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)

The present study was designed to investigate the effect of the calcium-channel antagonist gallopamil on myocardial ischemia during percutaneous transluminal coronary angioplasty (PTCA). Twenty-four adult patients with coronary artery disease and significant proximal stenosis of the left anterior descending coronary artery (LAD) were randomly assigned to receive gallopamil or placebo under double-blind conditions. Patients with recent myocardial infarction, apparent collateralization of the LAD, myocardial failure, sinoatrial or atrioventricular block, severe hepatic disease, or renal failure were excluded from the study. PTCA was performed with use of at least two balloon inflations, each of 2 min in duration. Gallopamil (0.4 mg) or placebo (0.9% sodium chloride) was administered during the 10-min interval between the two inflations. For determination of myocardial lactate and hypoxanthine release, blood samples were taken simultaneously from the great cardiac vein and the femoral artery before and immediately after each inflation. Electrocardiogram changes were analyzed by measuring ST-segment deviations (80 ms after the J point) and maximal T-wave deviations of the leads I, II, III, and V2, V4, and V6. The most sensitive leads for identification of myocardial ischemia in the LAD area were V2 and V4. If compared to the first balloon inflation, the degree of ST-segment/T-wave changes induced by the second inflation was significantly reduced only in the presence of gallopamil. Furthermore, if compared to placebo, ischemia-induced lactate and hypoxanthine release was decreased in the presence of gallopamil. These results suggest that intracoronary application of gallopamil attenuates myocardial ischemia during PTCA.
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PMID:Intracoronary gallopamil during percutaneous transluminal coronary angioplasty. 128 55

The purpose of the study was to evaluate the effect of enalapril on the frequency of ventricular premature beats in patients with congestive heart failure. The study group consisted of 30 patients with a mean age of 47 +/- 0.6 years with chronic congestive heart failure (NYHA classes III and IV) due to primary dilated cardiomyopathy and cardiomyopathy in the course of ischaemic heart disease. Initial therapy with digitalis and diuretics was supplemented with enalapril at a dose of 5-20 mg daily. Initially and at three months after enalapril, the following parameters were evaluated: NYHA functional class, the presence of premature ventricular beats in 24-hour ECG recording and left ventricular function by echocardiography. The scheduled therapy was completed by 23 patients; in 5 patients, the intake was discontinued because of hypotension, one patient died after 14 days due to worsening heart failure, and one patient was submitted for pacemaker implantation. Clinical improvement manifesting itself by a shift to lower NYHA classes was found in 20 patients. A reduced number of premature ventricular beats was observed in 52% of the patients. Termination of cardiac arrhythmias, especially of complex beats, was parallel to the circulatory improvement.
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PMID:The effect of enalapril on cardiac arrhythmias in patients with congestive heart failure. 128 55

In the postoperative period the alterations of blood pressure are the main hemodynamic complications. Hypotension or hypertension may compromise the coronary circulation and increase the metabolic demand of the myocardium. Pulmonary oedema is the most frequent manifestation of heart failure. The aim of its treatment is to increase myocardial contractility and decrease the metabolic demand. Myocardial ischemia is mostly silent and is an important correlate of adverse cardiac outcomes. The treatment of these hemodynamic events starts during the peroperative period by prevention of their risk factors.
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PMID:[Hemodynamic complications during the recovery period after anesthesia]. 130 45

Calcium channel blockers are widely used in the treatment of ischemic heart disease, hypertension, and supraventricular tachycardia. The prototype agents, verapamil, nifedipine, and diltiazem, represent three classes of calcium channel blockers, each of which has different pharmacologic effects. Nifedipine and the other dihydropyridines primarily are vasodilators and have no clinical effects on cardiac conduction or contractility. Diltiazem and verapamil also are vasodilators, but they possess, to varying degrees, negative inotropic, chronotropic, and dromotropic effects. Side effects of these drugs are relatively rare and usually not serious, with the exception of potential conduction disturbances and heart failure in patients with underlying cardiac disease. To assess patients taking these medications and provide the necessary teaching, the nurse needs an understanding of the pharmacologic properties, clinical indications, and potential adverse effects of the various drugs.
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PMID:Calcium channel blockers. 131 59

Single cardiac myocytes were isolated from the ventricles of failing and non-failing human hearts. The contraction amplitude, time-to-peak shortening and time to 50% and 90% relaxation were measured in cells stimulated at 0.2 Hz at 32 degrees C. The effects of increasing extracellular calcium and isoproterenol were investigated using cumulative concentration/response curves. Maximum contraction amplitude in high calcium or velocities of contraction or relaxation were not impaired in cells from failing hearts. Beta-adrenoceptor function in a single cell was assessed by the maximum contraction amplitude in the presence of isoproterenol relative to that with high calcium in the same cell (isoproterenol/calcium ratio). A decrease in the isoproterenol/calcium ratio correlated positively with an increase in the isoproterenol EC50 (concentration for half-maximal effect) for a cell (P less than 0.02, n = 39). The isoproterenol/calcium ratio in left ventricular myocytes decreased with increasing severity of disease, correlating with failure as defined by New York Heart Association class (P less than 0.001, n = 26 patients), left ventricular ejection fraction (P less than 0.001, n = 24), left ventricular end diastolic pressure (P less than 0.05, n = 21) and amount of diuretics prescribed (P less than 0.001, n = 26). In right ventricular myocytes, only increasing NYHA class correlated with decreasing isoproterenol/calcium ratios. There was a correlation of the isoproterenol/calcium ratio between right and left ventricular cells from patients with ischemic heart disease (P less than 0.05), n = 11). Beta-adrenoceptor subsensitivity occurred in mitral valve disease, ischemic heart disease, congenital abnormalities and congestive cardiomyopathy, but not in the right ventricle of patients with myocarditis. The isoproterenol/calcium ratio correlated negatively with the age of the patient (P less than 0.001, n = 26, left ventricle). Multiple regression indicated that the maximum contraction amplitudes in either high isoproterenol or high calcium declined significantly with age only, but that both age and severity of disease contributed to the decrease in isoproterenol/calcium ratio. Time-to-peak tension in isoproterenol, as well as relaxation times in high calcium also decreased with the age of the patient. Analysis of variance showed that between-patient variation was significantly greater than between-cell for most of the parameters measured. Beta-adrenoceptor desensitisation may be detected in individual myocytes from failing hearts, and this relates more to the severity of disease and the age of the patient rather than the etiology of heart failure. A decline in absolute contractility of muscle cells with age was detected.
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PMID:Isolated ventricular myocytes from failing and non-failing human heart; the relation of age and clinical status of patients to isoproterenol response. 132 14

Patients with different heart diseases, dilated cardiomyopathy, valvular heart disease, hypertension, ischemic heart disease or myocarditis showed manifestations of autoimmunity and down-regulation of beta-adrenergic receptors. Autoantibodies against beta-adrenergic receptors in these patients were detected with radioligand binding inhibition assay. The results suggested that the down-regulation of cardiac beta-adrenergic receptors in these patients may be mediated by autoimmunity. Autoantibodies against beta-adrenergic receptor were not related to any specific heart diseases, but to the severity of heart failure irrespective of its etiology. The significance of these autoantibodies in heart failure was discussed.
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PMID:[Circulating autoantibodies against beta-adrenergic receptors in patients with heart diseases]. 133 2

Several studies in the past have shown the long-term beneficial effects of beta-blockers in congestive heart failure. Despite the interest in this mode of therapy, their clinical application has been limited due to their negative inotropic effect. A subset of the heart failure patients do not show any improvements with standard beta-blocker therapy. Carvedilol, a new, non-selective beta-blocking agent with concurrent alpha-blocking properties, was evaluated in 17 patients with chronic heart failure secondary to ischaemic heart disease. All had resting left ventricular ejection fraction less than or equal to 45% and were maintained on diuretic therapy. Acute haemodynamic measurements were made after intravenous carvedilol (2.5-7.5 mg) and also after chronic therapy for 8 weeks (carvedilol 12.5-50 mg b.d.). Radionuclide ventriculography, ambulatory intra-arterial blood pressure monitoring and right heart catheterization were performed before and after 8 weeks of chronic therapy. Twelve patients completed the study and 5 were withdrawn. Symptomatic and haemodynamic improvement was demonstrated in 11 of the 12 patients after 8 weeks of therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Can intravenous beta blockade predict long-term haemodynamic benefit in chronic congestive heart failure secondary to ischaemic heart disease? A comparison between intravenous and oral carvedilol. 135 Apr 92

Several studies have demonstrated the long-term beneficial effects of beta-blockers in the treatment of congestive heart failure. Despite interest in this mode of therapy, clinical application of beta-blockers has been limited due to their negative inotropic effect. A subset of the heart failure patients do not show improvements with standard beta-blocker therapy. Carvedilol, a new nonselective beta-blocking agent with concurrent alpha-blocking properties, was evaluated in 17 patients with chronic heart failure secondary to ischemic heart disease. All had resting left ventricular ejection fraction less than or equal to 45% and were maintained on diuretic therapy. Acute hemodynamic measurements were made after administration of intravenous carvedilol (2.5-7.5 mg) and after chronic therapy for 8 weeks (12.5 to 50 mg b.i.d.). Radionuclide ventriculography, ambulatory intra-arterial blood pressure monitoring, and right heart catheterization were performed before and after 8 weeks of chronic therapy. Twelve patients completed the study (five were withdrawn). Symptomatic and hemodynamic improvements were demonstrated in 11 of the 12 patients after 8 weeks of therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Can intravenous beta-blockade predict long-term hemodynamic benefit in chronic congestive heart failure secondary to ischemic heart disease? A comparison of intravenous with oral carvedilol. 137 53

Calcium antagonists are useful for the management of patients with ischaemic heart disease, particularly when used prophylactically. At the cellular level, these drugs act primarily by limiting calcium ion (Ca++) entry through the voltage-sensitive Ca(++)-selective channels, an effect that contributes markedly to their 'energy sparing' properties. However, the long term use of these drugs has additional advantages, particularly with respect to their ability to slow Ca(++)-dependent processes involved in the formation of atherogenic lesions, partially antagonise the effects of the raised levels of circulating endothelin-1 encountered during ischaemia-induced heart failure and hypertension, and trap and immobilise oxyradicals. Prolonged episodes of ischaemia result in an irreversible loss of homeostasis with respect to Ca++. However, the increase in myocardial cytosolic Ca++ caused by relatively short periods of ischaemia is small, reversible, and markedly attenuated by the prophylactic use of calcium antagonists. In the isolated, perfused rat heart, verapamil pretreatment produces statistically significant inhibition of the increase in cytosolic Ca++ during 20-minute global ischaemia. This stereospecific effect is associated with a decrease in the rise in total tissue Ca++ during reperfusion and amelioration of the adenosine triphosphate depletion caused by ischaemia. In general, discussion relating to the molecular basis of the use of calcium antagonists in the management of patients with ischaemic heart disease needs to take into account the duration of the ischaemic event, the workload on the myocardium, the need for prophylactic therapy, and the presence of exacerbating factors such as atherosclerosis and tobacco smoking. The early rise in cytosolic Ca++, the source of which remains uncertain, appears to be an important focus for anti-ischaemic drug therapy.
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PMID:The molecular basis for the use of calcium antagonists in ischaemic heart disease. 137 84

In 109 out of 479 patients who were referred for cardiac transplantation it was considered to be too early to put them on the waiting list for a donor heart. The clinical course of these 109 patients was analysed in order to verify whether this decision had been right. The mean age of the patients was 43 years, half of them suffered from ischaemic heart disease. The systolic left ventricular function of the patients was severely depressed (mean left ventricular ejection fraction 21%) and the left ventricular cavity was markedly dilated (mean echocardiographic end diastolic dimension 73 mm). Functional capacity, measured by bicycle ergometry, was low: mean maximal workload 62% of the expected load for gender, height and age. The median follow-up duration was 31 months. The survival rate of the patients was better than that of 175 patients who were accepted for transplantation after referral, 92%, 87%, 81%, 71% and 73%, 73%, 71%, 68% after 1, 2, 3 and 4 years respectively. Re-assessment was necessary in 29% of the patients within 1 year and in 52% within 3 years. Twenty patients died: 12 patients died before re-assessment had been initiated (eight sudden deaths), six patients because of progressive heart failure before heart transplantation could be performed and two patients died after heart transplantation. Left ventricular ejection fraction, pulmonary capillary wedge pressure and transpulmonary gradient were not reliable predictors of the course of the patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Too early for cardiac transplantation--the right decision? 139 5


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