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: OBJECTIVES: Cardiocirculatory arrest during different types of interventions in the catheterization laboratory (cath-lab) requires mechanical cardiopulmonary resuscitation (CPR) to restore spontaneous circulation. However, mechanical chest compression leads to interruption of the procedure and can severely compromise the success of the percutaneous coronary intervention (PCI) or transcatheter aortic valve implantation (TAVI). Alternatives to mechanical chest compression are rare and mostly uncommon. The use of extracorporeal assistance for cardiopulmonary resuscitation (E-CPR) can be life-saving, but, up to now, it is not commonly and rapidly available in hospitals with cardiac-catheter laboratories but without cardiac-surgery departments. Here, we report our early experiences in using miniaturized extracorporeal membrane oxygenation (ECMO) systems for E-CPR in the cath-lab. We characterize the emergency uses and the bridging function of these simplified ECMO devices. METHODS: Patients who developed cardiocirculatory arrest during PCI and TAVI procedures were treated with E-CPR using percutaneous veno-arterial extracorporeal life-support. To provide extracorporeal life-support, we used two types of miniaturized ECMO systems that can act independently from wall their connection points for power and oxygen supply and are suitable for use in the cath-lab. RESULTS: Between 2006 and 2011, E-CPR was used in 10 PCI and 4 TAVI patients. The mean age was 73.6 ± 8.8 years. In all patients, E-CPR could be established using percutaneous veno-arterial vessel access. On extracorporeal assistance, the return of beating heart circulation could be rapidly re-established in all patients. In the PCI group, the procedure was successfully completed in all patients while on ECMO. Two patients in the TAVI group were bridged on ECMO to surgical aortic valve replacement. In the clinical follow-up, seven patients (50%) survived to hospital discharge. CONCLUSIONS: Miniaturized ECMO systems can be safe and highly effective in restoring circulation and gas exchange in patients with cardiocirculatory failure in the cath-lab. Additionally, the PCI and TAVI procedures can be finished successfully on ECMO, otherwise the patients can be bridged to cardiac surgery. Especially for patients in need of cardiac surgery, patient transfer to extracorporeal assistance can be more easily processed.
Abstract: Heart failure causes electrophysiological changes in the heart. Downregulation of repolarizing K+-currents leads to a prolongation of the cardiac action potential. Nevertheless, little is known about the differential expression of atrial and ventricular K+-channels in the failing heart. Ten rabbits underwent progressive rapid right ventricular pacing for 30 days. Digitized ECGs and echocardiograms were obtained. Left ventricular and left atrial tissue was harvested and mRNA levels of BNP, Kv4.3, rERG, Kv1.5, and KvLQT1 were measured by real time PCR. Experimental heart failure was characterized by left ventricular dilatation (13 ± 1 mm vs. 9 ± 1, p < .001), depressed fractional shortening (25 ± 5% vs. 40 ± 4, p < .001), and left atrial remodeling with increased diameter (16 mm ± 2 vs. 12 ± 1, p = .002) and weight (1.3 g ± 0.2 vs. 0.5 ± 0.1, p = .01). A prolongation of P-wave (44 ± 5 ms vs. 40 ± 4, p = .001) and PQ-interval (73 ± 10 ms vs. 66 ± 9, p = .009) occurred. In heart failure, BNP mRNA levels showed a significant upregulation in the left ventricle and atrium (1.83 AU ±1.31 vs. 0.67 ± 0.65, p < .05 and 7.16 AU ±1.76 vs. 0.77 ± 0.48, p < .05). Left ventricular Kv1.5 mRNA was reduced by 50% (p < .001) and KvLQT1 was reduced by 70% (p < .001). rERG and Kv4.3 mRNA were unchanged (n = ns). In contrast, left atrial Kv4.3 and KvLQT1 were reduced by 70% (p < .001), whereas rERG and Kv1.5 were unchanged (p = ns). Significant correlations were present between BNP and K+-channel expressions. Heart failure is characterized by significant changes in the gene expression of repolarizing K+-currents with a differential atrial and ventricular pattern. These molecular changes occur together with changes in cardiac function, geometry, conduction, and BNP expression and provide a functional basis for electrical vulnerability in heart failure.
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: Data on the effect of revascularization on outcome in patients with high-risk non-ST-segment elevation acute coronary syndrome (NSTEACS) and significant comorbidities are scarce. Recently, a simple comorbidity index (SCI) including 5 comorbidities (renal failure, dementia, peripheral artery disease, heart failure, and prior myocardial infarction [MI]) has shown to be a useful tool for risk stratification. Nevertheless, therapeutic implications have not been derived.
Abstract: To evaluate dipyridamole cardiac magnetic resonance (MR) imaging in the prediction of major events (MEs) in patients with ischemic chest pain in a large multicenter registry.
Abstract: INTRODUCTION AND OBJECTIVES: To evaluate by cardiovascular magnetic resonance those factors related to the amount of salvaged myocardium after a myocardial infarction and its value in predicting adverse ventricular remodeling. METHODS: One hundred eighteen patients admitted for a first ST elevation myocardial infarction (primary angioplasty, 65 patients; a pharmacoinvasive strategy, 53 patients) underwent magnetic resonance (6 [5-8] days and 6 months; n=83). The myocardial salvage index was quantitatively assessed as the percentage of area at risk (T2-weighted sequences) not showing late enhancement. RESULTS: Myocardial salvage index >31% (median) was associated with a shorter time to reperfusion (153min vs 258 min), a lower rate of diabetes (12% vs 32%), shorter time to magnetic resonance, and better cardiovascular parameters (P<.05 for all analyses). There were no significant differences depending on the reperfusion method. In a logistic regression analysis, delayed reperfusion (odds ratio=0.42 [0.29-0.63]; P<.0001), diabetes (odds ratio=0.32 [0.11-0.99]; P<.05) and a longer time to the performance of magnetic resonance (odds ratio=0.86 [0.76-0.97]; P<.05) were independently related to a lower probability of a myocardial salvage index >31%. Predictors of increased left ventricular end-systolic volume at 6 months were the number of segments showing an extent of transmural necrosis >50% (odds ratio =1.51 [1.21-1.90]; P<.0001) and left ventricular end-systolic volume at one week (odds ratio=1.12 [1.06-1.18]; P<.0001). CONCLUSIONS: Cardiovascular magnetic resonance enables the quantification of the salvaged myocardium after myocardial infarction. The celerity with which reperfusion therapy is administered constitutes its most important predictor. The possible effect of a delay in the performance of magnetic resonance on myocardial salvage needs to be confirmed. Salvaged myocardium does not improve the value of magnetic resonance for predicting adverse remodeling. Full English text available from:www.revespcardiol.org.
Abstract: Giant coronary artery aneurysms (gCAAs) with a diameter exceeding 5Â cm are extremely rare. The pathomechanisms and therapeutical measures in such cases have been controversial topics of discussion. Twenty-seven patients with gCAAs exceeding 5Â cm in size described in the literature were evaluated. A case with multiple gCAAs at our department was included in the analysis. Apart from atherosclerosis of all coronary arteries, a large (1.5Â 2.5Â cm) left anterior descending coronary artery aneurysm (CAA) and a gCAA (10.6Â 9.2Â cm) originating from the right coronary artery, the latter causing recurrent myocardial ischaemia with the occlusion of the peripheral right coronary artery and compressing the right cardiac cavities, were the pathological findings in our 43-year old male patient. gCAAs predominantly develop at the proximal right coronary artery. The majority of these aneurysms develop secondary to atherosclerotic lesions in young patients. We performed a successful surgical excision of the right gCAA, tightening of the left anterior descending artery aneurysm and concomitant coronary artery bypass grafting. A pathological examination confirmed advanced atherosclerosis. Microbiological examinations could find no signs of infectious causes. CAAs bear a significant risk of severe complications and have a high risk of mortality. A more aggressive surgical approach should be recommended.
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 (×1,000 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: 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: 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: 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: 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).
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: 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.
Abstract: To determine the prognostic and therapeutic implications of stress perfusion cardiovascular magnetic resonance (CMR) on the basis of the ischaemic cascade.
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: Congestive heart failure (CHF) is often associated with atrial fibrillation. The safety of many antiarrhythmic drugs in CHF is limited by proarrhythmic effects. We aimed to assess the safety of a novel atrial-selective K(+)-channel blocker AVE0118 in CHF compared to a selective (dofetilide) and a non-selective IKr blocker (terfenadine). For the induction of CHF, rabbits (n = 12) underwent rapid right ventricular pacing (330-380 bpm for 30 days). AVE0118 (1 mg/kg) dofetilide (0.02 mg/kg) and terfenadine (2 mg/kg) were administered in baseline (BL) and CHF. A six-lead ECG was continuously recorded digitally for 30 min after each drug administration. At BL, dofetilide and terfenadine significantly prolonged QTc interval (218 +/- 30 ms vs 155 +/- 8 ms, p = 0.001 and 178 +/- 23 ms vs. 153 +/- 12 ms, p = 0.01, respectively) while QTc intervals were constant after administration of AVE0118 (p = n.s.). In CHF, dofetilide and terfenadine caused torsades de pointes and symptomatic bradycardia, respectively, and prolonged QTc interval (178 +/- 30 ms vs. 153 +/- 14 ms, p = 0.02 and 157 +/- 7 ms vs. 147 +/- 10 ms, p = 0.02, respectively) even at reduced dosages, whereas no QTc-prolongation or arrhythmia was observed after full-dose administration of AVE0118. In conclusion, atrial-selective K(+)-channel blockade by AVE0118 appears safe in experimental CHF.
Abstract: OBJECTIVE: 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. METHODS: We analyzed 1030 consecutive patients admitted with ACPneg in our institution. Lymphocyte count was determined in the ED as a part of a routine diagnostic workup to rule out an acute coronary syndrome. Patients with inflammatory, infectious diseases, or active malignancy were excluded (final sample=975). The independent association between lymphocyte count and the composite endpoint (death/MI) was assessed by survival analysis for competing risk events (revascularization procedures). RESULTS: During a median follow-up of 36 months, 139 (14.3%) patients achieved the combined endpoint, with rates increasing monotonically across lymphocyte quartiles (6.2%, 10%, 20.6% and 24.1% for Q4, Q3, Q2 and Q1 (p<0.001), respectively). In a multivariable analysis, patients in lymphocytes' Q1 and Q2 as compared with those in Q4 had an increased risk for the combined endpoint: HR=2.45 (CI 95% 1.25-4.79, p=0.008) and HR=2.56 (CI 95% 1.30-5.07, p=0.007), respectively. CONCLUSION: In patients with ACPneg, low lymphocytes count was associated with an increased risk for developing the combined endpoint of death or MI.
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: INTRODUCTION: 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. METHODS: We analyzed 163 patients with a first ST-elevation myocardial infarction and a patent infarct-related artery treated with thrombolysis (67%) or primary angioplasty (33%). Using first-pass perfusion CMR, abnormal perfusion was defined as a lack of contrast arrival into the infarct area in >1 segment. Troponin I, creatine kinase MB and myoglobin were measured upon arrival and at 6, 12, 24, 48 and 96 hours after reperfusion. RESULTS: Abnormal perfusion was detected in 75 patients (46%) and was associated with a larger release of all 3 necrosis markers after reperfusion and higher peak values. This association was observed in the whole group and separately in patients treated with thrombolysis and primary angioplasty. Out of the 3 markers, troponin levels at 6 hours after reperfusion yielded the largest area under the receiver operating characteristic curve for prediction of abnormal perfusion (troponin: 0.69, creatine kinase MB: 0.65 and myoglobin: 0.58). In a comprehensive multivariate analysis, adjusted for clinical, angiographic, cardiovascular magnetic resonance parameters and all necrosis markers, high troponin levels at 6 hours after reperfusion (>median) independently predicted abnormal microvascular perfusion (OR 2.6 95%CI [1.2 - 5.5], p = .012). CONCLUSIONS: In ST-elevation myocardial infarction, a larger release of cardiac necrosis markers soon after reperfusion therapy relates to abnormal perfusion. Troponin appears as the most reliable necrosis marker for an early detection of cardiovascular magnetic resonance-derived abnormal microvascular reperfusion.
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: INTRODUCTION: 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). MATERIALS AND METHODS: We studied 105 patients with a first anterior STEMI treated with thrombolytic agents and an open left anterior descending artery. Microvascular perfusion was assessed using first-pass perfusion CMR at 7+/-1 days. CMR studies were repeated 184+/-11 days after STEMI. The ACE gene insertion/deletion (I/D) polymorphism was determined using polymerase chain reaction amplification. RESULTS: Overall genotype frequencies were II-ID 58% and DD 42%. Abnormal perfusion (> or = 1 segment) was detected in 56% of patients. The DD genotype associated to a higher risk of abnormal microvascular perfusion (68% vs. 47%, p=0.03) and to a larger extent of perfusion deficit (median [percentile 25 - percentile 75]: 4 [0-6] vs. 0 [0-4] segments, p=0.003). Once adjusted for baseline characteristics, the DD genotype independently increased the risk of abnormal microvascular perfusion (odds ratio [95% confidence intervals]: 2.5 [1.02-5.9], p=0.04). Moreover, DD patients displayed a larger infarct size (35+/-17 vs. 27+/-15 g, p=0.01) and a lower ejection fraction at 6 months (48+/-14 vs. 54+/-14%, p=0.03). CONCLUSIONS: The DD genotype associates to a higher risk of abnormal microvascular perfusion after STEMI.
Abstract: 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).
Abstract: AIMS: Experimental studies suggest that the autonomic nervous system modulates atrial refractoriness and conduction velocity in atrial fibrillation (AF). These modulatory effects are, however, difficult to assess in the clinical setting. This study sought to non-invasively characterize in patients with persistent AF, the influence of autonomic modulation induced by exercise on atrial fibrillatory rate as marker of atrial refractoriness and to identify clinical and electrocardiographic predictors of atrial rate response. METHODS AND RESULTS: In 24 patients (16 males, mean age 60 +/- 13 years) with persistent AF (16 +/- 25 months), continuous ECGs were recorded during bicycle exercise testing. Fibrillatory rate (in fibrillations per minute, fpm) was assessed at baseline and immediately after termination of exercise with spatiotemporal QRST cancellation and time-frequency analysis. Ventricular response was characterized by time-domain HRV indices. Exercise had no influence on mean fibrillatory rate (409 +/- 42 vs. 414 +/- 43 fpm, P = NS). Seven patients responded to exercise with an increase in fibrillatory rate (26 +/- 10 fpm, P < 0.001 and three with a decrease (-21 +/- 8 fpm, P < 0.001), while the remaining 14 patients did not show a response. Responders' HRV indices changed in response to exercise similarly to that of non-responders. Their baseline fibrillatory rate was, however, lower than that of non-responders (387 +/- 18 vs. 425 +/- 48 fpm, P = 0.028). No other clinical or echocardiographic variable was associated with fibrillatory rate response. Twelve weeks after cardioverson, responders were more likely to remain in sinus rhythm than non-responders (88 vs. 46 %, P = 0.04). CONCLUSIONS: Exercise-induced autonomic activation produces changes in atrial electrophysiological properties that can be detected by time-frequency analysis. Higher baseline fibrillatory rates are associated with an impaired atrial response to exercise that suggests advanced electrical remodelling and reduced sensitivity to autonomic stimuli.
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: 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.
