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)

Propranolol and practolol were tested in patients with repeated daily occurrence of spontaneous angina. Twenty-one showed ST segment depression (type I) and 15 ST segment elevation (type II) during angina. The efficacy of the treatment was evaluated in subjective (number of reported episodes of pain) and objective terms (number of episodes of electrocardiographic abnormalities documented during periods of continuous recording): practolol was fully effective in 42 per cent and propranolol in 38 per cent of type I cases; in type II angina 73 per cent of the cases fully responded to propranolol, none of the patients in this group given practolol improved. The study also showed that: (a) the effects on angina are strictly dose-dependent, and optimal results are achieved at individualized doses; (b) within the same subject the response may be preferential to one beta-blocker as opposed to the other; (c) propranolol is more effective in type II angina; (d) the occurrence of heart failure is uncommon even with high doses of beta blockers;(e) the relief of angina is due to prevention of ischaemia and not to a placebo or anaesthetic effect; (f) the prevention of ischaemia is not adequately explained by reduction of the mechanical effort and the oxygen need of the myocardium; (g) the antianginal effect is possibly dissociated from the beta blockade of the heart. The hypothesis that beta-blocking agents influence the conronary vasomotion is discussed.
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PMID:Treatment of spontaneous angina pectoris with beta blocking agents. A clinical, electrocardiographic, and haemodynamic appraisal. 77 91

Sixty-three patients with stable, severe typical angina pectoris (New York Heart Association functional class III or IV) were treated with propranolol and studied prospectively with a follow-up period of 5 to 8 years to assess the rate of complications and long-term effectiveness after an initial control period. The patients' mean age was 56 years; the mean daily dose of propranolol was 255 mg. The average yearly mortality rate was 3.8 percent with a cumulative 5 year mortality rate of 19 percent. Patients whose reduction of angina with propranolol was less than 50 percent had a nearly four-fold greater mortality rate than those whose reduction was 50 percent or more (P less than 0.01). Thirty-two percent of patients per year were angina-free with propranolol and 84 percent per year had 50 percent or more reduction in anginal episodes. There was no evidence for tachyphylaxis. Heart failure developed in 25 percent of patients, two thirds of whom had either congestive heart failure with an acute infarction or a prior history of congestive heart failure. All patients whose initial cardiothoracic ratio was greater than 0.5 had heart failure during the first 3 years of propranolol therapy. Of 12 patients who had an acute infarction during therapy, 7 died, 6 with cardiogenic shock; in contrast, 8 of 9 patients who had congestive heart failure without acute infarction survived. Eight percent of patients had other significant side effects, including gastrointestinal symptoms (three patients), hallucinations (one) and postural hypotension (one). The occurrence of asthma in three patients was dose-related and did not require drug discontinuation. Propanolol is an effective form of long-term therapy for severe angina pectoris; it does not induce tachyphylaxis or increase the overall mortality rate, although it may increase the risk of cardiogenic shock in acute myocardial infarction. Previous history of congestive heart failure, a cardiothoracic ratio of more than 0.5 without overt heart failure and mild asthma are relative contraindications. A 50 percent or greater reduction in anginal pain with propranolol predicts a low mortality group.
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PMID:Long-term propranolol therapy for angina pectoris. 81 88

The conditions associated with prolapse of the posterior leaflet of the mitral valve are multiple. The mechanisms of mitral valve prolapse as well as the pathogenesis of pain and ectopic impulse formation are reviewed. Propranolol appears to be the drug of choice for the symptomatic treatment of patients with this syndrome since it decreases myocardial oxygen demand and wall tension thus reducing or abolishing the discrepancy between myocardial oxygen demand and supply within the mitral apparatus. It has also been reported to modify the auscultatory findings associated with this condition. The frequency of this mitral valve abnormality in patients with obstructive coronary artery disease is reviewed. It appears that prolapse of the posterior leaflet scallops in patients with significant obstructive coronary artery disease represents an intermediate stage before mitral insufficiency occurs. This group of patients with papillary muscle dysfunction includes those with prolapsed leaflets without mitral insufficiency, those with systolic murmurs and compensated heart failure and others with progressive cardiac decompensation and severe mitral regurgitation.
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PMID:Mitral valve prolapse. Recent concepts and observations. 93 60

Statistical analysis of the realtion between blood pressure and renal function in 421 patients with CGN, referred to the Second Internal Medicine at Nihon University Hospital, and in 253 Hypertensive patients with CGN by questionaires sent to 29 Medical Universities were investigated. The relationship between survival rate and blood pressure of 84 patients with CGN in Surugadai Nihon University Hospital was also examined. These data show that antihypertensive therapy for CGN with hypertension has an important effect on prognosis. Propranolol was given to 10 hypertensive patients with CGN and hypotensive effect on renal function was observed. Our experience suggests that propranolol may be useful for treating a high renin component in the hypertension with non renal failure, and renal function does not become worse. But in renal failure, propranolol therapy must be used carefully because of inducement to cardiac failure.
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PMID:Therapy and prognosis of hypertension in chronic nephritis. 115 36

Between 1969 and 1991, 11 patients were followed up for permanent junctional reciprocating tachycardia. The average age at diagnosis was 2 years and 4 months (1 day to 14 years). The tachycardia was diagnosed at routine examination in 5 cases and following an episode of cardiac failure in the other 6. Digitalis was prescribed in all patients with 4 good results, 5 average and 2 poor results. One patient, who remained in mild cardiac failure with digitalis therapy, died suddenly at the age of 9 years. In more recent cases, amiodarone was used from the onset or secondarily with good results in all patients. In 2 patients, in whom amiodarone was withdrawn after 3 months and 3 years' treatment, there was a recurrence of the tachycardia. No side effects of amiodarone therapy were observed in this series. Three patients were prescribed flecainide with 1 good and 2 average results. Propranolol, used in 2 cases, was associated with 1 average and 1 poor result. Disopyramide and Verapamil were ineffective. These results suggest that amiodarone is the drug to choose in permanent junctional reciprocating tachycardia but it must be given long term. The persistence of cardiac failure, poor control of the tachycardia or secondary effects of drug therapy should lead to consideration of non-medical management of the tachycardia.
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PMID:[Permanent junctional reciprocating tachycardia in children and adolescents. Efficacy of medical treatment]. 153 Mar 93

Sympathetic activations may deteriorate myocardial failure due to progression of myocardial cell injury. In the present study, to test whether microtubules, calcium ion (Ca2+) sensitive cytoskeletons, are disrupted by norepinephrine (NE) and whether beta-adrenoceptor antagonist could attenuate the disruption of microtubules, structures of microtubules are studied in rat hearts with continuous subcutaneous infusions of norepinephrine. In the sham operated rats the microtubules stained by immunohistochemical technique showed normal network structures. A low dose of NE infusion (2 micrograms/kg/h) for 6 h resulted in a minimal change in microtubule structures. However, infusion for 24 h of NE (2 micrograms/kg/h) and a large dose of NE infusion (20 micrograms/kg/h) for 6h caused disruptions of microtubules in small patchy lesions (8 +/- 3%, 12 +/- 4% of area, respectively). A large dose of NE infusion for 24 h increased systolic blood pressure from 116 +/- 6 to 152 +/- 4 mmHg and increased plasma NE concentration from 430 +/- 40 to 17100 +/- 3700 pg/ml and further disrupted the network of microtubules in 40 +/- 6% of the total area. Propranolol (500 micrograms/kg/h) markedly attenuated NE-induced disruptions of microtubules. Disruptions of microtubules may be one of the underlying mechanism of deterioration of myocardial failure in chronic heart failure in which sympathetic activity is markedly activated.
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PMID:Norepinephrine disrupts cytoskeletal framework of microtubules in rat hearts. 160 97

Feline myocardial diseases today are largely represented by disorders involving LV hypertrophy. They may be attended by arrhythmias, congestive heart failure, systemic hypertension, thromboembolic complications, and sudden death. These structural myocardial disorders and their hemodynamic and electrocardiographic derangements may cause or result in variable degrees of diastolic dysfunction. Propranolol and aspirin represent two agents commonly employed to treat feline cardiomyopathies for more than 15 years. Nevertheless, clinical data describing their effect on morbidity and mortality are lacking. It is likely that propranolol administered at moderate to high doses effects favorable responses in some cats with clinical signs attributable to severe hypertrophy, outflow obstruction, or tachyarrhythmias. It is unknown whether clinical improvements are due to direct myocardial effects or (more likely) secondary responses to a beta-adrenergic blockade reduction in heart rate or contractility. Personal experience also indicates that high numbers of cats have received the drug for many years in combination with other therapies (especially furosemide) and remain in a compensated state of heart failure without untoward drug effects. On the other hand, many cardiomyopathic cats experience heart failure, arrhythmias, and death despite treatment with beta-blocking agents. Feline thromboembolism is a devastating complication of cardiomyopathic disorders. Until or unless the primary cause(s) of current diseases is elucidated to promote disease reversal, factors responsible for thrombus formation will accompany the heart diseases, protected from effective management. It appears unlikely that aspirin as currently recommended produces any obvious benefit in treating or preventing thromboembolism. Modifications of therapeutic protocols prescribing these frequently used drugs await well-constructed clinical trials evaluating their efficacy with respect to cardiovascular morbidity and mortality.
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PMID:Evidence for or against efficacy of beta-blockers and aspirin for management of feline cardiomyopathies. 168 44

The aim of this study was to evaluate the hemodynamic effects of extraaortic counterpulsation with a latissimus dorsi (LD) neurovascular flap in a canine heart failure model. Five dogs (8-18 kg) had a left LD neurovascular muscle flap raised. The muscle was brought into the chest through the second interspace and wrapped around the aorta. Parameters studied were heart rate (HR), systolic pressure (SP), diastolic pressure (DP) pulmonary artery pressure (PAP), mixed venous oxygen saturation (MVO2), and cardiac output (CO). Baseline measurements were obtained with the muscle nonstimulated and stimulated by a prototype burst stimulation. The only parameter that changed significantly with muscle stimulation was DP (55.8 +/- 3.8 mmHg to 72.4 +/- 4.8 mmHg, p less than 0.05). Propranolol (3-4 mg/kg) and verapamil (2-3 mg) were given intravenously to induce heart failure. Mean blood pressure decreased from 64.12 +/- 5.03 mmHg to 43.3 +/- 9.28 mmHg (p less than 0.05). Repeat measurements were obtained. With stimulation of the muscle flap there was an increase in DP from 36.8 +/- 9.2 mmHg to 55.4 +/- 19.3 mmHg (p less than 0.05). Although CO increased from 8% to 18% in all animals (1.42 +/- 0.33 L/mm to 1.58 +/- 0.34 L/mm) this did not reach statistical significance. This data indicates that both DP and CO can be improved by this method of cardiac assist in a heart failure model.
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PMID:Extraaortic counterpulsation with a latissimus dorsi flap: hemodynamic effects in a heart failure model. 180 2

In the present study: (a) physiopathology, (b) clinics, and (c) therapy of cardiothyreosis are discussed. (a) The hyperkinetic syndrome, the earliest clinical sign in thyrotoxicosis (vasodilatation, increase in inotropism, automatism, etc.), is mediated by a two-fold increase in the number of beta-receptors, and supported by an adequate synthesis of ATP and creatinphosphate (CP) in the young and, to a lesser extent, in the elderly. Genetical heart reserves are mobilized, thus significantly increasing the number and the size of mitochondria and also the enzymatic equipment (such as: the alpha-glycerophosphate-dehydrogenase, malic, pentosic cycles, etc.), a.s.o. Due to an excessive adrenergic action (glycogenolysis, an excessive oxygen consumption, up to necrosis, the ATP and CP syntheses dramatically drop; the phosphorus/oxygen ratio decreases to 2 (normal = 4). In this condition, the high functional cardiovascular performances are also impaired (the submaximal effort capacity is attained at a smaller and smaller oxygen consumption; Propranolol 2 mg i.v. decreased the cardiac output by above 30% (vs 10%--normal); electrocardiogram presents aspects of "coronary disease", tachycardia, etc.). An ultrastructural damage occurs: from "mitochondrial disease", partial lysis of myofibrils, to myofibrosis (revealed postmortem), in spite of a reduced degree of coronary atherosclerosis. Ultrastructural and biochemical experimental data support this point of view. (b) The incidence, precocity and severity of the thyrotoxic heart increase with age and the existence of a previous cardiovascular pathology. Cardiothyreosis is not present under 27 years; in 4,353 patients its incidence is of 25% (arrhythmia--21%, heart failure--12%, coronary insufficiency--1-3%). Of a major interest are tachyarrhythmias which may lead to a high mortality by hypodiastolic congestive heart failure, heart failure with secondary hyperaldosteronism, thromboembolic episodes and ventricular fibrillation. Thyrotoxicosis favours the disease of papillary muscles--mitral prolapse and insufficiency, reversible especially in children. (c) The treatment of thyrotoxic heart is an etiologic one (medical, surgical, radioactive--the last two being preferable after the adequate medical therapy). In particular, cardiothyreosis requires a reinforced irradiation (10,000 rads instead of 7,000 rads) in smaller 131I doses. The protection against the increased nocivity of catechols in thyrotoxicosis is very important (which explains the high mortality in the thyrotoxic "storm") and requires propranolol; doses above 2 mg/kilo body/day are recommended. In the elderly, the sensitivity to propranolol decreases: verapamil i.v. is more efficient in paroxysmal tachyarrhythmias (flutter, atrial fibrillation) and in those occurring intra-operatively during halothane narcosis. The anticoagulant therapy is administered in tachyarrhythmias with high ventricular rate, especially in the elderly, to avoid the embolic risk, higher in defibrillation condition.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cardiothyreosis. 182 Oct 70

We reviewed the records of 26 infants with congenital junctional ectopic tachycardia (JET) from seven institutions to examine the evolution in the management of this tachycardia that is difficult to treat. JET was defined electrocardiographically as an incessant tachycardia with normal QRS morphology and atrioventricular (AV) dissociation. The ventricular rate ranged from 140 to 370 beats/min (mean, 230 beats/min); 16 of 26 patients had cardiac failure. Treatment success was defined as a stable decrease in the rate of JET, below 150 beats/min; partial success was a significant decrease of JET rate with alleviation of symptoms. All patients received digoxin with no significant effect. Propranolol was given to 16 patients, with two successes and one partial success. Combinations of other conventional agents were used in 11 patients with two successes; 14 patients were treated with amiodarone, which resulted in eight successes and three partial successes; three patients died suddenly on medical treatment (amiodarone, one patient; propranolol, one patient; or amiodarone plus propranolol, one patient); sudden AV block was a possible cause and consequently, two later patients had pacemaker implantation as well as medical treatment. His catheter ablation was successfully performed twice but contributed to death in a newborn; three surgical His ablations were performed for intractable JET with two successes and one death. The overall mortality was 35%. Among survivors, treatment has been stopped without any complications in five patients ranging in age from 10 months to 8 years (mean, 3.5 years). It seems that amiodarone alone is the best drug for treatment of congenital JET; necessity for permanent pacing remains unsettled. His ablation should be reserved only for intractable JET.
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PMID:Evolving concepts in the management of congenital junctional ectopic tachycardia. A multicenter study. 218 49


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