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

Congestive heart failure (CHF) evolves either from an excessive workload or in response to loss of myocardium, both of which cause cardiac hypertrophy, increased cardiac pressure, and loss of functional reserve. Nearly 60% of patients in heart failure present with ischemic cardiomyopathy, which in its chronic form exhibits biventricular dilatation, elevated left ventricular mass, and extensive large-vessel atherosclerosis. The hypertrophy is proportional to the loss of myocardium, although animal studies suggest this varies with the infarct size. However, recent studies indicate that early afterload reduction may relieve the hypertrophic stimulus and prevent degeneration. Some 30% to 40% of patients in heart failure present with an idiopathic dilated cardiomyopathy, with a patchy but diffuse loss of tissue on microscopy, reactive hypertrophy in the surviving cells, and interstitial fibrosis and replacement scarring. The ultrastructural changes still await clarification. The role of pharmacologic intervention still remains unclear. However, any reduction in mortality will necessitate the identification of those cellular changes that inevitably lead to secondary degeneration of the remaining viable myocardium.
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PMID:The pathophysiologic profile of congestive heart failure. 315 47

Sudden death is common in patients with severe heart failure, but antiarrhythmic drug therapy has potential risks as well as benefits. Programmed electrical stimulation may offer a means of identifying lower risk patients who are less likely to benefit from antiarrhythmic therapy and who could potentially be spared the risk of adverse drug effects. Therefore 72 consecutive patients referred for management of severe heart failure (left ventricular ejection fraction 0.18 +/- 0.06) were studied. The mean age was 47 +/- 12 years; 45 (61%) patients had idiopathic dilated cardiomyopathy and 24 (33%) had coronary artery disease. Fifty-eight (82%) patients had nonsustained ventricular tachycardia. Following adjustment of vasodilators and diuretics, programmed stimulation was performed from the right ventricular apex with one, two, and three extrastimuli. Sustained ventricular tachycardia was initiated in nine (13%) patients and all received chronic antiarrhythmic drug therapy. During follow-up of 176 +/- 187 days, 1 of 13 patients treated for inducible ventricular tachycardia and 13 of 63 noninducible patients died suddenly (p = 0.20). The actuarial risk of sudden death in the noninducible patients was 13% at 6 weeks and 30% at 6 months. The only independent predictors of sudden death were pulmonary artery systolic pressure greater than 55% mm Hg and a pulmonary capillary wedge pressure with vasodilator therapy greater than 16 mm Hg. Of the 63 noninducible patients, 11 (17%) received long-term antiarrhythmic agents due to atrial fibrillation or referring physician preference, and antiarrhythmic therapy was not associated with a lower risk of sudden death in these patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inducible ventricular arrhythmias and sudden death during vasodilator therapy of severe heart failure. 319 28

A total of 110 patients with idiopathic dilated cardiomyopathy were followed prospectively for 53 +/- 8 (range 41 to 69) months to determine prognostic factors identifying patients at risk for sudden death or death from congestive heart failure. During the follow-up period 39 patients died, 14 of congestive heart failure and 25 suddenly. The incidence of cardiac death after 1 year was 18%, after 2 years 35%, and after 4 years 39%. Multivariate logistic regression analysis identified four independent prognostic factors: left ventricular ejection fraction, cardiac index, number of ventricular pairs/24 hours, and atrial rhythm (sinus rhythm or atrial fibrillation). With the final model of logistic regression 77 of 88 patients (88%) could be classified correctly as being at risk for death from chronic heart failure or sudden cardiac death. Patients who were likely to die of congestive heart failure were characterized by a markedly impaired left ventricular function (measured in terms of left ventricular ejection fraction, cardiac index, or both) and a low number of pairs/24 hours. The association between frequent complex ventricular arrhythmias and depressed left ventricular function identifies patients who are at risk for sudden death. The presence of atrial fibrillation significantly increases the risk of sudden death and death from congestive heart failure.
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PMID:Mode of death in idiopathic dilated cardiomyopathy: a multivariate analysis of prognostic determinants. 319 29

To diagnose latent dilated cardiomyopathy (latent DCM), we performed loading echocardiography with Angiotensin II and ergometer exercise in 41 patients. Twenty-one patients were suspected of having latent DCM because of histories, of heart failure of myocarditis; 10 patients had DCM; and 10 normal persons served as controls. On angiotensin II loading, cardiac function deteriorated in the DCM group, but it was maintained in the normal controls. Nine patients in the latent DCM group showed the same pattern as normals (L1-group), and 12 did as the DCM group (L2-group). Although % fractional shortening, end-diastolic and end-systolic dimensions of the left ventricle did not differ between the L1 and L2-groups, the A/R, the ratio of the pulsed Doppler echocardiogram at the left ventricular inflow tract, was larger and the exercise change of the % fractional shortening and exercise tolerance were less in the L2-group than in the L1-group. Furthermore, the biopsy findings of the L2-group were similar to those of the DCM group in terms of myocardial degeneration, myocardial hypertrophy and interstitial fibrosis. Thus, patients in the L2-group were thought to have a risk for DCM, and were cases of latent DCM. Angiotensin II loading is thought to be useful for diagnosing such cases.
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PMID:[A trial diagnosis of latent dilated cardiomyopathy]. 350 4

Peripartum cardiomyopathy is defined as left ventricular dilation and failure, first developing during the third trimester of pregnancy or in the first 6 months postpartum. In an effort to characterize this syndrome in a middle class population, 14 consecutive patients with peripartum cardiomyopathy underwent a detailed history and physical examination, right heart catheterization, M-mode and two-dimensional echocardiography, radionuclide ventriculography and right ventricular endomyocardial biopsy. These patients were then observed with sequential noninvasive studies to determine prognostic indicators. Eight (57%) of these 14 patients were primiparous and an equal number first presented with heart failure concomitant with or immediately before the onset of labor. When these women were compared with 55 patients with idiopathic dilated cardiomyopathy, only mean age at onset of symptoms (28.7 +/- 5.7 versus 48.2 +/- 13.6 years, p less than 0.001) and symptom duration (4.1 +/- 7.7 versus 19.0 +/- 18.4 months, p less than 0.001) differed between the groups. There was no difference in ventricular arrhythmia, left ventricular chamber size, ejection fraction or hemodynamics. Myocyte histologic findings were similar; however, myocarditis was identified in 29% of patients with peripartum cardiomyopathy and in only 9% of those with idiopathic dilated cardiomyopathy. In all patients with peripartum cardiomyopathy and myocarditis, the myocardial biopsy was performed within 1 week of onset of symptoms. Seven (50%) of the patients with peripartum cardiomyopathy had dramatic improvement within 6 weeks of follow-up, and 6 (43%) died.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Peripartum cardiomyopathy: clinical, hemodynamic, histologic and prognostic characteristics. 371 32

A prospective study was undertaken to assess the response of patients with idiopathic dilated cardiomyopathy to programmed electrical stimulation (PES). Fifteen patients undergoing evaluation of congestive heart failure were studied. All patients underwent cardiac catheterization and coronary angiography as well as endomyocardial biopsy to exclude known causes of heart failure. No patient had a history of syncope or sustained ventricular arrhythmias. All patients were found to have severe left ventricular dysfunction (mean ejection fraction 17%), as well as nonsustained ventricular tachycardia on ambulatory monitoring or exercise testing. A protocol using up to two premature stimuli and burst pacing, from two right ventricular sites, induced up to four repetitive ventricular responses but failed to induce a sustained ventricular arrhythmia in any patient. Patients with dilated cardiomyopathy, advanced ventricular arrhythmias, and depressed left ventricular function respond differently than do patients with coronary artery disease, advanced ventricular arrhythmias, and depressed left ventricular function, to PES. PES appears to have limited value in the evaluation of patients with dilated cardiomyopathy and nonsustained ventricular arrhythmias.
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PMID:The response of patients with complex ventricular arrhythmias secondary to dilated cardiomyopathy to programmed electrical stimulation. 375 63

Lymphocyte subsets were analyzed in patients with DCM, arrhythmias following influenza symptoms and acute perimyocarditis, respectively by an automated laser flow cytometry system with the use of monoclonal antibodies. A lower percentage of OKT8+ cells and a high OKT4/OKT8 ratio were found in the DCM and arrhythmias groups. No phenotypic abnormalities in the lymphocyte subsets were found in patients with acute perimyocarditis who were favorably progressing in clinical features. The results suggest that an immunological disturbance thought to play a part of the pathogenesis of DCM or heart failure may cause the abnormality of lymphocyte subsets.
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PMID:Lymphocyte subsets in patients with dilated cardiomyopathy and perimyocarditis. 375 3

To determine the factors conditioning the variability of positive inotropic response after intravenous acute amrinone administration, 14 patients with chronic cardiac failure were studied by quantitative M-mode and cross-sectional echocardiography. Six patients had idiopathic dilated cardiomyopathy and 8 patients had severe chronic aortic insufficiency. Myocardial contractility (evaluated as peak arterial systolic pressure/end-systolic volume ratio: PAP/ESV) did not change in patients with idiopathic cardiomyopathy, a significant increase of myocardial contractility occurred in patients with aortic regurgitation only if the control value of PAP/ESV was greater than 1. Mean systolic wall stress decreased significantly in all patients, independent of aetiology of cardiac failure and was the factor determining the improvement of left ventricular performance (evaluated as fractional shortening) in patients without changes in myocardial contractility. Maximum improvement in left ventricular performance occurred 10 minutes after amrinone administration. It is concluded that the possibility of detecting the positive inotropic properties of amrinone in man depends on the aetiology of the cardiac failure and on the basal level of myocardial contractility.
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PMID:Variability of positive inotropic response to acute amrinone administration in chronic cardiac failure. 375 94

Twenty-four patients, mean age 42 years, with idiopathic dilated cardiomyopathy (DC) and no history of symptomatic ventricular arrhythmias underwent right ventricular programmed stimulation with up to 3 extrastimuli. Ventricular tachycardia (VT) was induced in 8 patients and ventricular fibrillation (VF) in 2. The VT was unimorphic in 2 and polymorphic in 6. No significant differences were noted between patients in whom arrhythmias were inducible and and those in whom they were not with regard to age, symptomatic class, arrhythmia severity or hemodynamic indexes. Over a mean follow-up of 12 months, 4 patients died, 3 suddenly and 1 with progressive heart failure. Only 1 of the 3 who died suddenly had inducible VT. One other patient with induced sustained unimorphic VT later presented with spontaneous sustained VT similar in rate and configuration to induced VT. In conclusion, VT or VF may be induced in approximately 40% of patients with DC and no history of symptomatic VT or VF. Inducibility of polymorphic VT or VF does not correlate with clinical or hemodynamic variables or with the risk of sudden death. However, induction of unimorphic VT may predict later occurrence of spontaneous unimorphic VT.
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PMID:Prognostic usefulness of programmed ventricular stimulation in idiopathic dilated cardiomyopathy without symptomatic ventricular arrhythmias. 377 57

To characterize the abnormal pattern of instantaneous left ventricular (LV) ejection in heart failure, proximal aortic pressure, flow, acceleration, power and dW/dt were measured at rest and during supine bicycle exercise using high-fidelity, catheter-mounted pressure and velocity sensors in 16 patients with idiopathic dilated cardiomyopathy (IDC) and 11 normal control subjects. In patients with IDC, peak flow was lower than normal both at rest (454 +/- 155 vs 649 +/- 168 ml/s, p less than 0.01) and during exercise (569 +/- 213 vs 916 +/- 329 ml/s, p less than 0.01). Peak acceleration, power and dW/dt were also significantly reduced in patients with IDC at rest and during exercise. Time to peak flow (as a fraction of LV ejection time) was consistently prolonged in patients with IDC (rest, 0.40 +/- 0.08 vs 0.29 +/- 0.04; exercise, 0.36 +/- 0.06 vs 0.28 +/- 0.04, both p less than 0.01). Exercise-induced increments in peak flow, power and dW/dt were significantly blunted in patients with IDC. Studies during pacing tachycardia and nitroprusside administration failed to reproduce the abnormalities during exercise in patients with IDC. Thus, the instantaneous flow pulse in heart failure is both diminished in magnitude (decreased stroke volume and peak flow) and abnormal in shape (decrease peak acceleration and delayed time to peak flow). Exercise stress in IDC results in abnormalities of LV performance that can be detected using instantaneous ejection information. These abnormalities are unlikely to be explained by changes in heart rate or loading conditions.
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PMID:Effects of exercise and nitroprusside on left ventricular ejection dynamics in idiopathic dilated cardiomyopathy. 382 7


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