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Although idiopathic dilated cardiomyopathy is often viewed as an affliction of young of middle-aged adults, morbidity and mortality rates from idiopathic dilated cardiomyopathy rise sharply with age and are the highest in the elderly. To learn more about the determinants of this increasingly important cause of heart failure in the elderly, the authors conducted a pooled analysis of data from two case-control studies of idiopathic dilated cardiomyopathy carried out in Baltimore, Maryland (1984-1986), and in Washington, DC (1990-1992). Identical diagnostic criteria and interviewing procedures had been used in both studies. All of the cases of idiopathic dilated cardiomyopathy had evidence of ventricular dilation and hypokinesis, with a left ventricular ejection fraction of < 40%. Cases with a history of coronary artery disease were excluded along with those with known secondary forms of cardiomyopathy, Up to two neighborhood controls of the same sex and appropriate age (+/- 5 years) were selected for each case using a random digit dialing technique. The subjects or a suitable surrogate was interviewed by telephone to obtain medical history information. The present analysis was limited to 94 cases and 152 matched controls who were at least 60 years of age. Conditional logistic regression methods were used in the analysis. Significant associations were observed with lower educational attainment and a history of hypertension (P < 0.05). The association with hypertension (relative odds = 2.2, 95% confidence interval 1.1-4.6) persisted after adjustment for race, education, and diabetes and was not accounted for by coronary angiography utilization patterns. The association with diabetes was of borderline significance (p < 0.10). The pattern of risk factors identified in this analysis may allow for the early identification of elderly persons who are at increased risk of idiopathic dilated cardiomyopathy.
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PMID:Epidemiology of idiopathic dilated cardiomyopathy in the elderly: pooled results from two case-control studies. 861 Jul 1

Heart failure occurs when myocardial muscle dysfunction prevents the heart from pumping enough blood at normal cardiac pressures to meet the metabolic needs of the body, especially during exercise, and compensatory hemodynamic and neurohormonal mechanisms are overwhelmed or maladaptive. Pathologic classifications are broadly based on the presence of systolic dysfunction (dilated cardiomyopathy) and diastolic dysfunction (hypertrophic or restrictive cardiomyopathies). Coronary artery disease, idiopathic dilated cardiomyopathy, and hypertension are the most frequent causes, and myocardial function may be impaired by some drugs. When contractility is reduced, stroke volume and cardiac output are decreased, and alterations in the kidneys may induce fluid retention to compensate for the perceived low output and reduced circulating blood volume. Fluid retention, in turn, causes increased preload or filling pressure and symptoms of pulmonary congestion. Depressed contractility also results in a reduction in blood pressure, leading to compensatory neurohormonal activation and vasoconstriction, which significantly elevate afterload, further reduce stroke volume, and lead to deleterious cardiac remodeling. The overall clinical approach includes defining the etiology, identifying precipitant factors, and assessing the severity of myocardial dysfunction and clinical symptoms.
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PMID:Pathophysiology of heart failure: changing perceptions. 866 3

Pulmonary artery (PA) hypertension in transplant recipients increases mortality from right heart failure following heart transplantation. We examined the impact of long-term medical therapy on the severity of PA hypertension in patients with end-stage congestive heart failure on a transplant waiting list. The initial and final, quarterly right heart catheterization data on 60 patients (50 men, aged 50 +/- 9 years, New York Heart Association class III to IV) awaiting heart transplantation were analyzed and the patients divided into 2 groups: group A, those with persistent elevated systolic PA pressures throughout the 10-month follow-up (n = 31 of 60), and group B, those who had any decrease in systolic PA pressure during that period (n = 29 of 60). Group A had no change in hemodynamics. Group B had a significant decrease( +/- SD) in right atrial (11 +/- 7 to 5 +/- 4 mm Hg), PA (57 +/- 11 to 37 +/- 11 mm Hg), and PA wedge (25 +/- 9 to 14 +/- 7 mm Hg) pressures, with increases in cardiac output (3.8 +/- 0.9 to 4.7 +/- 1.1 L/min) and ejection fraction (18 +/- 6% to 27 +/- 11%) (p < 0.05). The combined end point of transplant or death occurred in 28 of 31 patients (90%) in group A versus 14 of 29 (50%) in group B (p = 0.0004). Ischemic etiology was present in 71 % of patients in group A versus 68% with idiopathic dilated cardiomyopathy in group B (p = 0.003). The reversibility of PA hypertension rather than its initial severity is predictive of patient clinical outcome. Idiopathic, as opposed to ischemic, cardiomyopathy responds better to medical therapy.
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PMID:Impact of medical therapy on pulmonary hypertension in patients with congestive heart failure awaiting cardiac transplantation. 875 90

This investigation was carried out to compare the clinical course of patients with chronic Chagas' heart disease with that of patients with dilated cardiomyopathy. A total of 125 patients (75 chagasic and 50 nonchagasic) prospectively followed up at the Cardiomyopathy clinic of Santa Casa Hospital from January 1990 to June 1993 entered the study. Patients underwent clinical history, physical examination, serological tests, resting electrocardiogram, chest X-ray and two-dimensional echocardiography. In nonchagasic patients, hypertensive cardiomyopathy was found in 17 of 50 (34%) patients, idiopathic dilated cardiomyopathy in 16 (32%), the association of hypertension and coronary artery disease in 12 (24%) and ischemic cardiomyopathy in two (4%). Twenty-one (23%) chagasic and three (6%) nonchagasic patients died during the study period (P = 0.02). Sudden cardiac death occurred in eight (38%) chagasic patients, pump failure death was detected in 10 (47%) and the mode of death could not be determined in three (14%) patients with chronic Chagas' heart disease. Thus, patients with chronic Chagas' heart disease have a clinical course worse than that of patients with nonchagasic dilated cardiomyopathy. This fact may be ascribed to the electrocardiographic and morphological peculiarities usually found in chronic Chagas' heart disease.
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PMID:Clinical course of Chagas' heart disease: a comparison with dilated cardiomyopathy. 922 90

It is unknown whether basal release of endothelium-derived nitric oxide in the coronary artery is altered in heart failure in humans. The aim of the present study was to evaluate the effect of inhibition of nitric oxide synthesis on basal tone of the conduit and resistance coronary arteries in awake patients. Coronary blood flow velocity (Doppler guide wire) and coronary arterial diameter (quantitative coronary angiography) were measured in 14 patients with heart failure caused by nonischemic left ventricular dysfunction (7 idiopathic dilated cardiomyopathy and 7 valvular insufficiency) and 7 patients with normal ventricular function (controls). Intracoronary N(G)-monomethyl-L-arginine (L-NMMA), an inhibitor of nitric oxide synthesis, at graded doses decreased coronary blood flow in both groups. However, the magnitude of flow reduction was smaller in patients with heart failure than in control patients (P<.0001). The magnitude of coronary blood flow reduction in response to L-NMMA inversely correlated to indexes of left ventricular contractile function (P<.01) but was not affected by the cause of heart failure. Constriction of the large epicardial coronary artery with L-NMMA also tended to be attenuated in patients with heart failure. In summary, vasoconstricting response to L-NMMA was blunted in the coronary resistance artery in heart failure in vivo. These findings suggest that basal release of nitric oxide in the coronary circulation is decreased in patients with heart failure.
Hypertension 1997 Jul
PMID:Basal release of nitric oxide is decreased in the coronary circulation in patients with heart failure. 923 20

It was first reported by our group in 1975 that heart failure due to idiopathic dilated cardiomyopathy (IDC) could be improved by long term treatment with a beta-blocker, starting at a low dose and continuing with a stepwise up-titration. Since then, many studies have been performed in patients with heart failure of various aetiologies and the beneficial effects of long term beta-blockade have been confirmed. About 3000 patients have been included in randomised studies in which beta-blockade, given for more than 2 months, mostly elicited significant improvements in functional class, exercise capacity, cardiac function, quality of life and/or morbidity. When started at a very low dose (one-tenth to one-twentieth of the doses generally used in angina or hypertension), the treatment is well tolerated in most patients. In these studies, various types of beta-blockers were used, including beta1-selective blockers and nonselective blockers with additional properties (vasodilator and antioxidative) such as metoprolol, bisoprolol, bucindolol and carvedilol. Several large studies have also reported benefits on mortality and morbidity. In the Metoprolol in Dilated Cardiomyopathy (MDC) trial, metoprolol treatment in patients with IDC resulted in a 34% reduction of the primary combined endpoint, total number of deaths and need for cardiac transplantation. In the Cardiac Insufficiency Bisoprolol Study (CIBIS), in patients with idiopathic as well as ischaemic cardiomyopathy, there was a nonsignificant 20% reduction in mortality. In the US carvedilol studies (n = 1094), also in patients with ischaemic and idiopathic cardiomyopathy, carvedilol reduced mortality by 65%, which was highly significant. A nonsignificant reduction in mortality was observed in the Australia-New Zealand (ANZ) Heart Failure Study with carvedilol. In all these studies there was a reduction in hospitalisations, with all drugs being generally well tolerated. It can thus be concluded that the beneficial effects of beta-blockers on cardiac function and morbidity have been documented in a large number of studies in selected groups of patients. The treatment has been accepted in some countries by the regulatory authorities. Larger, placebo-controlled studies are needed to convincingly demonstrate a reduction in total mortality as observed in the pooling of the 4 US carvedilol studies. Such studies are in progress for various beta-blockers, which may lead to acceptance of their routine clinical use in patients with congestive heart failure.
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PMID:The role of beta-blockers in left ventricular dysfunction and heart failure. 933 58

Allograft vascular disease is the major cause of late cardiac graft failure. A multifactorial etiopathogenesis is supposed. Our study investigated factors associated with allograft vascular disease occurrence. After stratifying our series on the basis of potential risk factors, we calculated allograft vascular disease incidence rate in 267 grafts from 258 patients who underwent transplant between November 1985 and August 1996. Chi-square test was used for the identification of univariate risk factors to be included in a multivariate model. Multivariate analysis was based on a Poisson model. Seventy of the 267 grafts (26.2%) were diagnosed with allograft vascular disease. Heart disease other than idiopathic dilated cardiomyopathy, donor's age, number of mismatches for HLA-B = 2, presence of systo-diastolic hypertension, number of acute rejection positive endomyocardial biopsies > or = 7 and the association of human Cytomegalovirus and hepatitis C virus infections proved to be univariate risk factors, and were included in the Poisson multivariate model. The association of Cytomegalovirus and hepatitis C infections multiplied allograft vascular disease incidence rate by 3.9, systo-diastolic hypertension by 2.2, occurrence of 2 HLA-B mismatches by 2, a high number (> or = 7) of acute rejection positive-endomyocardial biopsies by 1.8, and heart disease other than idiopathic dilated cardiomyopathy by 1.8. The association of human Cytomegalovirus and hepatitis C virus infections, of HLA-B mismatches, of acute rejection-positive endomyocardial biopsies, as well as post-transplantation hypertension and native heart disease other than idiopathic dilated cardiomyopathy, proved to be positively associated with an increased risk of allograft vascular disease. Given the concordance of our data with those of numerous prior series, we are going to adopt a special surveillance angiographic protocol for patients with these factors.
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PMID:Factors increasing the risk of allograft vascular disease in heart transplant recipients. 935 48

Three hundred and fifty nine cardiology units participated in a study (SEOSI) coordinated by the Association of Italian Hospital Cardiologists (ANMCO). The aim of the study was to: (1) evaluate how many patients with suspected or known heart failure consecutively approach a hospital cardiology unit; (2) assess their clinical characteristics; (3) define the diagnostic-therapeutic processes set in motion by cardiologists; (4) evaluate the social and emotional impact of the disease on the patient. In 12 days, 3921 patients were enrolled. Mean age was 67 +/- 12 years (median 69); 49% of the patients were in NYHA class III-IV; atrial fibrillation was present in 27%; 35% of the cases were scheduled for hospital admission. Ischaemic heart disease was the primary cause of heart failure (42%); arterial hypertension accounted for 20%, idiopathic dilated cardiomyopathy for 15% and cardiac valve disease for 15%. A chest X-ray, ECG and echocardiogram were performed in 70-80% of cases; ambulatory ECG in 36% and exercise testing in 11%. ACE inhibitors were administered to 63.5%, calcium antagonists to 19% and beta-blockers to 5.5%. No significant differences in drug prescription were noted in relation to NYHA classification. Multidrug use was common (3.6 +/- 1.6). Main advice was: salt restriction (47%) and rest (44%); physical activity and a formal exercise programme were prescribed to 10% and 5% of patients, respectively. Most patients were addressed to hospital follow-up. Thus, heart failure represents a heavy burden for hospital cardiology units. It can be estimated that about 190,000 patients with heart failure seek care at hospital cardiology units each year and about 65,000 are admitted as inpatients. Cardiologists are reasonably well oriented regarding both examinations required and the prescribing of drugs. Beta-blockers and physical exercise are prescribed very cautiously. The format of the present trial, characterized by brevity, simplicity and low cost, could be used as a tool to gain periodical information on several aspects of national health systems and physician behaviour.
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PMID:Survey on heart failure in Italian hospital cardiology units. Results of the SEOSI study. SEOSI Investigators. 945 52

Since the identification of an Insertion/Deletion polymorphism in the ACE gene, numerous studies have evaluated the potential risk of the DD genotype in cardiovascular disease and hypertension. The report of many conflicting publications reveals a strong need for reviewing the most important data. There is evidence of the absence of an association between the ACE polymorphism and hypertension in Caucasians. In blacks a positive association between the D allele and high blood pressure was seen, Japanese studies show discrepant results. Several studies showed no association between the ACE polymorphism and the risk of myocardial infarction. However, in certain subpopulations, such as low risk patients or coronary care unit patients, an increased risk of myocardial infarction in DD type is present, and a meta-analysis supports this proposition. Because of conflicting data, the potential association between the ACE polymorphism and coronary artery disease, cerebrovascular disease, left ventricular hypertrophy, hypertrophic and idiopathic dilated cardiomyopathy, carotid artery disease and diabetic and immunoglobin A nephropathy, remains inconclusive.
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PMID:Angiotensin I-converting enzyme insertion/deletion polymorphism: clinical implications. 948 29

We evaluated 3 patients with acromegaly who developed heart failure. Heart failure appeared to be due to acromegalic cardiomyopathy in 2 patients who did not have hypertension or evidence of coronary artery disease, and it was possibly due to acromegalic cardiomyopathy combined with familiar hypertrophic cardiomyopathy in 1 patient. The common echocardiographic findings in the present three cases were: 1) enlargement of the left atrium, 2) markedly dilated left ventricular cavity with diffuse hypokinesis, 3) decrease of indices of the left ventricular systolic function, and 4) no evidence of left ventricular hypertrophy. Echocardiographic findings in acromegaly with congestive heart failure resemble those of idiopathic dilated cardiomyopathy.
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PMID:Heart failure in 3 patients with acromegaly: echocardiographic assessment. 971 86


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