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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Peripartum cardiomyopathy (PC), an uncommon cause of peripartum heart failure, is defined as a cardiomyopathy presenting in the last trimester of pregnancy or the first 6 months postpartum, without evidence of preexisting cardiovascular disease. The etiology of PC and idiopathic dilated cardiomyopathy (IDC) remains uncertain. Several reports have addressed possible differences in clinical presentation and prognosis between these groups. A relatively high incidence of myocarditis has been recently reported in patients with PC, raising the possibility that this may represent a distinct difference between this condition and IDC. A retrospective review of endomyocardial biopsy specimens from 34 patients fulfilling the criteria for a diagnosis of PC was therefore performed to further evaluate this finding. Results indicate a lower incidence of myocarditis (8.8%, 3 of 34) than that reported in other studies. This incidence was comparable to that found in an age- and sex-matched control population undergoing transplantation for IDC (9.1%, 2 of 22). Factors that may influence the diverse range in the reported incidence of myocarditis are discussed.
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PMID:Incidence of myocarditis in peripartum cardiomyopathy. 805 28

The general cardiovascular performance of old people is determined by: a) inherent changes of the cardiovascular system which develop with age; b) delay of degenerative changes in some subjects caused by genetic factors, optimal physical activity and a proper diet; c) acquired diseases, in particular arteriosclerosis and hypertension. As a result of degenerative changes of the vascular wall the systolic pressure rises advancing age, some of the old people develop isolated systolic hypertension. Mild hypertrophy of the left ventricle develops also. The contracting ability of the heart muscle is preserved, the ejection fraction at rest and the cardiac output do not change. However, the diastolic function changes significantly-the elasticity of the left ventricle declines and its filling depends more on the atrial systole. A frequent cause of heart failure in old people is diastolic dysfunction. Pharmacotherapy of old people has some specific features which are discussed in more detail. A recent multicentre clinical investigation SHEP proved unequivocally, that effective treatment of systolic hypertension reduced in old people the risk of cerebrovascular attacks by 33%, of acute myocardial infarction by 27% and of cardiac failure by more than 50%! Based on these results it is clear that systolic hypertension must be treated equally systematically as diastolic hypertension. The approach to old people with cardiovascular disease must be strictly individual. Age alone must not be the reason for refusing access to the complete spectrum of modern diagnostic and therapeutic possibilities.
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PMID:[Old age from the viewpoint of the cardiologist]. 806 31

Spirometry was performed by 5,201 elderly participants of the Cardiovascular Health Study during their baseline examination and a subset of the ATS/DLD-78 respiratory questionnaire was administered by trained interviewers. In never smokers (46 percent of the cohort), the overall prevalence of chronic cough was 9 percent, chronic phlegm was 13 percent, attacks of wheezing with dyspnea were 8 percent, and grade 3 dyspnea on exertion was 10 percent. The prevalence of lung disease in current smokers (12 percent of the cohort) was 8/7 percent (men/women) with chronic bronchitis and 14/5 percent with emphysema. Overall, 6 percent reported asthma (a physician-confirmed history) and 12 percent reported hay fever. Using a logistic regression model, attacks of wheezing with dyspnea were strongly associated with a lower FEV1, coronary heart disease, heart failure, and a large waist size (in participants without a diagnosis of asthma, chronic bronchitis, or emphysema). Undiagnosed airways obstruction was twice as likely in women and those with lower income, and was associated with current and former smoking, pack-years of smoking, and chronic cough. Dyspnea on exertion (DOE) was three times or more likely if a participant reported heart failure, coronary heart disease, or emphysema; and much more likely if their FEV1 or FVC was substantially reduced. Dyspnea on exertion was also positively associated with older age, chronic bronchitis or asthma, a larger waist or hip size, pack-years of smoking, and less education. We conclude that DOE and attacks of wheezing with dyspnea are commonly associated with cardiovascular disease and a low FEV1 in those over 65 years and that airways obstruction frequently remains undiagnosed in the elderly.
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PMID:Prevalence and correlates of respiratory symptoms and disease in the elderly. Cardiovascular Health Study. 808 66

The pharmacological profile of carvedilol incorporating beta-adrenoceptor antagonism, weak alpha-blocking activity and slight calcium channel blockade indicates its anti-arrhythmic potential, but there are little data on its efficacy in this regard. Experimental animal studies have demonstrated that the drug reduces the number of premature ventricular contractions during both short-term and prolonged myocardial ischemia. In the relatively few open studies conducted in patients with hypertension, angina pectoris or heart failure complicated by a variety of ventricular arrhythmias, carvedilol improved the arrhythmia profile and significantly decreased the number of premature ventricular contractions. Further studies are need to extend the potential clinical usefulness of carvedilol in the treatment of the sinister ventricular arrhythmias that complicate so many common cardiovascular disease syndromes.
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PMID:Carvedilol--clinical experience in arrhythmias. 810 61

A total of 4676 patients and 1759 patients were treated with lisinopril and nifedipine respectively in a post-marketing surveillance study conducted in general practice in the UK. Patients were followed up for 12 months. Most of the lisinopril patients had hypertension, but a small number (180) had heart failure. Most of the nifedipine patients had uncomplicated hypertension, but some (22.57%) had other cardiovascular disease with or without hypertension. Lisinopril and nifedipine were equally effective in reducing blood pressure. During the study, 1.5% of hypertensive patients assigned to lisinopril died compared with 1.8% of patients assigned to nifedipine, and 15.1% of lisinopril patients compared with 19.7% of patients in the nifedipine group withdrew because of adverse events. Cough, malaise and fatigue, nausea and vomiting were more frequent causes of withdrawal from lisinopril than nifedipine. Conversely, headaches, pallor and flushing, oedema and palpitations caused more frequent withdrawals from nifedipine. Anaemia was more often encountered on nifedipine treatment than on lisinopril. In hypertensive patients, the frequency of first-dose hypotension was similar on both treatments. Serious events occurred in 0.8% and 0.5% of patients given lisinopril and nifedipine respectively. Lisinopril was well tolerated by heart failure patients: 16 patients (8.88%) died and an incidence of 4.44% of serious adverse events was reported, a pattern to be anticipated in such patients; dizziness, giddiness, dyspnoea, cough, nausea and vomiting were the most frequent causes of withdrawal; the incidence of first-dose hypotension was low (2.22%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Post-marketing surveillance of lisinopril in general practice in the UK. 811 50

The incidence of coronary heart disease and myocardial infarction fell gradually during the seventies. Reasons for this decline are not well understood. Speculations include changes of life style and health care. However, cardiovascular disease is still the leader of mortality in Western developed countries. Mortality of myocardial infarction has also declined. The major benefit was associated with broad establishment of coronary care units, smaller steps were achieved by various progresses in medical treatment. In contrast, the incidence of heart failure has increased. The major etiology of heart failure nowadays is coronary heart disease, especially large or recurrent myocardial infarction. The incidence of heart failure in patients having recovered from myocardial infarction is dramatically higher than in normal population. The Framingham Study showed an incidence of 14% in five years following a myocardial infarction. Prognosis of patients with manifestation of symptoms of heart failure is very poor. Patients with heart failure had an overall six years mortality of 55%. These observations suggest that coronary care units, thrombolysis and modern treatment as developed so far, suppressed in-hospital mortality and improved survival for the first year after a myocardial infarction. Thus, patients with larger infarcts who had succumbed early under previous regimens, survived. They carry, however, the burden of severely impaired left ventricular function, high probability to develop heart failure, and of a dubious long-term prognosis. Large efforts have put upon development of scores to estimate long-term prognosis after a myocardial infarction. With the development of techniques, composition of scores changed. However, residual ischemia, major left ventricular dysfunction, and ventricular arrhythmias are the basis of most scores indicating an adverse prognosis after an infarction. This review will be limited to the prognostic impact of left ventricular dysfunction and development of heart failure post myocardial infarction. A hypothetic cascade of events which may lead from myocardial infarction to heart failure and death is schematically outlined in Figure 1. Loss of contractile myocardium results in left ventricular dysfunction which may induce dilatation of the left ventricle, heart failure and ultimately death. This paper focuses on the evidence for the prognostic impact of the single steps and the whole cascade. Figure 1 shows in parenthesis the variables which were frequently measured to assess loss of contractile tissue, left ventricular dysfunction, and dilatation. Since heart failure is understood as a clinical syndrome of symptoms, it may only be semi-quantitated according to the classification of the New York Heart Association (NYHA).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Epidemiology and prognosis of myocardial infarct and chronic heart failure]. 812 20

Elderly patients with cardiovascular disease require slightly different management strategies compared with younger patients. Diagnosis is more difficult. Procedures, both diagnostic and therapeutic, are more dangerous. Despite higher risks, elderly patients have much to gain from aggressive therapies such as angioplasty, surgery, and thrombolysis. Decisions regarding these therapies are based on an incomplete data base and an understanding of the patients' needs. A review of the available data on cardiac surgery, angioplasty, myocardial infarction, and heart failure in the elderly is presented.
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PMID:Approach to ischemic heart disease, coronary care, and severe heart failure (including cardiogenic shock). 816 20

Sleep disordered breathing has increasingly been recognised as a frequent cause of ill-health in the community. Moderate or severe forms of the most common condition, obstructive sleep apnea (OSA), occur in up to 12% of the adult male population. A substantial body of literature has been published on the potential relationship between OSA and cardiovascular disease. In particular, OSA has been associated with cardiac failure, stroke, myocardial infarction and hypertension. Part of this association may be explained by other confounders, mainly obesity, which is common in OSA patients. The present review was prepared following a workshop aimed to critically review available scientific evidence suggesting that hypertension is a direct consequence of OSA. In addition, pathophysiologic mechanisms that may be involved in the relationship between OSA and cardiovascular disease, particularly brief intermittent elevation of blood pressure and sustained systemic hypertension, are discussed.
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PMID:Obstructive sleep apnea and blood pressure elevation: what is the relationship? Working Group on OSA and Hypertension. 820 10

Heart failure is the only cardiovascular disorder which is increasingly prevalent in North America. Several large clinical trials have emerged within the past 10 years. The results from some of these trials have had a significant impact on the way congestive heart failure is recognized and treated. The objective of this review is not to review exhaustively all recent clinical trials in heart failure but to present the most important ones selected because of their impact on how one understands and treats congestive heart failure in 1993. The results, as well as some important pathophysiological considerations related to these trials, will be addressed.
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PMID:Overview of clinical trials in congestive heart failure. 822 62

Heart failure, a major contributor to cardiovascular disease morbidity and mortality, is newly diagnosed in approximately 400,000 patients each year, and is particularly prevalent in individuals over age 65 years. Average mortality rates 5 years after diagnosis are 45-60%, and may be as high as 50% after 1 year for those with New York Heart Association class IV heart disease. 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 (dilated cardiomyopathy) or diastolic (hypertrophic or restrictive cardiomyopathies) dysfunction. The etiologies of heart failure may include inadequate coronary blood flow, pressure or volume overload, cardiomyopathy, or pericardial disease. Coronary artery disease, idiopathic dilated cardiomyopathy, and hypertension are the most frequent causes, and certain drugs may also worsen myocardial function. 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 preload or filling pressure to increase and symptoms of pulmonary congestion to emerge. Depressed contractility also results in a reduction in blood pressure, leading to compensatory neurohormonal activation and vasoconstriction, which significantly elevate afterload and further reduce stroke volume. The overall approach to heart failure includes defining the etiology, identifying precipitant factors, and assessing the severity of myocardial dysfunction and clinical symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathophysiology of heart failure. 823 96


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