Abstract: BACKGROUND: Takotsubo cardiomyopathy was described for the first time in Japan in the 1990s. It is very similar to the ischemic cardiopathy both for clinical and instrumental characteristics. His peculiarity is an alteration of the ventricular contraction mechanism with hypo-akinesis of the apex and lateral segments of the left ventricle, associated with hyper-kinesis of the heart base which is responsible for the typical echocardiographic aspect of a cruet during the systole. However, the etiology of this cardiomyopathy is still unknown despite the fact that numerous hypothesis have been made. A single study of 16 patients proved multivasal damage by a BLASH SCORE analysis of the coronary radiography. In our study, performed on 24 patients, we intended to assess the actual implication of the microcirculation by analyzing the TIMI frame count (TFC), so as reporting correlations between alterations of each single artery and its respective myocardial area. METHODS AND RESULTS: Six Cardiology Centres performed an International multi-centre collection of a consecutive series of 24 patients, of which 20 were women and four men. The average age was 67.4 years. All patients admitted to one of the Cardiology divisions were previously listed for symptoms and signs of Takotsubo cardiomyopathy. An electrocardiographic (ECG), echocardio-gram and a hemodynamic study were carried out on each patient. The patients were evaluated with a follow up lasting 7 weeks. On the coronary radiography film, the microcirculation was examined by an analysis of the TFC according to the Gibson technique. The value obtained was considered pathological if it was >30 frames. The evaluation of the microcirculation by the TFC analysis showed that in 23 of the 24 patients there was a pathological slow down of the flow in the coronary micro- circulation. By analysing the number of involved vessels it was noted that nine patients had a slowdown of the general flow in all three vessels, six patients in only two vessels and the remaining nine in one vessel. In particular: in 14 patients there was an abnormal TFC in left anterior descending coronary artery (LAD), 16 in the right coronary artery (RCA) and 18 in the left circumflex coronary artery (LCX), while in one patient the picture quality in the acute phase did not allow an evaluation of the score in the RCA and in another patient in the LDA. None of the explored vessels that was responsible for the disorder of the microcirculation showed any stenosis. CONCLUSION: From the data evaluated by us, microcirculatory dysfunction seems to be present very often during acute phases of Takotsubo illness, but it is not the only determining factor of the illness.
Abstract: BACKGROUND: It is well-known that a reduction of the cardiac frequency variability, measurable with the Heart Rate Variability (HRV) system, is an indirect expression of the sympathetic-autonomic tone. Another index, Heart Rate Turbulence (HRT), has been recently suggested as a possible unit of measurement for the sympathetic-autonomic tone: this system allows to estimate the baro-reflex response of the carotid arteries to an early ventricular extra-systole by analysing heart rate variations induced by a premature beat. METHODS AND RESULTS: In our research we have analyzed this phenomenon in patients affected by moderate or severe cardiac failure. In particular, we divided 110 patients into two arms: subjects with or without a history of resuscitated arrhythmic death, that is, patients with high or low arrhythmic potential. In a detailed analysis of the sympathetic-autonomic tone, using both the above-mentioned parameters, HRV showed an irrelevant statistical difference between the two arms; on the contrary, HRT showed a significant statistical difference. CONCLUSIONS: If our conclusions will be confirmed by next larger reports, HRT could become a reliable index for screening the arrhythmic potential of patients affected by cardiac failure, to select the ones who need a defibrillator implantation.
Abstract: Studies have shown that patients with compensated heart failure (HF) receiving high diuretic doses associated with normal sodium diet and fluid intake restrictions demonstrated significant reductions in readmissions and mortality compared with those who received low-sodium diets, and over a 6-month observation period, a reduction in neurohormonal activation was also observed. The aim of this study was to evaluate the effects of different sodium diets associated with different diuretic doses and different levels of fluid intake on hospital readmissions and neurohormonal changes after 6-month follow-up in patients with compensated HF. Four hundred ten consecutive patients with compensated HF (New York Heart Association class II to IV) aged 53 to 86 years, with ejection fractions <35% and serum creatinine <2 mg/dl, were randomized into 8 groups: group A (n = 52): 1,000 ml/day of fluid intake, 120 mmol/day, and 250 mg furosemide twice daily; group B (n = 51): 1,000 ml/day of fluid intake, 120 mmol/day, and 125 mg furosemide twice daily; group C (n = 51): 1,000 ml/day fluid intake, 80 mmol/day, and 250 mg furosemide twice daily; group D (n = 51): 1,000 ml/day fluid intake, 80 mmol/day, and 125 mg furosemide twice daily; group E (n = 52): 2,000 ml/day fluid intake, 120 mmol/day, and 250 mg furosemide twice daily; group F (n = 50): 2,000 ml/day fluid intake, 120 mmol/day, and 125 mg furosemide twice daily; group G (n = 52): 2,000 ml/day fluid intake, 80 mmol/day, and 250 mg furosemide twice daily; and group H (n = 51): 2,000 ml/day fluid intake, 80 mmol/day, and 125 mg furosemide twice daily. All patients received the treatments >or=30 days after discharge and for 180 days afterward. Signs of HF, body weight, blood pressure, heart rate, laboratory parameters, electrocardiograms, echocardiograms, brain natriuretic peptide, aldosterone, and plasma renin activity were examined at baseline and 180 days later. Group A showed the best results, with a significant reduction (p <0.001) in readmissions, brain natriuretic peptide, aldosterone, and plasma renin activity compared with the other groups during follow-up (p <0.001). In conclusion, these data suggest that the combination of a normal-sodium diet with high diuretic doses and fluid intake restriction, compared with different combinations of sodium diets with more modest fluid intake restrictions and conventional diuretic doses, leads to reductions in readmissions, neurohormonal activation, and renal dysfunction.
Abstract: BACKGROUND: beta-blockers in ST-segment elevation myocardial infarction (STEMI) are indicated for patients without a contraindication, particularly in patients with high heart rates (HR) or blood pressures. Epidemiological studies have shown that elevated HR represents a risk factor for cardiovascular morbidity. The study investigates the feasibility, tolerability, and the effects after 30 days of follow-up of ivabradine (IVA) versus metoprolol (METO) in early phases of anterior STEMI reperfused by percutaneous coronary intervention (PCI). METHODS AND RESULTS: Patients with a first anterior STEMI, Killip class I-II, an acceptable echocardiographic window, and admitted within 4hours of the onset of symptoms, with an ejection fraction <50%. METO or IVA, 12hours after PCI (double blind), were administered twice per day. Blood pressure (BP), heart rate (HR), electrocardiogram (ECG), and laboratory parameters were monitored during the study. At entry, day 10, day 30, and day 60, by echocardiography, the ESV, EDV, E/A ratio, E wave deceleration time, isovolumetric relaxation time were measured. A total of 155 (50 females, 105 males) patients were randomized in 2 groups: a group received METO (76 patients) 12hours after PCI and a group received IVA (79 patients) 12hours after PCI. The 2 groups were similar for clinical characteristics. No difference was evidenced in HR, systolic blood pressure, diastolic blood pressure, age (range, 39-73 years), sex, ejection fraction (EF), creatine kinase peak, between the 2 groups at entry. Both groups were similar for time to angiography and interventional procedures and number of vessels diseased. IVA group: the 79 patients showed 2 side effects and 5 readmissions: 4 for ischemic events and 1 for heart failure, and 1 sudden death; METO group: the 76 patients had 4 ischemic events, 2 side effects, and 1 patient died during re-acute MI (intrastent thrombosis) and 8 readmissions for heart failure signs. The systolic blood pressure and diastolic blood pressure showed a significant reduction in both groups, P < .0001, respectively), and significant lower values were observed in METO group, P=.0001). The HR was significantly reduced in both groups, P < .0001). IVA group showed a significant increase in EF, P=.0001, with concomitant reduction in ESV and EDV (P=.0001, and .048, respectively). The diastolic parameters were similar in both groups during study period. CONCLUSIONS: Our results suggest that ivabradine may be administered early (12hours after PCI) to patients with successful PCI for anterior STEMI with an impaired left ventricular function and high HR and sinus rhythm. A larger sample of patients and further studies are required to evaluate the effects of ivabradine on clinical end points.
Abstract: A 55-years-old woman, with a history of hypertension and ischemic stroke with residual left hemiparesis, was admitted to our hospital because of dyspnoea with clinical evidence of acute pulmonary edema. She was found to have a sinus tachycardia with ST-elevation in leads D1, aVL and V1-V4 in the electrocardiogram, and akinesis of the left ventricular apex with overall left ventricular systolic function being severely impaired and an ejection fraction of 28% on echocardiography. Orotracheal intubation was performed and mechanical ventilation was immediately started. Emergency cardiac catheterization was performed 2 h after the symptom onset. Coronary angiography showed no significant coronary artery disease. Blood analysis revealed an increase in the creatine kinase MB fraction, a significant positive detection in troponin T, a white blood cell count of 35000 per microliter, C-reactive protein of 59,9 mg/dl, and transient elevation in the concentration of free triiodothyronine, free thyroxine, thyroid globulin antibody, and thyroid peroxidase antibody. The symptoms improved during the next days, and follow-up echocardiography 18 days later showed complete resolution of the left ventricular dysfunction. These data suggest that tako-tsubo cardiomyopathy may be induced in patients with sepsis and transient hyperthyroidism.
Abstract: The aim of the present study was to evaluate the effects of a normal-sodium (120 mmol sodium) diet compared with a low-sodium diet (80 mmol sodium) on readmissions for CHF (congestive heart failure) during 180 days of follow-up in compensated patients with CHF. A total of 232 compensated CHF patients (88 female and 144 male; New York Heart Association class II-IV; 55-83 years of age, ejection fraction <35% and serum creatinine <2 mg/dl) were randomized into two groups: group 1 contained 118 patients (45 females and 73 males) receiving a normal-sodium diet plus oral furosemide [250-500 mg, b.i.d. (twice a day)]; and group 2 contained 114 patients (43 females and 71 males) receiving a low-sodium diet plus oral furosemide (250-500 mg, b.i.d.). The treatment was given at 30 days after discharge and for 180 days, in association with a fluid intake of 1000 ml per day. Signs of CHF, body weight, blood pressure, heart rate, laboratory parameters, ECG, echocardiogram, levels of BNP (brain natriuretic peptide) and aldosterone levels, and PRA (plasma renin activity) were examined at baseline (30 days after discharge) and after 180 days. The normal-sodium group had a significant reduction (P<0.05) in readmissions. BNP values were lower in the normal-sodium group compared with the low sodium group (685+/-255 compared with 425+/-125 pg/ml respectively; P<0.0001). Significant (P<0.0001) increases in aldosterone and PRA were observed in the low-sodium group during follow-up, whereas the normal-sodium group had a small significant reduction (P=0.039) in aldosterone levels and no significant difference in PRA. After 180 days of follow-up, aldosterone levels and PRA were significantly (P<0.0001) higher in the low-sodium group. The normal-sodium group had a lower incidence of rehospitalization during follow-up and a significant decrease in plasma BNP and aldosterone levels, and PRA. The results of the present study show that a normal-sodium diet improves outcome, and sodium depletion has detrimental renal and neurohormonal effects with worse clinical outcome in compensated CHF patients. Further studies are required to determine if this is due to a high dose of diuretic or the low-sodium diet.
Abstract: BACKGROUND: Exercise causes enhanced sympathetic discharge and results in physiologic tachycardia. However, in some patients with a diseased conduction system resulting from acute ischemia, exercise can precipitate heart block. METHODS AND RESULTS: In this report we describe a 51 years old male patient with transient advanced degree atrioventricular (AV) block developed during recovery from exercise stress testing, resolved after the administration of atropine. Nuclear perfusion imaging demostrated stress-induced ischemia of the inferior-apical segments, and recovery of perfusion in the images obtained at rest. Coronarography showed critical stenosis of the right coronary artery, which was treated by percutaneous coronary intervention (PCI) and drug eluting stent (DES) deployment. CONCLUSION: Nuclear myocardial perfusion imaging provides noninvasive evidence that transient ischemia of the infero-apical segment can result in advanced degree AV block in patient with critical severe right coronary disease.
Abstract: AIM: N-terminal pro-b-type natriuretic peptide (NT pro-BNP) is a neurohormone synthesized predominantly in ventricular myocardium. In patients with symptoms of heart failure, elevation in NT pro-BNP accurately identifies ventricular dysfunction. However, NT pro-BNP levels are not specific for ventricular dysfunction in patients who do not have overt symptoms of heart failure, suggesting that other cardiac processes such as myocardial ischemia may also cause elevation in NT pro-BNP. The study was aimed to determine whether NT pro-BNP elevations are associated with myocardial ischemia. METHODS: One hundred and thirty patients (104 males, 26 females, mean age 61+12 years), with ST elevation acute myocardial infarction (STEMI) and preserved left ventricular ejection fraction (>45%) at echocardiography performed at entry, from February 2003 and February 2004 were enrolled. In all patients NT pro-BNP plasma levels were checked at entry and 4-5 days after symptoms onset. In addition, maximal or symptom-limited exercise treadmill test (Bruce protocol), and myocardial perfusion scintigraphy using [(99m)Tc]Tetrofosmin single photon emission computed tomography (SPECT) imaging were performed within 30 days of STEMI. Ischemia was defined as reversible perfusion abnormalities. RESULTS: Of the 130 participants, 66 (51%) had inducible ischemia. Compared with patients in the lowest tertile, those in the highest tertile of NT pro-BNP had a greater significant risk of residual ischemia (odds ratio: 8.66; 95% CI, 3.90 to 19.24). Nevertheless patients in the highest tertile were older (64.19+/-10.80 years versus 55.90+/-9.67 years, P = 0.0001), had a lower left ventricular ejection fraction (49.70+13.46% versus 59.49+/-6.58%, P = 0.0001) and had a great rate of acute myocardial infarction (anterior acute myocardial infarction = 40.63% versus 25%). CONCLUSIONS: Elevated levels of NT pro-BNP are associated with residual myocardial ischemia among patients with STEMI and preserved left ventricular ejection fraction, as demonstrated by perfusion defect on SPECT imaging, suggesting that these patients may need further evaluation for stratification of the future risk of fatal events. The observed association between NT pro-BNP levels and ischemia may explain because tests for NT pro-BNP are not specific for ventricular dysfunction among patients with coronary artery disease.
Abstract: This is the first of a 2-part series. This article reviews the relationships among diuretics, neurohormonal activation, renal function, fluid and Na management, the cardiorenal syndrome, and heart failure. Part II will describe novel therapies based on these relationships, focusing particularly on vasopressin antagonists and treatment using hypertonic saline solution with high-dose loop diuretics. Heart failure (HF) is a complex hemodynamic disorder characterized by chronic and progressive pump failure and fluid accumulation. Diuretics are a vital component of symptomatic management, and enhancing diuretic response in the setting of diuretic resistance is therefore pivotal. In HF patients treated with diuretics, compensatory pathophysiologic mechanisms to maintain vascular resistance, such as nonosmotic stimulation of vasopressin secretion and activation of the renin-angiotensin-aldosterone system and sympathetic nervous system, promote renal Na and water reabsorption. Thus, there remains a need to develop novel therapies for HF patients who are refractory to conventional medical treatment. The conflicting results of diuretic treatments in HF and the importance of Na management in the context of the cardiorenal syndrome and neurohormonal activation have suggested novel and counterintuitive strategies, focusing primarily on the use of vasopressin antagonists and hypertonic saline solution with high doses of loop diuretics and neurohormonal interference. The authors review the current evidence for these therapies and suggest hypothetical bases for their efficacy.
Abstract: The conflicting results of diuretic treatments in heart failure (HF) and the importance of Na management in the context of the cardiorenal syndrome and neurohormonal activation in HF have suggested novel and counterintuitive strategies, focused primarily on the use of vasopressin antagonists and hypertonic saline solution with high doses of loop diuretics and their neurohormonal interference. The emerging novel therapies involving direct inhibition of vasopressin receptors appear to show promising results. The use of hypertonic saline solution mixed with a high dose of loop diuretics produces, probably by indirect mechanisms, a reduction or inhibition of the activated neurohormonal systems in HF patients. This treatment opens a new window on the role of sodium management in these patients and on the relation between sodium and the kidney's role and function in heart failure. The authors review the current evidence for these therapies and suggest hypothetical bases for their efficacy.
Abstract: BACKGROUND: Failure to reach 80% of maximal predicted heart rate (HR) during exercise may render a myocardial perfusion single photon emission computed tomography (SPECT) study non-diagnostic for ischemia detection. We sought to investigate the injection of atropine in patients who fail to achieve 80% of age-predicted HR during exercise performed for myocardial perfusion SPECT (MPS), defining its safety and efficacy to raise HR to adequate levels as well as its effect on MPS interpretation. METHODS AND RESULTS: Between January 2002 and December 2004, we studied 3,150 consecutive patients (2,253 men and 897 women, mean age 55 +/- 6 years) who were referred to a single office-based nuclear cardiology laboratory for MPS using SPECT imaging. One milligram of atropine was administered to patients that were unable to continue because of fatigue before reaching minimal HR, without an ischemic response (group A, n = 397). The scintigraphic results for group A were compared with those of patients who spontaneously achieved target HR (group B, n = 2,753). In group A, mean HR before atropine injection was 119.5 +/- 13.6 beats per minute (bpm), and it increased up to 137.3 +/- 13.5 bpm after drug administration, with an incremental of 17.8 +/- 6.9 bpm (P < 0.0001). The mean percentage of age-related HR achieved in this group was 83.5 +/- 8.1%. In 302 of this patients (76.1%) more than 80% of their aged-related HR (86.9 +/- 5.1%) was attained. No major adverse effects occurred. When groups A and B were compared, baseline and peak HR, rate pressure product, and maximal metabolic equivalents achieved were higher in group B. There were no significant differences in the percentage of total positive perfusion studies between both groups: 210/397 patients (52.9%) in group A and 1,342/2,753 patients (48.7%) in group B (P = 0.39). Ischemia or ischemia plus scar was found in 112/397 patients (28.2%) in group A and in 923/2,753 patients (33.5%) of group B (P = 0.14). CONCLUSION: Atropine added to exercise stress testing in patients who cannot achieve their 80% age-related HR is a safe, well-tolerated, and feasible method for MPS.
Abstract: BACKGROUND: Decreased exercise capacity is the main factor restricting the daily life of patients with chronic heart failure. N-terminal pro-brain natriuretic peptide (NT pro-BNP) is strongly related to the severity of and is an independent predictor of outcome in chronic heart failure. DESIGN: The study aimed to evaluate the effect of exercise training on functional capacity and on changes in NT pro-BNP levels and to assess the effect of exercise training on quality of life. MATERIALS AND METHODS: Sixty patients (45 men/15 women, mean age 52.7 years; +/-5.3 SD), with stable heart failure (45 ischaemic/hypertensive and 15 idiopathic patients), in New York Heart Association (NYHA) functional class II (n=35) to III (n=25), with an ejection fraction less than 40%, were randomly assigned to a training (n=30) and a control group (n=30). The training group (30 patients) performed 3 months of supervised physical training programme using a bicycle ergometer for 30 min three times a week at a load corresponding to 60-70% of their oxygen consumption (VO2) peak. The control group did not change their previous physical activity. A graded maximal exercise test with respiratory gas analysis and an endurance test with constant workload corresponding to 85% of the peak oxygen load at the baseline and after 3 months were performed, and at the same times NT pro-BNP levels were measured. RESULTS: The exercise capacity increased from 15.8 (+/-2.3 SD) to 29.9 (+/-2.1 SD) min (P<0.0001) and the peak VO2 tended to improve from 14.5 (+/-1.4 SD) to 17.7 (+/-2.6 SD) ml/kg per min (P<0.0001) during the supervised training period. VO2 at the anaerobic threshold increased from 12.9 (+/-1.0 SD) to 15.5 (+/-1.7 SD) ml/kg per min (P<0.0001). NT pro-BNP levels decreased from 3376 (+/-3133 SD) to 1434 (+/-1673 SD) pg/ml (P=0.043). The positive training effects were associated with an improvement in the NYHA functional class. CONCLUSION: Physical training of moderate intensity significantly improves the exercise capacity and neurohormonal modulation in patients with chronic heart failure. This is associated with an alleviation of symptoms and improvement in quality of life.
Abstract: BACKGROUND: There are several new strategies proposed to improve the outcome of patients with ST-elevation myocardial infarction (STEMI). One approach is the resurgent use of facilitated percutaneous coronary interventions (PCI). Until recently, deciding whether immediate PCI after combined treatment (facilitated PCI) is more appropriate than delayed PCI (short time) has not been investigated. The aim of this study, therefore, was to investigate the outcomes in patients initially successfully treated pharmacologically and immediate PCI < 2 hr, and in patients initially successfully treated with pharmacological therapy and with delayed PCI (12-72 h). METHODS: 451 reperfused STEMI patients, aged 18 to 75 years, class I-II Killip, with an acceptable echocardiographic window and admitted within 12 hs of the onset of symptoms were randomized into two groups. All patients had to have successful reperfusion, to receive the combination of a standard tirofiban infusion or abciximab plus half dose rtPA. Thereafter, patients were sub-grouped as follows:group 1 (immediate PCI) patients had PCI within 2 h; and group 2 (delayed PCI) patients in which PCI was performed after 12 hs and within 72 hs. RESULTS: The 225 reperfused (immediate-PCI) and 226 reperfused (delayed-PCI) patients (time from randomization to PCI 165 +/- 37 min in immediate PCI versus 45.1 +/- 20.2 h in delayed PCI group) showed similar results in ejection fraction, CK release and patency of the IRA. In addition, the delayed PCI group showed a significant reduction in ischemic events, restenosis and bleedings (P = 0.005, 0.01, 0.01 respectively) and significant reduced angiographic evidence of thrombus formation in the infarction-related artery (IRA) (p = 0.001). CONCLUSION: Our data suggest the safety and possible use of delayed facilitated PCI in patients with STEMI, and that delayed PCI in patients treated with combined lytic and IIb/IIIa inhibitors appears to be as effective and possibly superior (reduced ischemic events and repeat PCI) as immediate PCI. The patients in this study were successfully reperfused, with TIMI-3 flow and our data may not apply to patients with TIMI 0-2 flow. This strategy could allow transferring the reperfused patients and performing PCI after hours < 72 hours and not immediately, thereby reducing the number of urgent PCI and costs, obtaining similar results, but mostly causing less discomfort to the patient. Our results had to be interpreted with caution, because current guidelines do not recommend the combined therapy, but suggest further studies.The study was aimed to investigate the outcomes in patients initially successfully treated pharmacologically and immediate PCI < 2 h, and in patients initially successfully treated with pharmacological therapy and delayed PCI (12-72 h). All patients had to have successful reperfusion, to receive the combination of a standard abciximab or tirofiban infusion plus half dose rtPA. Similar results were observed in both groups. Delayed PCI group showed a significant lower incidence in restenosis (0.01), minor bleedings (0.005), ischemic events (0.01) and a reduced angiographic evidence of thrombus formation in IRA (0.001). Our data suggest the safety and possible use of delayed facilitated PCI in patients with STEMI. Our results had to be interpreted with caution, because current guidelines do not recommend the combined therapy, but suggest further studies.
Abstract: OBJECTIVES: The aim of this study was to evaluate the effect of a new treatment for refractory congestive heart failure (CHF) on brain natriuretic peptide (BNP) plasma levels and hydration station. BACKGROUND: The study was aimed at evaluating the effects of the combination of high-dose furosemide and small-volume hypertonic saline solution (HSS) in refractory CHF patients. METHODS: A total of 94 patients (34 women/60 men) with refractory CHF (age 55 to 80 years) were enrolled. They had to have an ejection fraction <35%, serum creatinine <2 mg/dl, blood urea nitrogen <60 mg/dl, a reduced urinary volume, and a low natriuresis (<500 ml/24 h and <60 mEq/24 h, respectively). Patients were divided (double-blind) into two groups: group 1 (18 women/30 men) received an intravenous furosemide (500 to 1,000 mg) plus HSS twice a day in 30 min. Group 2 (16 women/30 men) received an intravenous bolus of furosemide (500 to 1,000 mg/twice a day) alone, for four to six days. At entry, body weight, blood pressure, heart rate, and laboratory parameters were checked during hospitalization; BNP levels were measured on admission, 6 and 30 days after discharge, while on admission and 6 days after, impedance plethysmography was performed. The HSS group received 120 mmol of Na intake versus 80 mmol in non-HSS group. Fluid intake of 1,000 was given to both groups. RESULTS: The groups were similar for clinical characteristics. A significant increase in daily diuresis and natriuresis was observed in HSS group, p < 0.05. The BNP values showed significant intragroup and intergroup differences, 6 and 30 days after treatment. The patients from the HSS group reached a better hydration state than the non-HSS group after six days. In addition, the HSS group showed a significant reduction in hospitalization time and readmission rate. CONCLUSIONS: Our data show that the HSS group reached dry weight more rapidly, a significantly faster reduction in BNP levels, shorter hospitalization stay, and lower incidence in readmissions in the 30-day study period.
Abstract: BACKGROUND: An increasing number of studies with conflicting results regarding the association between angiotensin-converting enzyme (ACE) gene deletion polymorphism and cardiovascular disease has recently been published. The present prospective long-term study was conducted to evaluate whether the DD genotype could also be associated with a higher prevalence of hypertension in healthy subjects over 6 years of follow-up. We also investigated the effects of the ACE-I/D genotypes on diastolic function by echocardiography in healthy subjects without any risk factors and any events after 6 years of follow-up. METHODS: Population: 684 healthy volunteers (aged 25-55 years) normotensive and free of cardiovascular diseases, with acceptable echocardiographic window were enrolled. All subjects had to have a normal electrocardiogram (ECG) and echocardiogram (ECHO) at entry. All subjects have undergone a complete physical examination, 12-lead ECG and ECHO; DNA analysis and serum cholesterol have been performed on venous blood samples. All subjects underwent a clinical evaluation each year for the 6-year duration of the study. In addition, 275 subjects without any risk factors underwent an ECHO every year of the follow-up, to check the influence of genotypes on myocardial diastolic performances. RESULTS: All 684 subjects completed 6 years of follow-up. We obtained 3 genetically distinct groups: I) the ACE-DD group (n = 225, 80 F/ 145 M, mean age 43.4 +/- 7.6 years) with 42 hypertensive subjects (18.3%), 5 heart failure (HF) subjects and 6 subjects with acute coronary syndromes (ACS). There was no association between family history, smoking habit, hypercholesterolaemia and events. 2) the ACE-ID group (n = 335, 116 F/2 19 M, mean age 43.6 +/- 7 years) with 16 hypertensive subjects (4.7%) and 3 subjects with ACS. 3) the ACE-II group (n = 124, 45 F/79 M, mean age 42.5 +/- 6.9 years) with 2 hypertensive subjects (1.6%) and I HF subject. The incidence of hypertension and cardiovascular events, was significantly higher in the ACE-DD (53 cases, 23%) than in the ACE-ID and ACE-II groups (20 and 3 cases, 5.9% and 2.4%, respectively), p = 0.0001. The higher incidence of hypertension was observed in the older age groups (36-45 and 46-55 years) with ACE-DD and ACE-ID genotypes. Moreover, ACE-DD significantly and early affected myocardial diastolic properties in the total group examined, also when stratified for age. There was a reduction of E/A ratio and it was more evident in subjects aged 36-45 and 46-55 years, p = 0.0001. CONCLUSION: Our data suggest that ACE-DD polymorphism is associated with a higher incidence of hypertension in baseline healthy subjects, irrespective of other risk factors, and appears to affect the diastolic function. These effects were apparent predominantly in the older age groups.
Abstract: BACKGROUND: Non-invasive positive pressure ventilation (NIPPV) is an effective treatment for acute respiratory failure in patients with chronic obstructive pulmonary disease. We assessed the efficacy and safety of this therapy in acute cardiogenic pulmonary edema (ACPE). METHODS: In addition to routine therapy consisting of oxygen, nitrates and diuretics, 60 patients (39 male, 21 female, mean age 72.5 +/- 15.8 years) were started on full mask NIPPV using a Sullivan VPAP II ventilator delivering pressure support 15 cm H2O, PEEP 5 cm H2O, FiO2 100%. Pressure support were titrated to achieve oxygen saturation (SaO2) > 95%. Physiological measurements were obtained in the first 2 h and at 3 h, 4 h, and 10 h. Outcome measures included arterial blood gas (ABG), Borg dyspnea score, vital signs, and need for endotracheal intubation (ETI). RESULTS: Initial mean values on FiO2 100% by non nonrebreather mask: pH 7.11 +/- 0.25, paCO2 67.7 +/- 17.5 mmHg, paO2 71.5 +/- 29.7 mmHg, SaO2 83 +/- 12%, lactate concentrations 4.7 +/- 2.3 mmol/L, Borg score 8.6 +/- 1.3, respiratory rate (RR) 41 +/- 7. At 60 minutes of NIPPV, improvement was statistically significant: pH 7.35 +/- 0.18 (difference 0.24; p < 0.0001), paCO2 43 +/- 13 mmHg (difference 24.7; p < 0.0001), paO2 102 +/- 10 mmHg (difference 30.5; p < 0.0001), SaO2 99 +/- 5% (difference 16; p < 0.0001), lactate concentrations 1.2 +/- 0.8 (difference 3.5; p < 0.0001) Borg score 3.6 +/- 0.9 (difference 5; p < 0.0001), RR 24.6 +/- 5 (difference 17.1; p < 0.0001). NIPPV duration ranged from 40 minutes to 24 hours (median 3 hours, 30 minutes). Fifty-six patients (93.4%) improved allowing cessation of NIPPV. ETI was required in four (6.6%) of 60 patients. There were non complications of NIPPV. CONCLUSION: In this study of acute cardiogenic pulmonary edema, NIPPV is an effective treatment and may help prevent ETI.
Abstract: BACKGROUND: The ACE-D allele has been associated with cardiovascular disease. The study evaluates the relationship between the ACE-ID genotypes and diastolic function in healthy subjects after 6 years of follow-up. METHODS: Two hundred and seventy-five healthy volunteers aged 25-55 years had normal physical examination, 12-lead ECG, acceptable echocardiographic windows and echocardiogram at entry. Venous blood was drawn for DNA analysis. RESULTS: Two hundred and forty-two subjects completed 6 years of follow-up. Three genetically distinct groups were obtained: ACE-DD group (n=71, 26F/45M, mean age 48 +/- 7 years); ACE-ID (n=115, 39F/76M, mean age 40 +/- 7 years); and ACE-II (n=56, 20F/36M, mean age 47 +/- 6 years). Significant differences in E/A ratio were found between ACE-DD and ACE-ID, and ACE II (p=0.028, <0.0001, 0.0001), respectively. After 6 years, echocardiography showed a significant reduction of E/A ratio in the ACE-DD group, p=0.0001. CONCLUSION: The data suggest that ACE-DD is associated with deteriorating myocardial diastolic properties.
Abstract: INTRODUCTION: Patients with a negative troponin (TnT) result showed 1.4% mortality during a mean follow-up of 9-10 weeks. Mortality was greater in patients with an evidence of ischemic ECG changes and a negative TnT test (1.6-4.4%). Few studies have examined the efficacy of echocardiography (2DE) in patients with chest pain. The purpose of the present study was to determine the clinical utility, sensitivity and specificity of the combination of TnT levels and 2DE in patients presenting with chest pain, ST-depression, T-wave negative and no diagnostic ECG. METHODS: 280 consecutive patients with chest pain and presence of ST depression, T-wave inversion, and non-diagnostic ECG, acceptable 2DE window, evidence or no evidence of alterations of the segmentary motion, and evidence and no evidence of injury, as assessed by TnT and normal value of CK-CK MB, were enrolled. 2DE, blood CK, and TnT levels were controlled at entry and subsequent samples were obtained every 4 h for the first 12 h and then every 12 h. All patients performed angiography within 12-72 from admission. PTCA or CABG were performed according to angiographic findings and left ventricular function. RESULTS: The 280 patients (98 F/M 182), mean age 59.7+/-11.9 years, who met the entry criteria, were divided as follows: group 1: ST-segment depression (192 patients); group 2: T-wave inversion (36 patients); and group 3: non-diagnostic ECG (52 patients). The combination of positive TnT and wall motion alterations showed a higher sensitivity, specificity and predictive values in comparison with alone TnT or 2DE. Patients, with the concordance between TnT and 2DE, were at higher risk. Patients with negative combination in all groups (94), showed a low incidence of coronary stenosis (10.6%), as well as negative 2DE alone (102 patients) (12.7%), while patients with negative TnT (128) showed higher incidence of coronary stenosis (39%), p < 0.0001. CONCLUSION: Our results suggest that the combination of negative TnT test and negative 2DE in patients presenting to EDs with chest pain either with ECG changes or without ECG changes is a useful tool to identify those who can be discharged safely. We think that our data are important because by the combination we can identify the high risk (when positive) patients, reduce incidence of the false negative, but mostly it allows us to identify true negative patients to discharge safely.
Abstract: AIM: The aim of this study was to evaluate glycoprotein IIb/IIIa receptor inhibitor effectiveness in AMI patients with unsuccessful thrombolysis. METHODS: Eighty-four patients hospitalised within 4 h of symptom onset were randomised (single blind) into two groups. Regardless of the group, placebo or GP IIb/IIIa inhibitors were administered to patients who did not present with reperfusion signs 30 min after starting thrombolysis and 30-60 min after the end of full thrombolysis in patients with pain recurrence and ST-segment elevation. Reperfusion was assessed by the creatine kinase peak occurring within 12 h, by the observation of rapid ST-segment reduction (50-70% within 1 h) in 12-lead ECG continuous monitoring, by the rapid regression of pain and by the development of early ventricular arrhythmias. Group 1 (GP IIb/IIIa) (42 patients) received treatment with GP IIb/IIIa inhibitors i.v., heparin according to TIMI-14 trial and aspirin during failed thrombolysis or after 30-60 min effective thrombolysis because of pain recurrence and ST segment elevation. Group 2 (placebo) (42 patients) received a full dose of rtpA (100 mg) and placebo either during failed thrombolysis or after 30-60 min effective thrombolysis because of pain recurrence and ST segment elevation and standard heparin treatment and aspirin. RESULTS: Thirty-nine group 1 (GP IIb/IIIa) patients showed rapid reperfusion (6 +/- 4 min) after abciximab treatment; 22 patients received rtpA 65 mg and 20 patients received rtpA 100 mg and subsequent GP IIb/IIIa inhibitor treatment. Coronarography, performed after 3-12 h, showed patency of infarct related artery (IRA) in 39 patients whose clinical picture was suggestive of rapid reperfusion during administration of a bolus of GP IIb/IIIa inhibitors. No group 2 (placebo) patients showed reperfusion and they were submitted to rescue PTCA. SIDE EFFECTS: Four cases in the GP IIb/IIIa group and two cases in placebo group (major bleeding). Patients receiving GIIb/IIIa inhibitors showed a reduced incidence of stent treatment (ns) and a significant reduction of events (angina) within 30 days of treatment. CONCLUSION: Our data suggest the possibility of using IIb/IIIa glycoprotein receptor inhibitors in patients with AMI and failed thrombolysis. The increased risk of bleeding was acceptable. The most important results were the safety of this combination.
Abstract: BACKGROUND: ST segment depression (STD) is a standard electrocardiographic sign of myocardial ischemia. Although STD may represent reciprocal changes in patients with previous myocardial infarction, studies of reciprocal changes during exercise testing are scarce. METHODS: From December 1999 to December 2000, 160 patients (119 males, 41 females, mean age 54 +/- 8 years), undergoing, maximal or symptom-limited exercise treadmill test (Bruce-protocol), myocardial perfusion scintigraphy using technetium-99m tetrofosmin single photon emission computed tomography (SPECT) imaging, within 30 days of an uncomplicated inferior Q wave myocardial infarction. The location of STD at the electrocardiogram (ECG) was defined as anterior (V1-4), high lateral (I, aVL), and lateral (V5-6). Ischemia was defined as reversible perfusion abnormalities. RESULTS: STD occurred in anterior leads in 29 patients (18.1%), in the lateral leads in 41 patients (25.6%), in the high lateral leads in 20 patients (12.5%). In 70 patients (43.8%) no significant STD occurred during the exercise test. ST segment elevation occurred in 28 patients (17.5%) in inferior leads. High lateral STD was associated with inferior ST elevation in 16 patients (80%), whereas only eight patients (19.5%) with lateral STD and nine patients (31%) with anterior STD were associated with inferior ST elevation. Ischemia was detected in 63 of 90 patients (70%) with and in 10 of 70 patients (14.3%) without STD (p < 0.0001). Patients with high lateral STD had a higher prevalence of fixed perfusion defects in the inferior wall (95 vs. 27.8%) and in posterolateral wall (75 vs. 18.9%) compared with other patients (p = 0.003 and 0.002, respectively). Ischemia was more prevalent in patients with lateral STD than without (87.8 vs. 14.3%, p < 0.0001). CONCLUSION: In patients with inferior Q wave, the presence of exercise-induced STD in lateral and anterior leads appears to be a sign of myocardial ischemia, and may require invasive evaluation; on the other hand, the presence of STD in high lateral leads should be recognized as a reciprocal change for ST elevation in the inferior leads, and may not be an indication for invasive evaluation.
Abstract: BACKGROUND: The aim of this study was to evaluate the effectiveness of glycoprotein (GP) IIb/IIIa receptor inhibitors in acute myocardial infarction (AMI) patients in case of unsuccessful and failed thrombolysis. METHODS: Eighty-four patients hospitalized within 4 hours of symptom onset were randomized (single blind) into two groups. Regardless of the group, placebo or GP IIb/IIIa inhibitors were administered to patients who did not present with reperfusion signs (failed thrombolysis) 30 min after starting thrombolysis and 30-60 min after the end of full thrombolysis in patients with pain recurrence and ST-segment elevation (unsuccessful thrombolysis). Reperfusion was assessed by the creatine kinase peak occurring within 12 hours, by the observation of rapid ST-segment reduction (50-70% within 1 hour) in the 12-lead ECG continuous tracing, by the rapid regression of pain and by the development of early ventricular arrhythmias. Group 1 patients (n = 42) received, during failed thrombolysis or after 30-60 min of effective thrombolysis but with pain recurrence and ST-segment elevation (unsuccessful thrombolysis), treatment with i.v. GP IIb/IIIa inhibitors, heparin according to the TIMI 14 trial, and aspirin. Group 2 patients (n = 42) received a full dose of recombinant tissue-type plasminogen activator (rt-PA 100 mg) and placebo either during failed thrombolysis or, after 30 min of effective thrombolysis but with pain recurrence and ST-segment elevation, and standard heparin treatment and aspirin. RESULTS: In group 1, 39 patients showed rapid reperfusion (4 +/- 3 min); 22 patients received rt-PA 65 mg and 20 patients received rt-PA 100 mg and subsequent GP IIb/IIIa inhibitor treatment. Coronary angiography, performed after 12-72 hours showed patency of the infarct-related artery in 39 patients whose clinical picture was suggestive of rapid reperfusion during administration of a bolus of GP IIb/IIIa inhibitors. In group 2, no patients showed reperfusion and they were submitted to rescue coronary angioplasty (p < 0.05). Side effects occurred in 3 cases in group 1 and in 2 cases in group 2. Patients receiving GP IIb/IIIa inhibitors showed a reduced incidence of stent treatment (p = NS) and a significant reduction in the occurrence of events (angina) within 30 days of treatment (p = NS). CONCLUSIONS: Our data suggest that in patients with AMI and failed thrombolysis, treatment with GP IIb/IIIa receptor inhibitors is feasible. The increase in the risk of bleeding was acceptable. The most important result was that this combination is safe.
Abstract: BACKGROUND: The goal of therapy in acute myocardial infarction (AMI) is the complete and timely restoration of coronary blood flow. Platelets have a pivotal role in the pathophysiology of AMI. The study was aimed at evaluating the safety and efficacy of the combination of 50 mg alteplase plus tirofiban vs 100 mg alteplase in AMI patients. METHODS: One hundred twenty patients (83 males, 37 females; mean age 54.3 +/- 8 years) were hospitalized for suspected AMI within 6 hours of the onset of symptoms. All patients presented pain and persistent ST-segment elevation, were suitable candidates for thrombolysis (1st episode) and were randomized (double blind) into two groups. Group A (n = 60,42 males, 18 females) received 50 mg alteplase (15 mg as bolus, followed by an infusion of 35 mg over 60 min) in combination with tirofiban (0.4 mcg/kg/min for 30 min followed by an infusion of 0.1 mcg/kg/min for 3 days). Group B (n = 60, 41 males, 19 females) received 100 mg of accelerated-dose alteplase alone. Reperfusion criteria were defined as follows: > 50% reduction in the ST-segment elevation; resolution of chest pain; double marker of creatine kinase (CK) and CK-MB activity 2 hours after the start of thrombolysis; reperfusion arrhythmias within the first 120 min of thrombolysis. The blood pressure, heart rate and ECG were continuously monitored. The mortality, re-AMI, recurrent angina, major and minor bleeding, and emergency bypass surgery or coronary angioplasty were checked. RESULTS: The groups were similar with regard to clinical data, risk factors, time elapsed from the onset of symptoms to thrombolytic therapy and AMI localization. Forty-seven patients (78.3%) from group A showed reperfusion (15-60 min) vs 25 patients (41.7%) from group B (43-105 min after the end of full-thrombolysis, p = 0.01). Group A patients showed an earlier CK peak and lower CK and CK-MB peaks than those in the control group (p = 0.0001, p = 0.011, p = 0.005, respectively). Nine patients (7.5%) died: 6 (10%) in group B and 3 (5%) in group A (p = NS). A non-fatal re-AMI occurred in 8 patients from group A and in 4 patients from group B (p = NS). Recurrent angina occurred in 27 patients (45%) from group A and in 11 (18.3%) from group B (p = 0.037). Twenty-three of these patients underwent urgent coronary angioplasty (17 from group A and 6 from group B) and 3 from group A and 1 from group B underwent urgent coronary artery bypass grafting (p = NS). The frequency of minor bleeding was higher in group A than in group B (56.7 vs 25%, p = 0.033). No major bleeding was observed in the study groups. At the predischarge echocardiogram, the ejection fraction was higher in group A than in group B (50 +/- 9 vs 44 +/- 7%, p = 0.001). CONCLUSIONS: Our data suggest that the combination of glycoprotein IIb/IIIa inhibitors plus alteplase is feasible in AMI patients and that the increased risk of bleeding is an acceptable risk considering the advantage in terms of the reduction in the extent of an AMI. In addition, this combination can allow one to gain time when it is necessary to perform mechanical revascularization in patients admitted to a hospital without an interventional cardiology laboratory or in those who have to be referred to another hospital for urgent coronary artery bypass grafting.
Abstract: BACKGROUND: Recent evidence suggests that, via the mineralocorticoid receptors present in cardiovascular tissues, aldosterone exerts profibrotic effects, and that partial aldosterone escape occurs during ACE-inhibitor treatment. METHODS: A double-blind, randomized study was performed in order to evaluate the feasibility, tolerability, and the effects of the administration of 25 mg/day of canrenoate plus captopril versus captopril alone to patients with anterior acute myocardial infarction (AMI) unsuitable for or not receiving thrombolytic treatment and to patients in whom such treatment resulted or did not result in reperfusion. One hundred eighty-seven patients with anterior AMI were included in the present study. In all cases serum creatinine concentrations and serum K concentrations were < 2.0 mg/dl and < 5.5 mmol/l respectively. The patients were randomized in two groups: the canrenoate group included 94 patients who received captopril and 25 mg i.v. of canrenoate (1 mg/hour for the first 72 hours and then orally 25 mg/day) whereas the placebo group (93 patients) received captopril and placebo. On admission and on days 10, 90 and 180 all patients underwent echocardiography in order to determine the end-systolic volume (ESV), the ejection fraction (EF), the end-diastolic diameter, the E/A ratio, the E deceleration time as well as the isovolumetric relaxation time (IVRT) and the E and A peak velocities. RESULTS: Unreperfused patients did not show patency of the infarct-related artery whereas in reperfused patients this vessel was patent (7-10 days after AMI). The two groups were similar in age, sex, incidence of diabetes, smoking habits, hypertension, creatine kinase enzymatic peak, adjuvant therapy, baseline EF, ESV, and incidence of coronary artery bypass grafting/coronary angioplasty. Following 10 days of treatment (canrenoate group), only 9 patients presented with serum K and creatinine concentrations respectively > 5.5 mmol/l and > 2.0 mg/dl. Among those patients receiving canrenoate, the mitral E/A ratio was higher compared to the placebo group (p = 0.001) whereas the ESV was significantly reduced (p < 0.05). The deceleration time for reperfused patients receiving canrenoate was higher than that observed for reperfused patients in the placebo group. The intragroup EF was significantly increased (p = 0.042). Compared to the placebo group, the IVRT was significantly higher for unreperfused patients receiving canrenoate than in the placebo group (p = 0.001). Serum creatinine, blood urea and K levels as well as the incidence and extent of vessel disease were similar for both groups. No side effects were observed during the study period. CONCLUSIONS: Our data suggest that the combination of captopril plus canrenoate is feasible for the initial treatment of patients presenting with AMI. Besides, compared to captopril alone it is more efficacious in improving the E/A ratio, the ESV, the EF, and the IVRT.
Abstract: BACKGROUND: Thrombolysis reduces mortality in patients with acute myocardial infarction hospitalized within 6 hours of the symptom onset. Infarctions involving a small area of the myocardium show a lower mortality in comparison to those involving a large area. The aim of this study was to evaluate the safety and efficacy of rescue thrombolysis in patients with large acute myocardial infarction who had failed standard thrombolysis. METHODS: From January 1995 to December 1997, ninety patients (69 males, 21 females, mean age 56.7 +/- 9 years), hospitalized for suspected acute myocardial infarction within 4 hours of the symptom onset, suitable for thrombolysis (first episode), and who experienced pain and showed persistent ST segment elevation 120 min after starting thrombolysis, were randomized (single blind) into two groups: Group A (n = 45) received an additional thrombolytic treatment (rt-PA 50 mg), 10 mg as a bolus plus 40 mg in 60 min; Group B (n = 45) received conventional therapy. Positive non-invasive markers were defined as follows: resolution of chest pain; > 50% reduction in ST segment elevation; double marker of creatine phosphokinase (CPK) and CK-MB activity 2 hours after the start of thrombolysis; occurrence of reperfusion arrhythmias within the first 120 min of thrombolytic therapy. Blood pressure, heart rate and ECG were continuously monitored. Echocardiogram was carried out at entry and before discharge to control ejection fraction and segmental wall motion. Adverse events such as death, reinfarction, recurrent angina, incidence of major and minor bleeding, and emergency bypass surgery or coronary angioplasty were checked. RESULTS: Thirty-five patients (77.7%) showed reperfusion (10-50 min) after the start of additional rt-PA. In patients who did not receive additional thrombolysis, only 12 (26.6%) showed reperfusion 65-115 min after the end of rt-PA infusion. Group A showed an earlier and lower CK and CK-MB peak than Group B (p = 0.0001, p = 0.009, and p = 0.002, respectively). Mortality (n = 16, 17.7%) was higher in Group B (n = 13) than in Group A (n = 3) (28.8 vs 6.6%, p = 0.041). Seven patients from Group A showed non-fatal reinfarction. Angina was observed in 18 (40%) patients from Group A and 3 (6.6%) from Group B (p = 0.006). Ten of these patients underwent urgent coronary angioplasty (9 from Group A and 1 from Group B) and 3 from Group A urgent bypass surgery. Minor bleeding was higher in Group A than in Group B (44.4 vs 15.5%, p = 0.047). A major bleeding was observed in Group A (non-fatal stroke). At predischarge echocardiogram ejection fraction was higher in Group A than in Group B (46 +/- 8 vs 38 +/- 7%, p = 0.0001). CONCLUSIONS: Our data suggest that an additional dose of a thrombolytic drug in patients with unsuccessful thrombolysis is feasible, and the bleeding increase is an acceptable risk in comparison with the advantages obtained from a reduced infarct extension. Rescue thrombolysis could save time and allow mechanical revascularization to be carried out in patients admitted to a hospital without interventional cardiology laboratory or in those who have to be refereed to other hospitals for urgent bypass surgery.
Abstract: Thrombolysis reduces mortality in patients with acute myocardial infarction (AMI) who are hospitalized within 6 hours from the onset of symptoms. AMIs involving a small area of myocardium show a lower mortality in comparison with AMI involving a large area. The present study was aimed at evaluating the safety and efficacy of rescue thrombolysis in patients with large AMI who had failed thrombolysis. Ninety patients (69 Males and 21 Females), mean age 56.7 +/- 9 years, hospitalized for suspected AMI within 4 hours from the onset of symptoms, suitable for thrombolysis (First episode), and showing pain and persistent ST segment elevation 120 minutes after starting thrombolysis, were randomized (double-blind) into two groups. Group A (45 patients: 10 females and 35 males) received an additional thrombolytic treatment (rTPA 50 mg), 10 mg as bolus plus 40 mg in 60 minutes. Group B (45 patients: 11 females and 34 males) received placebo. Positive noninvasive markers were defined as follows: (1) resolution of chest pain, (2) > or = 50% reduction in ST segment elevation, (3) double marker of creatine kinase (CK) and CK-MB activity 2 hours after the start of thrombolysis, and (4) occurrence of reperfusion arrhythmias within the first 120 minutes of thrombolytic therapy. Blood pressure, heart rate, and ECG were continuously monitored. An echocardiogram was carried out at entry, and before discharge, to control ejection fraction and segmentary kinetics. Adverse events such as death, re-AMI, recurrent angina, incidence of major and minor bleeding, and emergency CABG/PTCA were checked. The groups were similar in terms of age, sex, diabetes, smoking habits, hypertension, and adjuvant therapy (beta-blockers). No significant difference was observed between the two groups regarding the time elapsed from the onset of symptoms to thrombolysis and AMI localization. Thirty-five patients (77.7%) showed reperfusion (10-50 minutes) after commencement of additional rTPA. Of the patients receiving placebo, 12 (26.6%) showed reperfusion within 35-85 minutes. Group A showed an earlier and lower CK and CK-MB peak than the control group, (respectively, p = 0.0001-0.009 and 0.002). Mortality (17.7%, 16 patients) was higher in group B than in the additional rTPA group, i.e., 6.6% (3 patients) in group A versus 28.8% (13 patients) in Group B (p = 0.041). Seven patients from group A showed nonfatal re-AMI. Angina was observed in 18 patients (40%) from group A and 3 (6.6%) from group B (p = 0.006). Ten of these patients underwent urgent PTCA (9 from group A and 1 from group B), and 3 from group A underwent urgent CABG. Minor bleeding was higher in group A than in group B (44.4% versus 15.5%, p = 0.047). Major bleeding was observed in group A (nonfatal stroke). At predischarge, the echocardiogram ejection fraction was higher in group A than in group B (46 +/- 8% versus 38 +/- 7%, p = 0.0001). Our data suggest that an additional dose of thrombolytic drug in patients with unsuccessful thrombolysis is feasible and also that the bleeding increase is an acceptable risk in comparison with the advantages obtained in reducing AMI extension. Rescue thrombolysis can allow a gain in time to perform mechanical revascularization in patients admitted to hospital without an interventionist cardiology laboratory or in those who have to be referred to another hospital for urgent CABG.
Abstract: It is common practice to hospitalize patients with chest pain for a period of observation and to perform further diagnostic evaluation such as exercise treadmill testing (ETT) once acute myocardial infarction (AMI) has been excluded. This study evaluates the safety and efficacy of immediate ETT for patients admitted to the hospital with acute chest pain. One hundred and ninety non-consecutive low-risk patients admitted to the hospital from emergency department with acute chest pain underwent ETT using Bruce protocol immediately on admission to the hospital (median time 165+30 min). Fifty-seven (30%) patients had positive exercise electrocardiograms, 44 (77.2%) of whom had significant coronary narrowing by angiography. An uncomplicated anterior non-Q-wave AMI was diagnosed in one patient. One hundred and eleven (58.4%) patients had negative and 22 (11.6%) patients had non-diagnostic exercise electrocardiograms. Of these 133 patients, 86 (64.7%) were discharged immediately after ETT, 19 (14.3%) were discharged within 24 h, and 28 (21%) were discharged after 24 h of observation. There were no complications from ETT. During the 17+/-6 months follow-up no patients died, and only eight (7.2%) patients with negative ETT experienced a major cardiac event (one AMI and seven angina). In conclusion, our results suggest that immediate ETT of low-risk patients with chest pain who are at sufficient risk to be designated for hospital admission, is effective in further stratifying this group into those who can be safety discharged immediately and those who require hospitalization.
Abstract: Two cases of severe intoxication after ingestion of cooked tuna fish were observed. Symptoms and clinical signs were consistent with the scombroid syndrome. Cardiovascular shock was observed in both patients and was associated with subendocardial myocardial infarction in 1 case and acute pulmonary edema with myocardial ischemia in the other. The importance of ECG monitoring in the Intensive Coronary Care Unit is stressed.
Abstract: BACKGROUND: A prospective study has been done on 46 patients with suspected coronary artery disease (CAD). They had no history of myocardial infarction (MI) and a normal basal kinetic echocardiography. This was done in order to evaluate the overall accuracy of dobutamine-atropine stress echocardiography (DAS) compare to exercise stress test (ET) for the diagnosis of CAD. METHODS: All the patients after suspension of coronary therapy, performed a casual sequence with both maximal or symptom limited exercise testing (treadmill-Bruce protocol) and DAS. The dobutamine has been given while monitoring systemic blood pressure, electrocardiography and echocardiography in steps of 10 mcg/kg/min' per 3 min' up to a maximum of 40 mcg/kg/min'. Atropine has been added (0.25-1 mg) in patients who did not reach the theoretical maximal cardiac frequency. The test is considered positive when kinetic segmental left ventricular dysfunction appeared. CAD was defined as 50% luminal area stenosis in at least 1 coronary artery at coronary angiography. RESULTS: Significant CAD was present in 27/46 patients (59%). Compared with ET, DAS had significantly higher sensitivity (59% vs 92%, p = 0.01). The different sensibility between the two tests was higher on these patients with a 1 vessel disease (40% vs 86%, p = 0.02). There were no significant differences in specificity among the two tests (79% vs 84%, respectively). Differences in overall accuracy between ET and DAS were significant (67% vs 89%, p = 0.02). CONCLUSIONS: The results of our study show that the DAS is a safe and feasible technique with high sensibility (especially in patients with single CAD) and specificity. This is a valid alternative to the traditional ET, especially for these patients unable to exercise or these who are poorly motivated to achieve a work load sufficient to make the test interpretable.
Abstract: The usefulness of high-dose (< or = 0.84 mg/kg over 10 minutes) dipyridamole echocardiography testing was compared with that of exercise thallium-201 scintigraphy in detecting restenosis (> 70% lumen reduction) in 50 asymptomatic patients with ST-segment depression during maximal exercise testing 3 months after successful coronary angioplasty. Dipyridamole echocardiography testing and exercise thallium scintigraphy showed a similar sensitivity (75 vs 83%; p = NS) and specificity (90 vs 84%; p = NS) for the detection of restenoses, which occurred in 12 patients. It is concluded that dipyridamole echocardiography testing is as accurate as exercise thallium testing for the noninvasive detection of severe restenosis in patients with exercise-induced asymptomatic ST-segment depression after successful angioplasty. Furthermore, the site, extent and severity of the thallium perfusion defects during exercise are correlated to those of the dyssynergy during dipyridamole echocardiography.
Abstract: Although thrombolytic therapy reduces mortality in patients with acute myocardial infarction (AMI), it is associated with a greater incidence of successive coronary events, and there is still no ideal diagnostic and therapeutic strategy for such patients. The present study verifies the value of negative predischarge exercise testing in identifying low-risk patients treated with thrombolysis after AMI. One hundred fifty-seven consecutive patients with an uncomplicated clinical course underwent maximal or symptom-limited exercise testing (Bruce treadmill protocol) within 15 days of AMI in the absence of therapy. The location of the AMI was anterior in 51 patients, inferior in 85 and non-Q-wave in 21. All of the patients were followed for 6 months. Death and nonfatal reinfarction were considered as major coronary events, and the recurrence of angina as a minor event. Exercise test results were negative in 105 patients (group 1) and positive for angina or ST depression greater than or equal to 0.1 mV in 52 (group 2). No deaths occurred during follow-up; there were 3 reinfarctions (3%) and 7 cases (7%) of postinfarction angina in group 1, and 2 reinfarctions (4%) and 21 cases (40%) of postinfarction angina in group 2. By the end of follow-up, 90% of the patients with negative exercise test results were event-free (97% in the case of major events). These results show that thrombolytic therapy does not affect the value of negative postinfarction exercise testing in identifying low-risk patients.
