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 clinical efficacy of xamoterol, alpha beta 1-adrenoceptor partial agonist, was determined in a multicentre double-blind, randomized, parallel group study of 240 patients with mild to moderate heart failure. At entry, 62% of patients were receiving diuretics (thiazides, or loop diuretics at a dose no greater than the equivalent of 80 mg of frusemide); 32% were taking nitrate formulations and 14% digoxin for control of atrial fibrillation. Assessments were carried out after a 1-week placebo run-in and after 3 months of treatment with either xamoterol or placebo. 198 patients completed the study of whom 186 had valid exercise tests. Mean exercise duration increased by 7% after placebo and by 19% after xamoterol during a progressive treadmill exercise protocol. Xamoterol significantly reduced peak exercise heart rate compared with placebo. Subjectively, there was improvement in breathlessness on the visual analogue scale after treatment with xamoterol compared with placebo, but no change in fatigue. We conclude that xamoterol produces sustained improvement in symptoms and exercise duration in mild to moderate heart failure.
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PMID:Clinical efficacy of xamoterol, a beta 1-adrenoceptor partial agonist, in mild to moderate heart failure. U.K. Xamoterol Study Group. 257 8

The renin-angiotensin-aldosterone system plays an important role in the development of congestive heart failure (CHF). In patients with chronic heart failure, angiotensin-converting enzyme (ACE) inhibitors, such as captopril, enalapril, and quinapril, have been shown to improve hemodynamics, reduce symptoms of fatigue and dyspnea, increase exercise capacity, correct hyponatremia, reduce diuretic requirements and ventricular arrhythmias, and conserve potassium and magnesium. ACE inhibitors reduce circulating levels of angiotensin II and aldosterone and may reduce plasma norepinephrine and vasopressin levels. They are equally effective in patients with mild to moderate heart failure and in patients with severe cardiac impairment. ACE inhibitors are at least as beneficial as digitalis in patients with mild heart failure, and they may even be considered as first-line therapy. Promising results have also been obtained in patients with myocardial infarction, in whom long-term therapy with ACE inhibitors has prevented an increase in heart size. ACE inhibitors improve prognosis in patients with severe heart failure and in patients with hyponatremia; the question of effect on survival in mild to moderate heart failure has yet to be answered.
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PMID:ACE inhibitors in congestive heart failure. 267 Feb 20

The patient was a 70-year-old male with complaint of macrohematuria at the first visit to our clinic on June 10, 1986. At that time, cystoscopy revealed a thumb sized papillary tumor and a rice sized non papillary tumor, and the biopsy specimen was pathologically diagnosed as undifferentiated carcinoma. But, he refused admission. On January 30, 1987, he came back to our clinic with complaints of dyspnea, general fatigue and weight loss. Moderate lt. gynecomastia was found and the level of serum hCG-beta was detected as high as 101 ng/ml. Excretory urogram and enhanced CT revealed a large mass in the bladder. In the seventeenth day after admission, he died of lung edema and heart failure. The findings of autopsy showed a large light greenish to light brownish tumor of 10 X 10 X 3 cm in the bladder. Distant metastases were observed in internal, common iliac and paraaortic lymph nodes, but without other distant metastasis. In histological and immunohistochemical studies, the final diagnosis is choriocarcinoma of the bladder, containing syncytiotrophoblastic giant cells with hCG-beta granules as an undifferentiated carcinoma. To our knowledge this case is the eighth described in Japan. Herein we report a new case of primary choriocarcinoma of the bladder and make a brief review of the literatures.
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PMID:[Primary choriocarcinoma of the bladder: a case report of autopsy]. 267 66

Dynamic cardiomyoplasty is a new surgical procedure proposed for treatment of the failing heart. Clinically, the latissimus dorsi muscle is raised as a pedicled flap and wrapped around the heart. The skeletal muscle is transformed to produce a myocardium-like fatigue-resistant muscle. It is stimulated to contract in synchrony with the heart in hope of assisting the myocardial contraction. An R-wave synchronous pacemaker provides a pulse-train form of stimulation to simulate, for the skeletal muscle, the contractile characteristics of the myocardial syncytium. We have undertaken a critical review of the clinical results of dynamic cardiomyoplasty reported to date. Objective evidence of clinical improvement after dynamic cardiomyoplasty resulting from the contractile assistance of the myoplasty has been modest. Many of the beneficial results reported could be explained by concomitant procedures done, such as aneurysmectomy or coronary artery bypass grafting. Hemodynamic studies have failed to demonstrate consistent and convincing improvement as a result of the cardiomyoplasty stimulation. We have, however, identified an interesting subgroup of patients, in whom a striking hemodynamic response to cardiomyoplasty stimulation has been reported. These patients all possess large resting heart volumes characteristic of dilated cardiomyopathy. Thus, case selection may ultimately be one of the most important factors in determining the success of dynamic cardiomyoplasty for the treatment of heart failure.
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PMID:Dynamic cardiomyoplasty for treatment of heart failure. 269 90

The authors developed a new measure of subjective health status for patients with heart failure. Eighty-eight patients with heart failure were asked about the impact of their condition on 123 items related to physical and emotional function. The most frequently chosen and important items were included in a 16-item Chronic Heart Failure Questionnaire (CHQ) that examines dyspnea during daily activities, fatigue, and emotional function. The CHQ was tested in a controlled trial of digoxin in heart failure patients in sinus rhythm. When administered serially to 25 patients in the run-in phase of the trial, the CHQ proved reproducible. Subsequently, CHQ results distinguished those who reported improvement or deterioration from those who did not. The CHQ showed moderate correlations with patient global ratings, walk test scores, and clinical assessments of heart failure. The authors conclude that the CHQ may be useful for measuring health status in clinical trials in heart failure.
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PMID:Development and testing of a new measure of health status for clinical trials in heart failure. 270 67

A case of malignant fibrosarcoma originated from pericardium was reported. A 31 year-old female who complained of general fatigue and back pain showed dilated cardiac shadow in chest X-ray. Cardiac blood pool scan with 99mTc-RBC revealed avascular mass in pericardial cavity which push the heart up and left side. It was suspected to be malignant, since the mass had increased 67Ga uptake. CT and MRI also demonstrated that the tissue characterization of the pericardial mass was irregular, and the mass compressed venous return. The large mass originated from pericardium caused the right sided cardiac failure. In 12 years ago, she had a history of operation which resected benign hemangioma in the same space (pericardium). We could suspect the malignant transformation between the two rare pericardial tumors; benign hemangioma and malignant fibrosarcoma.
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PMID:[Pericardial fibrosarcoma demonstrated by Ga-67 scintigraphy]. 279 5

Skeletal muscle grafts can be used to mechanically assist the failing heart. In 13 mongrel dogs, latissimus dorsi muscle was preconditioned in situ for 6-8 weeks. Biopsy samples of the muscles were obtained for histochemical analysis. In seven dogs, muscle force and fatigue were compared in conditioned and contralateral unconditioned (controls) muscles. In six dogs, latissimus dorsi cardiomyoplasty was performed in propranolol-induced acute heart failure, and its effects were evaluated by hemodynamic and echocardiographic parameters. Muscle conditioning was responsible for latissimus dorsi transformation to a muscle with predominantly fatigue-resistant type I fibers. Conditioned muscles developed less initial force (-27 +/- 6%) and a longer contraction time (+32 +/- 4%) (p less than 0.05) but did not show fatigue for less than 15 minutes. With synchronous pulse-train stimulation of the muscle flap, cardiac output increased from 1.4 +/- 0.1 (mean +/- SD) to 2.0 +/- 0.2 l/min (p less than 0.05), pulmonary wedge pressure decreased from 16.3 +/- 0.9 to 12.1 +/- 1.4 mm Hg (p less than 0.05), and left ventricular end-diastolic pressure decreased from 18 +/- 2.0 to 13.5 +/- 1.4 mm Hg (p less than 0.05). Echocardiographically derived ejection fraction increased from 39.3 +/- 2.4% to 59.6 +/- 2.9% (p less than 0.05), and fractional shortening increased from 15.4 +/- 1.1% to 26.3 +/- 1.7% (p less than 0.05). Thus, chronic stimulation of skeletal muscles induces fiber transformation and increases resistance to fatigue and force development. Cardiomyoplasty, on the other hand, improves ventricular function in the presence of acute heart failure. This surgical technique represents an alternative method of treatment for advanced myocardial failure.
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PMID:Stimulated preconditioned skeletal muscle cardiomyoplasty. An effective means of cardiac assist. 280 2

Six patients suspected to have "pacemaker syndrome" were studied with hemodynamic and electrophysiologic methods. Symptoms appeared after implantation of ventricular pacemaker (VVI). Mile symptoms such as dizziness and fatigue and severe symptom of heart failure were noted. The results of the study suggested that cardiac output decreases due to loss of atrial contribution to ventricular filling and also as a result of increase of systemic venous pressure. If the patient has V-A conduction, cardiac output will decrease further. Restoration of atrioventricular synchronization is essential in the treatment of the pacemaker syndrome.
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PMID:[Pacemaker syndrome: a report of 6 cases]. 280 51

During 10 years of clinical use involving almost 3 million patient-years, acebutolol has become established as a remarkably safe and well-tolerated beta-blocking agent, effective in treating essential hypertension and cardiac arrhythmias. The existence of a long-lived active metabolite (diacetolol) confers a 24-hour duration of action, which permits effective use of a once-daily regimen, particularly for hypertension. Acebutolol has low lipid solubility and low protein binding; the former property reduces the risk of central side effects, and the latter means that displacement interactions with other drugs are unlikely. Because acebutolol and its metabolite normally have both renal and hepatic excretion pathways, an alternative pathway is available should either be compromised through disease. Acebutolol is cardioselective, and clinical use has borne out the low incidence of bronchospasm in patients with impaired lung function. The possession of intrinsic sympathomimetic activity (ISA) leads to only modest reductions in cardiac output, which in turn reduces the chance of excessive bradycardia and the likelihood of precipitating heart failure. A combination of selectivity and ISA may be responsible for the low incidence of tiredness and cold extremities observed with acebutolol compared with other beta blockers. The unique pharmacologic and pharmacokinetic profile of acebutolol confers several therapeutic advantages and may be responsible for the generally low level of side effects experienced in clinical use.
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PMID:Acebutolol: ten years of experience. 285 85

Symptoms of dyspnea and fatigue limit effort tolerance in patients with chronic cardiac failure. These symptoms may be consequent to an abnormal cardiocirculatory response to the increased O2 demand that accompanies exercise as manifested by: reduced ability to augment cardiac output in response to increased left ventricular filling pressure, inadequate vasodilatory response in exercising limbs, the onset of lactate production by muscle at relatively low levels of work, and increased work of breathing that accompanies pulmonary venous hypertension and abnormal compliance of the lung secondary to left ventricular dysfunction. The clinical experience with new positive inotropic agents in the long-term treatment of patients with chronic cardiac failure is accumulating rapidly. Attention has focused on the ability of these agents to improve exercise performance, particularly their ability to increase the aerobic capacity. The experience to date suggest that beta-adrenergic receptor agonists offer little advantage in this regard while causing ventricular arrhythmias. On the other hand, the phosphodiesterase inhibitors, MDL 17,043 and MDL 19,205, and the bipyridine derivatives, amrinone and milrinone, may improve exercise performance in many patients and exert a sustained effect during long-term therapy. Placebo-controlled, randomized trials will need to be performed, however, to determine the ultimate efficacy and safety of these agents. The most meaningful results for analysis will be obtained when objective parameters of exercise performance, such as aerobic capacity and anaerobic threshold, are monitored that are free of patient or physician bias.
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PMID:Effects of new inotropic agents on exercise performance. 286 37


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