Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with very poor ventricular function have been thought to be highly vulnerable to elective myocardial revascularization. Ischemic cardiomyopathy is now the major indication for cardiac transplantation. The 2-year survival of medically treated patients with ejection fractions less than 20%, but who are not sufficiently symptomatic for cardiac transplantation, is less than 25%. At our institution we have taken an aggressive approach by using myocardial revascularization for chronic ischemic cardiomyopathy. Between 1983 and 1988, 39 patients with preoperative ejection fractions less than 20% underwent coronary artery bypass. Patients were excluded if they had valvular heart disease other than mild to moderate mitral regurgitation, required resection of a left ventricular aneurysm, or required emergency operation for acute coronary occlusion. Mean age was 63.3 years (range, 43 to 80 years) and 31 were men. Mean preoperative ejection fraction was 18.3% (range, 10% to 20%) and the mean preoperative left ventricular end diastolic pressure was 22 mm Hg (range, 8 mm Hg to 38 mm Hg). There was one operative death (2.6%). Mean follow-up was 21 months (range, 3 to 60 months) with eight late deaths (a total mortality rate of 21%). Seven deaths were due to arrhythmias. Three patients continued to have severe heart failure, one of whom underwent successful cardiac transplantation. By life table analysis, there was a 3-year survival rate of 83%. With the present shortage of cardiac transplant donors, myocardial revascularization for ischemic cardiomyopathy is a reasonably effective means for preserving residual ventricular function.
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PMID:Coronary revascularization rather than cardiac transplantation for chronic ischemic cardiomyopathy. 267 84

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

The purpose of this study was to assess the hemodynamic effects of intravenous digoxin in patients with New York Heart Association class IV heart failure, who had never previously been treated with digitalis drugs, and who were initially treated only with diuretics and systemic vasodilators to clinical end points of compensation. Eleven male patients, 5 with idiopathic and 6 with ischemic cardiomyopathy, had sinus rhythm and were hospitalized with congestive heart failure not precipitated by an acute ischemic event. All 11 patients were treated with intravenous furosemide and various vasodilators without invasive hemodynamic monitoring for a mean period of 4.3 +/- 2.1 days. This therapy resulted in subjective and objective improvement in all patients as reflected by a significant decrease in heart failure score from 9.5 +/- 2.2 to 2.7 +/- 2.3 (p less than 0.001). When compensation was achieved by clinical criteria, the patients were instrumented and hemodynamics obtained before and serially thereafter for 6 hours after the intravenous administration of digoxin given in two 0.5 mg doses 2 hours apart. In response to digoxin, cardiac index increased from 2.6 +/- 0.7 liters/min per m2 to a peak of 3.3 +/- 0.6 liters/min per m2 (p less than 0.005); left ventricular stroke work index (g X m/m2) increased from 27 +/- 16 to 43 +/- 23 (p less than 0.005) and the ejection fraction (eight patients) increased from 21 +/- 13% to 29 +/- 11% (p less than 0.04). Mean pulmonary capillary wedge pressure decreased from 24 +/- 7 to a minimum of 17 +/- 4 mm Hg (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic effects of intravenous digoxin in patients with severe heart failure initially treated with diuretics and vasodilators. 355 83

Patients with congestive heart failure have been considered to have augmented sympathetic drive both at rest and during dynamic exercise. The augmentation observed during exercise may be related to the state of near exhaustion experienced by patients with heart failure at relatively low work loads. To compare the response of the sympathetic nervous system to exercise in normal subjects and patients with heart failure when they are working in a comparable physiologic frame of reference, the data for both groups can be expressed as percent peak oxygen consumption achieved (percent peak VO2) rather than as a function of absolute oxygen consumption (VO2). Ten healthy control subjects and 31 patients with chronic clinical class II and III heart failure were studied during upright maximal bicycle exercise. Eighteen of the 31 patients had primary cardiomyopathy and 13 had ischemic cardiomyopathy. The average ejection fraction at rest was 24 +/- 10% (+/- SD) in the group with heart failure. Heart rate, systolic blood pressure, VO2 and plasma norepinephrine levels were measured at rest and throughout exercise. When the data were expressed as a function of percent peak VO2 achieved, patients with heart failure demonstrated a flatter slope (p = 0.004) than normal in the response of plasma norepinephrine to exercise, indicating a relative blunting of sympathetic drive. This was accompanied by attenuated heart rate (p = 0.001) and blood pressure (p less than 0.001) responses. These differences were not apparent when the data are expressed as a function of absolute VO2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relative attenuation of sympathetic drive during exercise in patients with congestive heart failure. 397 88

This article reports the treatment with continuous ambulatory peritoneal dialysis of a patient with intractable congestive heart failure secondary to an ischemic cardiomyopathy. Although the use of peritoneal dialysis to treat refractory heart failure is not new, the advent of an effective continuous peritoneal dialysis system has allowed its use over prolonged periods of time. The two-year treatment interval described herein represents the longest reported application of this technique, to the best of our knowledge.
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PMID:Long-term therapy for heart failure with continuous ambulatory peritoneal dialysis. 400 39

The coronary hemodynamic effects of vasodilator therapy with angiotensin-converting enzyme inhibitors (captopril and teprotide) were studied in 11 patients with ischemic heart disease and severe congestive heart failure (CHF). Over 2 hours, systemic vascular resistance was reduced from 2,408 +/- 240 to 1,715 +/- 170 dynes . s . cm-5 (p less than 0.001), and cardiac output improved 18%, resulting in lower arterial pressure (101 +/- 8 to 86 +/- 5 mm Hg, p less than 0.001) and left ventricular filling pressure (30 +/- 2 to 21 +/- 2 mm Hg, p less than 0.001). Coronary sinus thermodilution blood flow paralleled perfusion pressure but did not significantly vary overall (160 +/- 20 to 133 +/- 12 ml/min, difference not significant [NS]). Coronary vascular resistance was unchanged. Although the left ventricular stroke work index rose slightly (37.7 +/- 8.8 to 41.3 +/- 7.9 g l m/m2, p less than 0.05), there was no change in the coronary arteriovenous oxygen content difference (10.8 +/- 1.0 to 10.4 +/- 1.0 ml/10 ml, NS) or calculated myocardial oxygen consumption (16.4 +/- 1.9 to 13.9 /- 1.6 ml/min, NS). The heart rate-systolic blood pressure product declined significantly during this period (8,824 +/- 703 to 7,087 +/- 514 beats . mm Hg, p less than 0.02); this relief of cardiac effort was a function of the pretreatment plasma renin activity. A derived index of external myocardial efficiency improved 37% (19 +/- 3 to 26 +/- 6, p less than 0.05), reflecting greater left ventricular work without increased oxygen demand. Enhancement of myocardial performance after converting enzyme inhibition appears dependent on reduction of angiotensin-mediated ventricular afterload and preload. The lack of coronary vasomotor effects in patients with advanced ischemic cardiomyopathy may reflect limited coronary vascular reserve. Improvement of heart failure in these patients developed without evidence of myocardial ischemia, since balance was maintained between oxygen supply and demand.
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PMID:Coronary hemodynamic effects of angiotensin inhibition by captopril and teprotide in patients with congestive heart failure. 618 86

We evaluated long-term combined vasodilator therapy (hydralazine or ecarazine + isosorbide dinitrate) in 29 patients with chronic congestive heart failure resistant to the optimal conventional therapy. There were 24 men and 5 women, aged 28 to 76 years (mean 52 y/o). The etiology of heart failure was congestive cardiomyopathy in 24 patients, ischemic cardiomyopathy in 4 patients and advanced mitral regurgitation due to calcified mitral annulus in 1 patient. There were 21 patients in NYHA class III and 8 patients in NYHA class IV. All patients continued their previous therapeutic regimen during the period of this study. Hemodynamic measurements were performed with a triple lumen flow-directed balloon-tipped catheter in 20 patients to evaluate the effects of vasodilator therapy. In the rest of 9 patients, heart rate, blood pressure, chest X-ray examination for heart size (CTR) and M-mode echocardiograms for ejection fraction (EF) were monitored. The hemodynamic responses to the combined vasodilator therapy in 20 patients showed significant decreases in afterload and preload concomitant with an increase in cardiac output. The noninvasive evaluation of combined vasodilator therapy in 9 patients resulted in significant improvement in CTR and EF. We also noted a significant improvement in their symptoms of 29 patients. Side effects and drug toxicity were uncommon during vasodilator therapy. It is concluded that the combined vasodilator therapy is most useful adjunctive therapy in the management of severe refractory heart failure. Moreover, long-term nonparenteral vasodilators can be administered even at outpatient clinic without hemodynamic monitoring.
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PMID:Ambulatory long-term vasodilator therapy for chronic refractory heart failure: hemodynamic evaluation and clinical response. 642 26

In a double-blind cross-over study with 9 patients suffering from ischemic cardiomyopathy with cardiac failure, the effect of 3 different drug preparations on pulmonary artery pressure (PA-pressure) was studied. Iso-Ameritrat is a new drug-combination consisting of a sweet-tasting wrap containing 2.5 mg Isosorbide Dinitrate (ISDN) and of a bitter-tasting core containing 10 mg Pentaerythritol Tetranitrate (PETN) and 200 mg Meprobamate. A statistically significant decrease of PA-pressure values could be observed already 3 minutes after administration of Iso-Ameritrat. Within the next minutes this decrease even augmented and lasted over the whole period of measurement (30 minutes). After administration of the second drug preparation (Ameritrat), containing 10 mg PETN and 200 mg Meprobamate in the core, but not any nitrate in the wrap a slight but also statistically significant decrease of PA-pressure values could be documented. Therefore a sublingual resorption of PETN can be assumed. The precise beginning of the effect of PETN couldn't be assured, but it must be within 5 minutes. A thir preparation, containing only 200 mg Meprobamate in the bitter tasting core caused no significant decrease of PA-pressure values.
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PMID:[Pulmonary artery pressure measurement for assessment of bioavailability of isosorbide dinitrate and pentaerythritol tetranitrate (author's transl)]. 699 69

Two patients abruptly developed congestive heart failure and elevation in serum transaminase levels when given disopyramide phosphate; enzyme abnormalities and hemodynamic status corrected upon withdrawal of the drug. Both patients had underlying ischemic cardiomyopathy. Myocardial infarction, pulmonary embolism, and viral hepatitis were ruled out in both patients. One patient had a liver biopsy documenting central hepatic necrosis with congestion, consistent with hepatic ischemia and not toxic hepatitis. In the other patient, cardiac decompensation and hepatocellular enzyme elevation were reproduced on rechallenge with the drug. Disopyramide should be used with caution in patients with heart failure.
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PMID:Acute cardiac failure and hepatic ischemia induced by disopyramide phosphate. 722 41

Recently published data of the controlled MDC- and CIBIS-trials confirm the favorable effect of beta-blocker therapy on the hemodynamics and clinical course of patients with chronic heart failure due to dilatated and/or ischemic cardiomyopathy. However, mortality remains unchanged. The mechanisms by which beta-blocker therapy improves hemodynamics in chronic heart failure are not known reliably. It is postulated that the negative chronotropic effect of beta-blockers improves the cellular calcium metabolism and thereby increases myocardial contractility. Further effects of beta-blockers are protection of myocardial cells from enhanced catecholamine concentrations. This prevents cell necrosis and economizes the use of cell energy. The reversion of down-regulation of beta-1-receptors in beta-blocker therapy is most probably only an epiphenomenon. Major randomized clinical trials are ongoing to investigate whether improved hemodynamics and clinical course are correlated with decreased mortality. It also still remains open which substance is most beneficial (e.g., selective beta-blockers, beta-blockers with additional vasodilatatory effect).
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PMID:[Beta receptor blockers in chronic heart failure]. 750 69


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