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

To assess left ventricular diastolic filling in valvular aortic stenosis, pulsed Doppler echocardiography was used prospectively in 35 patients with severe aortic stenosis (valve area less than 1 cm2) and in 38 age-matched normal subjects. Twenty-seven patients had a normal left ventricular systolic function at rest (ejection fraction greater than 0.50) and a normal or only slightly increased mean pulmonary capillary wedge pressure (mean 11 +/- 4 mm Hg). Eight patients had a poor left ventricular systolic function (ejection fraction: 0.28 +/- 0.10) and an elevated mean pulmonary capillary wedge pressure (mean: 36 +/- 9 mm Hg). The Doppler derived filling parameters were correlated with hemodynamic data, left ventricular wall thickness derived from M-mode echocardiograms, heart rate and atrio-ventricular (A-V) conduction delay using stepwise multiple correlation. The data of this study suggest that left ventricular filling is significantly impaired in patients with severe aortic stenosis and left ventricular hypertrophy with an increase in late diastolic (A-wave) velocity, an increase in the A/E ratio, a decrease in the first one-half filling fraction and a prolongation of early diastolic deceleration time. These changes in filling hemodynamics are associated with alterations in mean pulmonary capillary wedge pressure, left ventricular wall thickness, heart rate and A-V conduction delay. When heart failure develops as a result of impaired left ventricular systolic function, an increase in left atrial filling pressure is associated with a shift of left ventricular filling towards early diastole with a 'normalisation' of the transmitral flow velocity curve. In extreme cases, a progression towards a 'restrictive' filling pattern is found with a marked shortening of the left ventricular early diastolic deceleration time. In the presence of high filling pressures, increased left atrial driving pressure (derived from the mean pulmonary capillary wedge pressure) is associated with changes in the left ventricular filling pattern irrespective of the presence and the degree of myocardial hypertrophy.
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PMID:The spectrum of left ventricular filling in severe aortic stenosis. 183 32

Reports in the literature have suggested that a complex alteration in beta-receptor pathway takes place in failing human myocardium. The purpose of our study was to evaluate the beta-adrenergic receptor system in an experimental model of heart failure induced by monocrotaline in rats. Monocrotaline, administered with a single intraperitoneal injection (50 mg/Kg), causes pulmonary hypertension and right ventricular hypertrophy, associated with congestive heart failure. beta 1 and beta 2-receptors were characterized in the right ventricle by direct radioligand binding utilizing [125I] Iodocyanopindolol and selective beta 1-(CGP 20712A) and beta 2-(ICI 118551) antagonists. Adenylate cyclase was measured in basal condition and in the presence of different stimulators as isoproterenol with ICI 118551 (beta 1-receptor-stimulated activity), isoproterenol with CGP 20712A (beta 2-receptor-stimulated activity), Gpp(NH)p, NaF and forskolin. In the right ventricle of the failing hearts the beta 1-receptor density decreased selectively (-55.8%) while the beta 2-receptor density was unchanged. Modifications in the adenylate cyclase system were demonstrated: a reduction in the basal and beta 1- and beta 2-stimulated adenylate cyclase activity; a decrease in adenylate cyclase activation elicited by Gpp(NH)p, but not by forskolin and NaF. In conclusion, these data suggest that in monocrotaline-induced heart failure in the rat there is a selective beta 1-receptor down-regulation and an impaired coupling efficiency of G proteins. These results are in line with biochemical changes found in patients with heart failure.
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PMID:[The adrenergic beta system in an experimental model of heart failure]. 196 56

The cause of severe right heart failure and of equal diastolic pressures in both ventricles (as seen in constrictive pericarditis) in a 56-year-old woman was suspected to be cardiac amyloidosis on the basis of findings in both the echocardiogram (biventricular hypertrophy) and the electrocardiogram (prominent Q waves, absent hypertrophy signs). The endomyocardial biopsy was at first unremarkable. But later, serial modified Congo-red staining unequivocally demonstrated amyloid deposits. In a second case, a 66-year-old man with global cardiac failure and echocardiographic pointers towards hypertrophic cardiomyopathy, was treated with verapamil, 240 mg daily. When this was not tolerated he was hospitalized. He, too, had prominent Q waves but no signs of ventricular hypertrophy. Cardiac amyloidosis was confirmed by biopsy. Both cases underline the special importance of echo- and electrocardiographic changes, taken together, in the diagnosis of cardiac amyloidosis.
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PMID:[Significance of electro- and echocardiogram for the diagnosis of cardial amyloidosis]. 198 99

We have observed that many spontaneously hypertensive rats (SHR) between the ages of 18 and 24 mo develop findings suggestive of heart failure, including pleural and pericardial effusions, left atrial thrombi, and right ventricular hypertrophy. Isolated left ventricular papillary muscle function was studied in these animals (SHR-F), in age-matched SHRs without evidence of heart failure (SHR-NF), and in nonhypertensive controls (WKY). Preparations from SHR-F showed depression of active tension development (3.58 +/- 1.75 g/mm2, means +/- SD) compared with both SHR-NF (7.17 +/- 0.94) and WKY (6.17 +/- 1.00) (P less than 0.01). Shortening velocity was also depressed in SHR-F (0.95 +/- 0.38 lengths/s) compared with SHR-NF (1.60 +/- 0.30; P less than 0.05) and WKY groups (2.15 %/- 0.48; P less than 0.01). Depression of muscle function was not found before 18 mo of age. Thus the aging SHR is a model in which one can observe the transition from chronic stable left ventricular hypertrophy to overt heart failure. Furthermore, left ventricular papillary muscles from SHRs with heart failure show evidence of significant contractile dysfunction, suggesting that impairment of intrinsic myocardial function underlies the development of heart failure.
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PMID:Impaired myocardial function in spontaneously hypertensive rats with heart failure. 199 92

Analysis of 34 years of follow-up of Framingham Study data provides clinically relevant insights into the prevalence, incidence, secular trends, prognosis, and modifiable risk factors for the occurrence of heart failure in a general population sample. Heart failure was found to be highly prevalent, affecting about 1% of persons in their 50s and rising progressively with age to afflict 10% of persons in their 80s. The annual incidence also increased with age, from about 0.2% in persons 45 to 54 years, to 4.0% in men 85 to 94 years, with the incidence approximately doubling with each decade of age. Women lagged slightly behind men in incidence at all ages. Male predominance was because of a higher rate of coronary heart disease, which confers a fourfold increased risk of heart failure. Heart failure, once manifest, was highly lethal, with 37% of men and 33% of women dying within 2 years of diagnosis. The 6-year mortality rate was 82% for men and 67% for women, which corresponded to a death rate fourfold to eightfold greater than that of the general population of the same age. Sudden death was a common mode of exitus and accounted for 28% of the cardiovascular deaths in men and 14% in women with heart failure. Hypertension and coronary disease were the predominant causes for heart failure and accounted for more than 80% of all clinical events. Factors reflecting deteriorating cardiac function were associated with a substantial increase in risk of overt heart failure. These include low vital capacity, sinus tachycardia, and ECG evidence of left ventricular hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Epidemiology of heart failure. 200 Jul 73

A health risk appraisal function has been developed for the prediction of stroke using the Framingham Study cohort. The stroke risk factors included in the profile are age, systolic blood pressure, the use of antihypertensive therapy, diabetes mellitus, cigarette smoking, prior cardiovascular disease (coronary heart disease, cardiac failure, or intermittent claudication), atrial fibrillation, and left ventricular hypertrophy by electrocardiogram. Based on 472 stroke events occurring during 10 years' follow-up from biennial examinations 9 and 14, stroke probabilities were computed using the Cox proportional hazards model for each sex based on a point system. On the basis of the risk factors in the profile, which can be readily determined on routine physical examination in a physician's office, stroke risk can be estimated. An individual's risk can be related to the average risk of stroke for persons of the same age and sex. The information that one's risk of stroke is several times higher than average may provide the impetus for risk factor modification. It may also help to identify persons at substantially increased stroke risk resulting from borderline levels of multiple risk factors such as those with mild or borderline hypertension and facilitate multifactorial risk factor modification.
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PMID:Probability of stroke: a risk profile from the Framingham Study. 200 1

Four young horses of various breeds and suffering from atrial fibrillation died of heart failure. All had markedly high pulmonary arterial pressure, right-sided cardiomegaly, and lack of histologic lesions in the right atrium or pulmonary parenchyma. Three horses had hypertrophy and/or necrosis of the tunica media of the pulmonary vasculature. Clinical signs of disease, physiologic data, and pathologic findings indicated that these horses had primary pulmonary hypertension with secondary right-sided cardiac ventricular hypertrophy and dilatation, atrial fibrillation, and heart failure.
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PMID:Pulmonary hypertension as a cause of atrial fibrillation in young horses: four cases (1980-1989). 201 43

More than the character of the blood pressure elevation, the cardiovascular risk profile should be the prognostic guide for antihypertensive therapeutic decision-making. Hypertension tends to occur in association with other risk factors which augment the risk and need to be considered in evaluating the hazard of hypertension, the urgency for treatment, and the choice of treatment. Elevated blood pressure is often accompanied by blood lipid abnormality, obesity, electrocardiograph (ECG) abnormality, glucose intolerance, and elevated fibrinogen and hematocrit, all of which enhance the risk of cardiovascular sequelae of hypertension. Hypertensive patients at particularly increased risk of cardiovascular events are those with an increased total/HDL-cholesterol ratio, ECG abnormality, impaired glucose tolerance, or the cigarette smoking habit. The risk of a cardiovascular event among hypertensive patients varies over more than a 10-fold range depending on the number of these coexistent risk factors. Multivariate risk formulations are available to allow a composite estimate of the joint conditional probability of a cardiovascular outcome in hypertensive patients with multiple risk factors. Since some antihypertensive agents can adversely affect blood lipids, glucose tolerance, or uric acid values, the risk profile must also be taken into account in choosing the optimal antihypertensive therapy. Also, hypertension is commonly associated with angina, myocardial infarction, left ventricular hypertrophy, stroke, or cardiac failure. These too must be taken under consideration in judging the urgency for treatment and the choice of agents. Thus, hypertension is best regarded as a component of a cardiovascular risk profile in implementing optimal therapy and in assessing its efficacy.
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PMID:The clinical heterogeneity of hypertension. 204 9

The overall cardiovascular mortality in patients with chronic renal failure is about 30 per cent of which 10 per cent is attributed to myocardial infarction. This prevalence led some workers to propose a hypothesis of "accelerated atherosclerosis" due to the hyperlipidaemia observed in 30 to 70 per cent of patients. However, the concept of accelerated atherosclerosis, which was based essentially on clinical studies, has been questioned. Pericardial effusion is a common complication of chronic renal failure and has been reported in over 62 per cent of patients in echocardiographic studies. There are many causes and symptoms are often mild; systematic echocardiographic examination of patients with renal failure undergoing haemodialysis has shown 32 per cent of pericardial effusions to be asymptomatic. There are two potential complications: cardiac tamponade and, lesser frequently, constrictive pericarditis. Cardiac failure is a common cause of death in patients undergoing long-term dialysis. The myocardial histological appearances are those of fibrosis, the etiology of which is not fully understood although the dialysis membranes and hypotensive episodes occurring during haemodialysis have been thought to play a role. Left ventricular hypertrophy and fibrosis may give rise to ventricular arrhythmias which could explain some of the cases of sudden death observed in patients with renal failure and often wrongly attributed to ischemic heart disease. Another form of myocardial disease which is observed later is characterised by an alteration of systolic function with left ventricular dilatation and hypokinesia and increased end diastolic pressures without an increase in left ventricular wall thickness. Valvular heart disease may also result from renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[So-called uremic heart diseases]. 210 35

Guinea pig myocardium resembles human myocardium with respect to the mechanisms which regulate contractility (enzymatic activity of myosine, functional activity of the sarcoplasmic reticulum). Guinea pig left ventricular hypertrophy (LVH) is therefore a good experimental model for the study of human LVH. The mechanical properties of 5 months old female guinea pigs' left ventricular papillary muscle, 3 weeks after constriction of the abdominal aorta (N = 10), were investigated. Ten papillary muscles of operated control animals and eight of normal guinea pigs submitted to 20 minutes hypoxia were also studied. The animals had no signs of cardiac failure after constriction of the abdominal aorta but the increase in the ratio of heart to body weight (p less than 0.001) confirmed the LVH. When compared with the operated controls, there was a decrease of the maximum velocity of contraction at zero load, of the velocity of contraction with preload alone (Vc), of the total isometric force normalized for the section of the muscle(s) and of the positive peak of the derivative of the isometric force normalized for section (+ dF/s) (p less than 0.001 for each parameter). The parameters of relaxation were also abnormal: decreased velocity of isotonic relaxation with preload only (Vr) and of the negative peak of the derivative of the isometric force normalized for section (- dF/s) (p less than 0.001 for each parameter), and an increase in the half relaxation time (t1/2) (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Changes in contraction-relaxation coupling in experimental cardiac hypertrophy in the guinea pig]. 212 20


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