCTION: In acute coronary syndromes, myocardial damage markers and acute-phase reactants predict adverse cardiac events. The aim of this study was to define the fitted prognostic value of the most widely used variables of necrosis and inflammation as well as of homocysteine. METHODS AND RESULTS: Troponin I, high-sensitivity C-reactive protein, fibrinogen and homocysteine were measured in 515 consecutive patients admitted to our institution for non-ST elevation acute coronary syndrome. The risk for major events (death or nonfatal myocardial infarction) through 6 months of follow-up was analysed. In the univariate analysis, all markers were related to major events (p<0.01 in all cases). In a multivariate model fitting for baseline characteristics and electrocardiographic changes, the only biomarkers related to major events were C-reactive protein >11 mg/l (2.1 [1.2-3.8] p=0.007) and troponin I >3 ng/ml (1.9 [1.1-3.4] p=0.03). Moreover, the rate of major events was significantly higher (p<0.0001) only when both C-reactive protein and troponin I were increased (31.4% vs. 9.3% if any or both markers were normal). CONCLUSION: In non-ST elevation acute coronary syndromes elevated levels of troponin I, C-reactive protein, fibrinogen and homocysteine are strongly related to the risk of major events. The prognostic value of troponin I and C-reactive protein is independent and additive with respect to each other.
Abstract: INTRODUCTION AND OBJECTIVES: Although traditionally an elevated white blood cell count (WBC), an indicator of systemic inflammation, has been accepted as part of the healing response following acute myocardial infarction (AMI), it has frequently been shown to be a predictor of adverse cardiovascular events. The present study was designed to assess the association between WBC and long-term mortality in AMI patients either with ST-segment elevation (STEMI) or without ST-segment elevation (non-STEMI). Patients and method. The study included 1118 consecutive patients who were admitted with the diagnosis of AMI: 569 non-STEMI and 549 STEMI. The WBC was measured in the 24 hours following admission. Patients were divided into 3 groups: WBC1 (count, <10 x 103 cells/mL), WBC2 (count, 10-14.9 x 10(3) cells/mL), and WBC3 (count, > or =15x10(3) cells/mL). All-cause mortality was recorded during a median follow-up period of 10+/-2 months. The relationship between WBC and mortality was assessed by Cox regression analysis for both types of AMI. RESULTS: Long-term mortality during follow-up was 18.5% in non-STEMI patients and 19.9% in STEMI patients. In non-STEMI patients, the adjusted hazard ratios for those in the WBC3 and WBC2 groups compared with those in the WBC1 group were 2.07 (1.08-3.94; P=.027) and 1.61 (1.03-2.51; P=.036), respectively. The corresponding figures in STEMI patients were 2.07 (1.13-3.76; P=.017) and 2.22 (1.35-3.63; P=.002), respectively. CONCLUSIONS: WBC on admission was an independent predictor of long-term mortality in both non-STEMI and STEMI patients.
Abstract: OBJECTIVES: We sought to evaluate the usefulness of a comprehensive assessment of four cardiovascular magnetic resonance imaging (CMR)-derived myocardial viability indexes in the setting of myocardial stunning. BACKGROUND: Cardiovascular magnetic resonance imaging allows the simultaneous assessment of several viability indexes. METHODS: We studied 40 patients with a first ST-segment elevation myocardial infarction (MI) and an open infarct-related artery. At the first week, using CMR, wall motion (WM), and four viability indexes were determined: wall thickness, WM improvement with low-dose dobutamine, perfusion, and transmural extent of necrosis. We created a comprehensive score based on the presence and the relative power of these viability indexes for predicting normal WM at the sixth month. RESULTS: Of 153 dysfunctional segments at the first week, 59 (39%) exhibited normal WM at the sixth month. According to the odds ratio of viability indexes for predicting normal WM, we developed a five-level predictive score. The proportions of segments showing normal WM at sixth month were as follows; Level 1 (0 indexes): 0 of 13 (0%); Level 2 (normal thickness and/or perfusion): 14 of 82 (17%); Level 3 (dobutamine response): 5 of 11 (45%); Level 4 (non-transmural necrosis): 20 of 26 (77%); Level 5 (non-transmural necrosis and dobutamine response): 20 of 21 (95%), p < 0.0001 for the trend. These proportions were similar in a matched prospective validation group comprising 16 patients (0%, 18%, 62%, 77%, and 90% for levels 1 to 5, respectively, p < 0.0001 for the trend). CONCLUSIONS: A comprehensive analysis of the four more widely used CMR-derived viability indexes is useful for predicting late systolic function after myocardial infarction.
Abstract: AIMS: The significance of exercise-induced ST segment elevation in Q leads in patients with a recent myocardial infarction and without significant residual stenosis in the infarct-related artery has not been defined. We aimed to elucidate the role of myocardial perfusion and viability in this scenario. METHODS AND RESULTS: Sixty-six patients with a first myocardial infarction, single-vessel disease and an open artery were studied. Myocardial perfusion was assessed with angiographic blush, intracoronary myocardial contrast echocardiography and magnetic resonance. Myocardial viability was quantified by means of magnetic resonance (transmural extent of necrosis). Exercise-induced ST elevation in Q leads was observed only in 13 cases (20%); 53 patients (80%) did not show this finding. The group with ST elevation had fewer cases with normal perfusion: Blush 3 (15% vs. 74%, p=0.001), myocardial contrast echocardiography score >0.75 (8% vs. 81%, p=0.001) and magnetic resonance score >0.75 (31% vs. 68%, p=0.03). Similarly, myocardial viability (necrosis <50%) was less frequent in patients with ST elevation (8% vs. 72%, p=0.001). CONCLUSION: In patients with a first myocardial infarction and without residual ischemia, exercise-induced ST segment elevation in Q leads is an uncommon finding and it is related to a more damaged coronary microcirculation and to less viable myocardium.
Abstract: OBJECTIVES: The purpose of this research was to develop a risk score for patients with chest pain, non-ST-segment deviation electrocardiogram (ECG), and normal troponin levels. BACKGROUND: Prognosis assessment in this population remains a challenge. METHODS: A total of 646 consecutive patients were evaluated by clinical history (risk factors and chest pain score according to pain characteristics), ECG, and early exercise testing. ST-segment deviation and troponin elevation were exclusion criteria. The primary end point was mortality or myocardial infarction at one year. The secondary end point was mortality, myocardial infarction, or urgent revascularization at 14 days (similar to the Thrombolysis In Myocardial Infarction [TIMI] risk score). RESULTS: Primary and secondary end point rates were 6.7% and 5.4%. A risk score was constructed using the variables related to the primary end point: chest pain score > or =10 points (hazard ratio [HR] = 2.5; 1 point), > or =2 pain episodes in last 24 h (HR = 2.2; 1 point), age > or =67 years (HR = 2.3; 1 point), insulin-dependent diabetes mellitus (HR = 4.2; 2 points), and prior percutaneous transluminal coronary angioplasty (HR = 2.2; 1 point). Patients were classified into five categories of risk (p = 0.0001): 0 points, 0% event rate; 1 point, 3.1%; 2 points, 5.4%; 3 points, 17.6%; > or =4 points, 29.6%. The accuracy of the score was greater than that of the TIMI risk score for the primary (C index of 0.78 vs. 0.66, p = 0.0002) and secondary (C index of 0.70 vs. 0.66, p = 0.1) end points. CONCLUSIONS: Patients presenting with chest pain despite no ST-segment deviation or troponin elevation show a non-negligible rate of events at one year. A risk score derived from this specific population allows more accurate stratification than when using the TIMI risk score.
Abstract: OBJECTIVE: To investigate the outcome of patients with acute chest pain and normal troponin concentrations. DESIGN: Prospective cohort design. SETTING: Single centre study in a teaching hospital in Spain. PATIENTS: 609 consecutive patients with chest pain evaluated in the emergency department by clinical history (risk factors and a chest pain score according to pain characteristics), ECG, and early (< 24 hours) exercise testing for low risk patients with physical capacity (n = 283, 46%). All had normal troponin concentrations after serial determination. MAIN OUTCOME MEASURES: Myocardial infarction or cardiac death during six months of follow up. RESULTS: 29 events were detected (4.8%). No patient with a negative early exercise test (n = 161) had events versus the 6.9% event rate in the remaining patients (p = 0.0001). Four independent predictors were found: chest pain score > or = 11 points (odds ratio (OR) 2.4, 95% confidence interval (CI) 1.1 to 5.5, p = 0.04), diabetes mellitus (OR 2.3, 95% CI 1.1 to 4.7, p = 0.03), previous coronary surgery (OR 3.1, 95% CI 1.3 to 7.6, p = 0.01), and ST segment depression (OR 2.8, 95% CI 1.3 to 6.3, p = 0.003). A risk score proved useful for patient stratification according to the presence of 0-1 (2.7% event rate), 2 (10.2%, p = 0.008), and 3-4 predictors (29.2%, p = 0.0001). CONCLUSIONS: A negative troponin result does not assure a good prognosis for patients coming to the emergency room with chest pain. Early exercise testing and clinical data should be carefully evaluated for risk stratification.
Abstract: Spontaneous Valsalva sinus pseudoaneurysm is a rare and highly lethal condition. Below we present a clinical case of a young woman with spontaneous Valsalva sinus pseudoaneurysm diagnosed presenting with acute myocardial infarction (AMI) and ischemic stroke.
Abstract: INTRODUCTION AND OBJECTIVES: We report the impact on prognosis of an invasive strategy used at our center for non-ST-segment elevation acute coronary syndrome. PATIENTS AND METHOD: We analyzed 504 consecutive patients with typical chest pain, electrocardiographic changes or increased troponin I serum values, who were divided into 2 cohorts: a) conservative group, 272 patients admitted between October 2001 and September 2002 and managed with a conservative strategy, and b) invasive group, 232 patients admitted between October 2002 and September 2003 for whom an invasive strategy was recommended. We recorded major events (death or reinfarction) and minor events (readmission or need for postdischarge revascularization) within a 12-week follow-up period. RESULTS: In the invasive group in-hospital angioplasty (21% vs 35%, P<.0001) and in-hospital revascularization (33% vs 48%, P=.001) increased. There were no significant differences between the conservative and the invasive group regarding major events (17% vs 15%). The invasive group was associated with a reduction in minor events (17% vs 9%, P=.01). The incidence of any event was reduced (28% vs 20%, P=.04). In the multivariate analysis for the whole group (n=504) the invasive strategy significantly reduced minor events (hazard ratio 0.5 [0.3-0.8], P=.008) and any event (hazard ratio 0.5 [0.3-0.8], P=.005), but not major events (hazard ratio 0.6 [0.4-1.1], P=.09). CONCLUSIONS: The results observed in recent randomized clinical trials regarding the use of an invasive strategy were confirmed in the real world. In the short term, the benefits seem to be confined to a reduction in minor events, i.e., fewer readmissions and less need for postdischarge revascularization.
Abstract: The additional prognostic information provided by C-reactive protein (CRP) to parameters of left ventricular function in survivors of acute myocardial infarction (AMI) was investigated in 665 patients (326 with ST elevation and 339 with non-ST elevation). Cox multivariable analysis identified the following predictors of 6-month cardiac death: age (per 5 years hazard ratio [HR] 1.2, 95% confidence interval [CI] 1.1 to 1.4, p = 0.004), Killip class >I at presentation (HR 2.4, 95% CI 1.3 to 4.5, p = 0.0001), a reduced ejection fraction (per 5% HR 1.3, 95% CI 1.2 to 1.4, p = 0.0001), and greater CRP (per 5 mg/L HR 1.02, 95% CI 1.01 to 1.04, p = 0.02); the C-index of the model was 0.77 without and 0.78 with CRP. CRP is associated with mortality in addition to age and parameters of ventricular function (Killip class and ejection fraction) in survivors of AMI, although the relevance of its additive predictive role seems marginal.
Abstract: INTRODUCTION AND OBJECTIVES: The Charlson comorbidity index (CCI), an indicator of comorbidity, has been used as an adjusting variable in multivariate models. Because of its prognostic value per se for cardiovascular complications after acute myocardial infarction (AMI), we sought to determine the predictive value of the CCI for all-cause mortality and recurrent AMI 30 days and 1 year after the index event. PATIENTS AND METHOD: We analyzed 1035 consecutive patients admitted with the diagnosis of AMI (ST elevation=508 and non-ST elevation=527). The composite endpoint was determined after 30 days (13.9%) and 1 year (26.3%) of follow-up. The CCI was calculated on admission, and other variables with prognostic value were also recorded. CCI was stratified in 4 categories: 1: CCI=0 (control), 2: CCI=1, 3: CCI=2,4: CCI> or =3. Cox proportional risks analysis was used for the multivariate analysis, and the C-statistic was calculated to assess the discriminative power of the models. RESULTS: Hazard ratios (95% CI) estimated for each category of CCI were: 2=1.69 (1.10-2.59), 3=1.78 (1.08-2.92) and 4=1.57 (0.87-2.83) at 30 days; 2=1.62 (1.18-2.23), 3=2.00 (1.39-2.89) and 4=2.24 (1.50-3.36) at 1 year. Comparisons with the C-statistic between the nested multivariate models (with and without CCI) yielded values of 0.765 vs 0.750 after 30 days, and 0.751 vs 0.735 after 1 year. CONCLUSIONS: Our data indicate that CCI is an independent predictor of mortality or recurrent AMI 30 days and 1 year after the index AMI.
Abstract: BACKGROUND AND OBJECTIVE: We intended to determine whether C-reactive protein (CRP) provides independent prognostic information after a non-ST elevation acute coronary syndrome. PATIENTS AND METHOD: We prospectively studied 630 consecutive patients admitted with a diagnosis of non-ST elevation acute coronary syndrome. Cut-off values were: troponin I > 1 ng/ml (n = 354; 56%) and CRP > 11 mg/l (n = 273; 43%). RESULTS: Within a one-year follow-up period, 56 (9%) cardiac deaths, 85 (13%) myocardial infarctions (MI) and 127 (20%) first major events were detected. Patients with increased CRP showed higher rates of death at one-month (8% vs 1%), death at one-year (15% vs 4%), myocardial infarction at one-month (8% vs 4%), myocardial infarction at one-year (19% vs 9%), major events at one-month (15% vs 5%) and major events at one-year (30% vs 13%). In the multivariate analysis, once adjusted for baseline and electrocardiogram data and for myocardial damage markers, CRP was an independent predictor of death at one-month (odds ratio [OR] 4.6) and death at one-year (OR = 2.7), major events at one-month (OR = 1.8) and major events at one-year (OR = 1.8). Troponin I predicted MI at one-month (OR = 2.5) and MI at one-year (OR = 2.2). CONCLUSIONS: CRP provided independent information to predict major events in non-ST elevation acute coronary syndromes. Troponin I was a more powerful predictor of MI than PCR. The analysis of CRP and myocardial damage markers in the short-term and long-term risk stratification seems worthy.
Abstract: BACKGROUND: Atrial fibrillation is one of the most common complications of cardiac surgery. Beta blockers have been demonstrated to decrease the incidence of postoperative atrial fibrillation. Preliminary investigations reporting sotalol and atenolol to be effective in preventing postoperative atrial fibrillation are encouraging, but no studies have been conducted comparing both drugs. METHODS: A total of 253 consecutive eligible patients (66 +/- 8 years; mean +/- standard deviation) scheduled to undergo cardiac surgery were enrolled in this study. Patients were randomized in a prospective open manner 1.5:1 to atenolol group (50 mg/daily; 153 patients) or sotalol group (80 mg twice daily; 100 patients). RESULTS: Atrial fibrillation occurred in 44/253 patients (17.45%). A significant difference was found in the occurrence of atrial fibrillation in the atenolol group (34 patients, 22%) compared with those receiving sotalol (10 patients, 10%; p = 0.013). Therapeutic efficiency and efficacy was 12% and 54%, respectively. Stepwise logistic regression analysis revealed that age more than 68 years old (odds ratio = 2.72; 95% confidence interval [CI] = 1.37-5.41; p = 0.004), the use of beta-adrenergic agents (odds ratio = 2.74; 95% CI = 1.5-5; p = 0.001), and sotalol (odds ratio = 0.46; 95% CI = 0.23-0.95; p = 0.035) were independently associated with development of atrial fibrillation. CONCLUSIONS: Oral low-dose sotalol provides a considerable reduction in the occurrence of atrial fibrillation. A selective approach based on clinical risk prediction should decrease the occurrence of atrial fibrillation after cardiac surgery.
Abstract: BACKGROUND AND OBJECTIVE: We aimed to delineate the sex differences in short-term (one-month) and long-term (one-year) cardiac death after an acute coronary syndrome. PATIENTS AND METHOD: After the publication of the new myocardial infarction definition, we prospectively analyzed 1,324 consecutive patients admitted with a diagnosis of acute coronary syndrome to a tertiary hospital. 483 (37%) of these patients had myocardial infarction with ST-elevation, 439 (33%) had myocardial infarction without ST elevation (troponin I > 1 ng/ml) and 402 (30%) had an unstable angina (troponin I < 1 ng/ml). RESULTS: Within 1-year of follow-up, 177 deaths (13.4%) were detected. There was a similar rate of cardiac death in female and male patients with 'non-ST elevation myocardial infarction' (one-month: 9.7% vs 7.1%, p = NS; one-year: 16.7% vs 13.2%, p = NS) and with unstable angina (one-month: 3% vs 1.9%, p = NS; one-year: 3% vs 5.6%, p = NS). Among patients with 'ST-elevation myocardial infarction' women showed a higher rate of cardiac death at one-month (21.5% vs 9.8%; p < 0.0001) and at one-year (28.9% vs 14.1%, p < 0.0001) than men. In the multivariate analysis, independent predictors of cardiac death in 'ST-elevation myocardial infarction' at one-year were age > 70 years (p < 0.0001), Killip class > 1 (p < 0.0001) and lack of reperfusion (p = 0.003) but not having a female sex. CONCLUSIONS: Patients with 'non-ST elevation acute coronary syndromes' did not display sex differences with regard to mortality. Women with 'ST-elevation myocardial infarction' had a higher mortality; however, these differences were not independently related to a female sex but to a worse baseline clinical profile and a lesser rate of reperfusion.
Abstract: The relationship between troponin I and systolic function (quantitative contrast ventriculography) was evaluated in 137 consecutive patients with a first acute coronary syndrome (60 with and 77 without ST elevation). In general, a larger troponin I peak value was related with a more depressed ejection fraction and poorer regional systolic function (p < 0.0001). Nevertheless, this correlation was weaker than expected, especially in those cases without ST-segment elevation, suggesting that other factors apart from systolic dysfunction must be taken into account in order to explain the worse prognosis of those patients with increased serum levels of this marker of myocardial damage.
Abstract: OBJECTIVES: To determine the effects of long-term nocturnal intermittent positive-pressure ventilation (NIPPV) on symptoms, pulmonary function test results, sleep, and respiratory muscle performance in patients with ventilatory insufficiency due to severe kyphoscoliosis. DESIGN: A prospective study in which 16 severe kyphoscoliotic patients were treated with NIPPV delivered by volume-cycled and pressure-cycled ventilators, over a period of 36 months. INTERVENTIONS AND MEASUREMENTS: At baseline, pulmonary function tests, blood gas measurements, polysomnography, and respiratory muscle strength (measured by noninvasive indexes) were obtained. Symptoms and the number of hospitalizations in the previous 6 months also were recorded. Patients then began using a ventilator for > 1 to 2 days, in order to select the type of ventilator and the appropriate interface. Patients returned for evaluation (in outpatient setting) every 6 months for a follow-up period of 3 years. At 6 months, polysomnography was repeated, and by the third year clinical and functional parameters had been reassessed. RESULTS: All symptoms improved significantly with NIPPV therapy, when compared with the baseline values. The mean (+/- SD) PaO(2) and FVC values increased at 36 months compared with baseline values (62.6 +/- 7.1 vs 67.8 +/- 8.8 mm Hg, respectively; and 37.9 +/- 7.2% vs 47.5 +/- 11.9%, respectively; p < 0.05 for both). There were significant improvements in mean maximal inspiratory pressure (55.8 +/- 17.4 to 78.5 +/- 17.5 cm H(2)O), maximal expiratory pressure (53.8 +/- 17.7 to 72.3 +/- 11.0 cm H(2)O), mouth pressure (0.28 +/- 0.08 to 0.22 +/- 0.02 cmH(2)O), and pressure-time index (0.18 +/- 0.05 to 0.11 +/- 0.02; p < 0.05 for all comparisons). There were no significant differences in breathing pattern and ventilatory drive. After 6 months, nocturnal oxyhemoglobin saturation improved, however, there was no significant change in sleep architecture. All patients subjectively perceived a better quality of life after beginning ventilation, which persisted over the course of the study. CONCLUSIONS: Long-term NIPPV therapy improves daytime blood gas levels, respiratory muscle performance, and hypoventilation-based symptoms in patients with severe kyphoscoliosis.
Abstract: OBJECTIVES: We analyzed whether the study of systolic function by echocardiography adds independent information to that afforded by biochemical markers in predicting six-month major events after non-ST elevation acute coronary syndrome. PATIENTS AND METHOD: Baseline clinical and electrocardiographic data as well as serum concentrations of troponin, myoglobin, C-reactive protein, fibrinogen and homocysteine were recorded prospectively in 515 consecutive patients admitted because of non-ST elevation acute coronary syndrome. Ejection fraction (echocardiogram) was determined in 248 cases (48%). Predictors of cardiac death or infarction within the following six months were analyzed. RESULTS: In the 248 patients in whom ejection fraction was analyzed, 38 major events were recorded. Increased biochemical markers were related to major events (p < 0.05 for all markers). In the final multivariate model, which included clinical, electrocardiographic, serological and systolic function data, ejection fraction was the most powerful predictor of six-month major events: age > 70 years (p = 0,04), insulin-dependent diabetes (p = 0.03), C-reactive protein > 11 mg/l (p = 0.004) and ejection fraction < 50% (p < 0.0001); C-statistic = 0.80. CONCLUSIONS: Apart from the clinical and biochemical profile, analysis of systolic function is advisable for correct risk stratification of patients with non-ST elevation acute coronary syndrome.
Abstract: BACKGROUND: Management of acute chest pain in the emergency room constitutes a challenge. METHODS: Seven hundred and one consecutive patients were evaluated by clinical history (chest pain score and risk factors), ECG, troponin I and early (<24 h) exercise testing in low risk patients (n=165). A composite end-point (recurrent unstable angina, acute myocardial infarction or cardiac death) was recorded during hospital stay or in ambulatory care settings for patients discharged after early exercise testing. RESULTS: The end-point occurred in 122 patients (17%). Multivariate analysis identified the following predictors: chest pain score > or =11 points (OR=1.8, 2-2.8, 95% CI, P=0.007), age > or =68 (OR 1.6, 1.1-2.4 CI 95%, P=0.03), insulin-dependent diabetes mellitus (OR 1.9, 1.1-3.4 CI 95%, P=0.02), a history of coronary surgery (OR 3.3, 1.5-7.2 CI 95%, P=0.003), ST-segment depression (OR 1.9, 1.2-3.0 CI 95%, P=0.009) and troponin I elevation (OR 1.6, 1.1-2.5, CI 95%, P=0.05). ST-segment depression produced a high end-point increase (31 vs. 13%, P=0.0001). Troponin I elevation increased the risk in the subgroup without ST-segment depression (20 vs. 11%, P=0.006) but did not further modify the risk in the subgroup with ST depression (31 vs. 28%, ns). Nevertheless, the negative ECG and troponin I subgroup showed a non-negligible end-point rate (16% when pain score > or =11 or 7% when pain score <11, P=0.004). Finally, no patient with a negative exercise test presented events compared to 7% of those with a non-negative test (RR=2.5, 2.1-3.1 95% CI, P=0.01). CONCLUSIONS: Emergency room evaluation of chest pain should not focus on a single parameter; on the contrary, the clinical history, ECG, troponin and early exercise testing must be globally analysed.
Abstract: OBJECTIVES: To investigate the prognostic factors in patients who come to the emergency room with chest pain but without ST segment elevation. PATIENTS AND METHOD: 743 consecutive patients were evaluated by recording clinical history, electrocardiogram and troponin I determination, and early (<24 h) exercise testing was done for the low-risk subgroup of patients (n=203). All patients were followed during 3 months for major events (acute myocardial infarction or death). RESULTS: Major events occurred in 71 patients (9.6%). Multivariate analysis (C statistic=0.79; 95% CI 0.73-0.84; p=0.0001) identified the following predictors: age > or =72 years (OR=1.7; 95% CI, 1.0-2.9; p=0.05), insulin-dependent diabetes mellitus (OR=2.9; 95% CI, 1.5-5.4; p=0.001), previous ischemic heart disease (OR=1.9; 95% CI, 1.1-3.2; p=0.02), ST depression (OR=2.1; 95% CI, 1.2-3.8; p=0.01) and troponin I elevation (OR=2.9; 95% CI, 1.5-5.3; p=0.001). These five predictors were used to construct a risk score based on their odds ratios, which allowed event rate stratification by quartiles of the score: 0-2 points (1.6% events), 3-4 points (8.1% events), 5-7 points (11.9% events) and > or =8 points (26.2% events); p=0.0001. No patient with negative findings in the early exercise testing had major events. CONCLUSIONS: In patients with chest pain, the combination of clinical, electrocardiographic and biochemical data available on admission to the emergency service allows rapid prognostic stratification. Early exercise testing is advisable for the final stratification of low risk patients.
Abstract: INTRODUCTION: C-reactive protein is an important prognostic indicator for early risk stratification in patients with an acute coronary syndrome. The mechanisms underlying the elevation of C-reactive protein in these patients have not been fully understood. We studied the factors related to the increase of this acute-phase reactant. METHODS AND RESULTS: Within a single-centre registry, 419 consecutive patients admitted for a non-ST elevation acute coronary syndrome were studied. Serum high sensitivity C-reactive protein was measured late (median 3 days) after admission. Clinical, electrocardiographic, biochemical and angiographic variables were recorded. In the multivariate analysis, an increased C-reactive protein (n=162) was related to high levels of troponin I (OR 2.5 (1.6-4) P<0.001) and to a Killip class>1 at presentation (OR 2.9 (1.6-5.4) P<0.001). The coronary angiographic characteristics were not related to C-reactive protein. Finally, in 52 patients with no previous heart disease in whom regional dysfunction was quantified by left ventriculography the presence of a significant (>6 chords) regional dysfunction was significantly related to C-reactive protein (OR 5.1 (1.7-15.3) P=0.006) CONCLUSION: Our results indicate that in acute coronary syndromes elevated levels of C-reactive protein late after admission are mainly related to clinical, biochemical and angiographic evidences of myocardial damage. The prognostic utility of this parameter could be in part explained by its relationship with a major regional dysfunction.
Abstract: Early exercise testing (first 24 hours) was evaluated in the stratification of patients seen in the emergency room for chest pain. One hundred and forty-two consecutive patients without ischemia in the ECG or troponin I elevation were included. Ninety-two patients were discharged after the exercise testing (group I, 82 negative and 10 inconclusive test results) and 50 patients were hospitalized (group II, 29 positive and 21 inconclusive test results). In group I, cardiac events (unstable angina and non-fatal infarction) occurred in the next 30 days of follow-up in 2 patients with inconclusive test results; no cardiac events occurred in patients with negative test results. In group II, unstable angina was diagnosed in 30 patients and 3 presented recurrent angina. There were no complications during exercise testing. In conclusion, early exercise testing is safe and useful in the stratification of patients seen in the emergency room for chest pain. Only patients with negative test results should be discharged early.
Abstract: OBJECTIVES: The relative value of classic markers, myocardial damage variables, and levels of acute-phase reactants in establishing the pre-discharge prognosis of acute coronary syndrome without ST-segment elevation was analyzed. METHOD: We prospectively studied 385 consecutive patients admitted from our chest pain unit with a high-probability diagnosis of acute coronary syndrome without ST-segment elevation. The clinical and electrocardiographic data, myocardial damage markers (troponin I, CK-Mb mass, myoglobin), and acute-phase reactants (high-sensitivity C-reactive protein, fibrinogen) were recorded. RESULTS: During admission, 15 deaths (3.9%) and 16 complicative infarctions (4.2%) occurred, for a total of 31 major events (death and/or infarction: 8.1%). Age (p = 0.03), insulin-dependent diabetes (p = 0.009), and C-reactive protein (p = 0.05) were independently related to death. Fibrinogen was related to infarction (p = 0.01); by fibrinogen quartiles: 1.4%; 1.4%; 2.9%, and 11.7% (p = 0.02). Age (p = 0.01), insulin-dependent diabetes (p = 0.02), and C-reactive protein (p = 0.04) were independent predictors of major events; by C-reactive protein quartiles: 1.4%; 5.5%; 5.4%, and 16.7% (p = 0.004). Troponin I was related to major events (p = 0.03), but it was not an independent predictor. CONCLUSIONS: Acute-phase reactants add independent information to clinical variables in the short-term risk stratification of patients with an acute coronary syndrome. The predictive power of troponins is lower than that of other variables.
