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)

A random single-blind study of oxprenolol against perhexiline has been undertaken in angina pectoris. Both drugs were effective in treatment (P less than 0.01) but perhexiline was better than oxprenolol (P less than 0.05), 12 of the 14 patients preferring perhexiline. Offset against this was the greater incidence of side effects with perhexiline, including one patient who later developed peripheral neuropathy. Despite the greater efficacy of perhexiline, it is suggested that side effects should preclude its routine prescription as a drug of first choice in angina pectoris. It should remain of value in the special situations of resistant angina and angina with heart failure or bronchospasm, when its use should be carefully monitored for these side effects.
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PMID:Comparative trial of perhexiline maleate and oxprenolol in patients with angina pectoris. 36 44

Following a case of mannitol-induced respiratory and circulatory collapse, the effects of hyperosmolar injections on pulmonary arterial pressure, systemic blood pressure, and cardiac output were studied in dogs. The injection of 20 ml of 10% NaCl into the pulmonary artery increased pulmonary arterial pressure and decreased systemic blood pressure by approximately 50% of control values. Injections of solutions of equal hyperosmolar strength, 50 ml of 25% mannitol or 50 ml of 4% NaCl into the pulmonary artery produced no significant elevation of pulmonary arterial pressure, but were associated with comparable decreases in systemic blood pressure. When allowed to vary, cardiac output increased with injections of all three hyperosmolar solutions, yet was still accompanied by falls in systemic blood pressure as large as when cardiac output was held constant. Vagotomy did not prevent these changes in systemic and pulmonary arterial pressure, nor the increase in cardiac output. After five to 10 injections, the decreases in system blood pressure with any of the solutions and the increases in pulmonary arterial pressure with 10% NaCl disappeared and further injections were without effect. It is concluded that adminstration of mannitol probably does not cause pulmonary edema due to fluid overload, nor does it cause heart failure as evidenced by increases in pulmonary arterial pressure. However, rapid injection may cause a fall in blood pressure and may on occasion be accompanied by bronchospasm, especially in sensitive subjects.
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PMID:Hypotension and respiratory distress caused by rapid infusion of mannitol or hypertonic saline. 57 Dec 22

In a multicentre, double-blind, between-patient study the hypotensive effect of oxprenolol was investigated in 329 patients with mild to moderate hypertension. A factorial experimental design with three factors was chosen: oxprenolol--none or daily doses of 20, 40, 60 and 80 mg; dihydralazine and hydrochlorothiazide, respectively, none or 30 mg daily. Each treatment was given for 4 weeks after an adequate period of withdrawal from any other possible hypotensive therapy and one week of placebo wash-out. Irresponsive of the association with dihydralazine and/or hydrochlorothiazide, oxprenolol had a hypotensive effect linearly related to dose for standing systolic (P less than 0.05) and diastolic (P less than 0.01) pressure, and for lying diastolic (P less than 0.05) pressure. The additional of dihydralazine enhanced the time-course of the hypotensive effect of oxprenolol, particularly the 80 mg dose level. In general, the combination of oxprenolol with dihydralazine and hydrochlorothiazide caused larger reductions in blood pressure, particularly with oxprenolol 80 mg. In the latter group, the eventual falls in blood pressure were 30.5 and 14.4 mmHg for lying systolic and diastolic, respectively; and 32.1 and 20.0 mmHg for the standing systolic and diastolic pressures. The drug was well tolerated; major side effects (heart failure and bronchospasm) occurred in three patients.
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PMID:Hypotensive effect of oxprenolol in mild to moderate hypertension: a multicentre controlled study. 78 73

Bronchospasm due to cardiac disease results from increased pulmonary capillary pressure and impaired lymphatic drainage. Bronchospasm can usually be attributed to cardiac disease if physical and roentgenographic examination support the diagnosis of cardiac failure. The latter is especially helpful in revealing interstitial edema and redistribution of blood flow to the upper lobes. Therapy is directed at decreasing lung water, improving gas exchange and searching for the underlying mechanism of cardiac failure.
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PMID:Cardiac asthma--its origin, recognition and management. 82 80

Asthma bronchiale (a.b.) is defined as paroxysmal or permanent, partly or completely reversible dyspnoea due to a bronchospasm resulting from pathological hyperreactivity of the bronchial system. In the pathogenesis participate allergic, immuno-infiltrative and genetic factors, irritating substances (environment) and infectious. The allergic constituent acts via sensitization and allergization of the mast cell, to its degranulation with release of mediators (histamine, serotonin, leukotrienes, thromboxane, PAF) with subsequent bronchoconstriction and production of viscous mucus. As to adrenergic factors, a block of beta-adrenergic receptors and reduced adrenal function is involved. As to non-adrenergic factors an increased sensitivity of the parasympathetic--vagus is involved which conditions bronchoconstriction and hyperkrinia. From the clinical aspect extrinsic (atopic) and intrinsic (cryptogenic) asthma bronchiale can be differentiated. The former is encountered more frequently in childhood and adolescence, in subjects with a positive family-history, high IgE and positive skin tests and a known allergen. The latter type of a.b. is found in adolescence, in subjects with a negative family-history, with eosinophilia; it is conditioned by infection (e.g. chronic bronchitis), strain, cold and takes a dangerous course (aspirin). As to the course, attacks of a.b. are involved with a symptom-free interval (extrinsic a.) easily controlled by treatment. Then there is the chronic form with a variable course and the necessity of permanent treatment. Status asthmaticus is in recent years with increasing frequency the cause of death and thus calls for maximal treatment. It is the third most serious form of a.b. Assessment of arterial blood gases is very important as a check of treatment as well as from the prognostic aspect (cross-over intubation). From the differential diagnostic aspect we must consider the asthmoid component in chronic bronchitis, pulmonary embolism, left-sided cardiac failure, tracheal or bronchial compression by an aortal aneurysm, tumour. The differential diagnosis is not always easy.
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PMID:[Bronchial asthma. Pathogenesis and clinical aspects]. 145 62

Acute aortic dissection is a devastating condition requiring prompt intensive pharmacologic management geared toward control of blood pressure and reduction in myocardial contractility (change in velocity/change in time). The treatment of choice currently is sodium nitroprusside and intravenous propranolol hydrochloride. During acute aortic dissection, hemorrhage may spread into the interatrial septum, extending to the atrioventricular junctional tissues, thus causing conduction abnormalities. Adverse effects of long-acting beta-blockers, including bradycardia, heart failure, and bronchospasm, may limit their usefulness because these effects persist for a long time after discontinuation. This may be detrimental, especially in patients with compromised cardiac function, bronchospastic disease, or both. We report a case of a 64-year-old woman with compromised cardiac function and aortic dissection who was successfully treated with esmolol hydrochloride (an ultrashort-acting beta-blocker) and sodium nitroprusside.
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PMID:Intravenous esmolol in acute aortic dissection. 168 74

The safety and efficacy of oral sotalol, an investigational beta-adrenergic blocker with class III antiarrhythmic drug properties, were examined in a multicenter study in 236 patients with sustained ventricular tachyarrhythmias. In 104 patients, the index arrhythmia was a cardiac arrest, and all patients had undergone at least 3 previous unsuccessful antiarrhythmic trials (mean = 5 per patient). In the 106 patients assessed by programmed electrical stimulation, sotalol completely suppressed induction of ventricular tachycardia (VT) in 33 (31%) and rendered VT slower (greater than 100 ms prolongation of cycle length) or more difficult to induce in 29 (27%). Using continuous 24-hour ambulatory monitoring methods, sotalol complete- and partial-response rates were 51 and 12%, respectively. Of the 236 acute-phase patients, 151 were discharged receiving long-term sotalol therapy. The median sotalol dose was 480 mg/day. At a mean follow-up of 346 +/- 92 days, 27 patients (18%) had recurrence of sustained arrhythmia; 9, sudden death; 11, sustained VT; 5, automatic defibrillator discharge; and 2, syncope. Adverse effects forced discontinuation of therapy in 10 patients (7%): 6 secondary to symptomatic bradyarrhythmia, 2 due to refractory heart failure, 1 due to torsades de pointes, and 1 from bronchospasm. Life-table analysis of sotalol's overall long-term efficacy at 6, 12 and 18 months were 80, 76 and 72%, respectively. Although mean follow-up was short (less than 1 year), neither acute-phase programmed stimulation nor 24-hour ambulatory monitoring responses were significantly predictive of subsequent arrhythmic outcome. Proarrhythmia was documented in 18 patients (7%), 17 during the acute phase and 1 during long-term follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Safety and efficacy of sotalol in patients with drug-refractory sustained ventricular tachyarrhythmias. 229 89

Six cases of systemic reactions to topical treatment with beta-blocking eyedrops are reported, bradycardia and faintness due to an overdosage of ophthalmic timolol; decompensated heart failure one month after the prescription of carteolol eyedrops: bronchospasm after two weeks of treatment with metipranolol eyedrops; crippling Raynaud's phenomenon of otherwise unknown origin, which had begun with timolol eyedrops, continued with carteolol eyedrops and regressed after discontinuation of ophthalmic beta-blockers; aggravation of an anaphylactoid shock in a patient treated with ophthalmic timolol, and myocardial infarction possibly due to the abrupt withdrawal of timolol eyedrops. It cannot be overstressed that the rules governing the prescription of oral beta-blockers also apply to ophthalmic preparations of these drugs: respect of contra-indications, strict adherence to the dosage recommended, gradual drug withdrawal and regular supervision. Only controlled studies and long-term follow-up will be able to demonstrate differences in safety between the five beta-blockers commercialized as eyedrops in this country.
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PMID:[Systemic complications of beta-blocking eyedrops. Apropos of 6 cases]. 256 93

Salbutamol (albuterol) is a beta 2-selective adrenoceptor agonist which accounts for its pronounced bronchodilatory, cardiac, uterine and metabolic effects. During the intervening years since salbutamol was first reviewed in the Journal (1971), it has become extensively used in the treatment of reversible obstructive airways disease. Numerous studies in this disease (including severe acute, childhood and exercise-induced asthma) have confirmed the bronchodilatory efficacy of salbutamol, and it has been shown to be at least as effective as most of the currently available bronchodilators, if not more effective. The onset of maximum effect of salbutamol is dependent on the formulation used and the route by which it is administered. In most patients inhaled salbutamol is a first-line therapy, since it offers rapid bronchodilation, usually relieving bronchospasm within minutes. Although oral salbutamol has often proved to be less efficacious than the inhaled formulation, it still affords clinically significant bronchodilation, and it is particularly useful in those patients unable to coordinate the use of inhalers. Parenteral formulations of salbutamol are generally reserved for the treatment of severe attacks of bronchospasm and they are one of the treatments of choice in these life-threatening situations. Studies of the concomitant use of salbutamol and other agents such as anticholinergics, methylxanthines and beclomethasone dipropionate have usually shown a complementary response in the majority of patients, as might be expected from the different mechanisms of action of these groups of drugs. Salbutamol is generally well tolerated and any side effects observed are a predictable extension of its pharmacology. Since the frequency of side effects is dose related, and therefore dependent on the route of administration, it is not surprising that they are much more common following intravenous and oral rather than inhalation therapy. Tremor, tachycardia and hypokalaemia are the most frequently reported adverse effects. After nearly 20 years of use, salbutamol is well established as a 'first-choice' treatment in reversible obstructive airways disease. Indeed, throughout this time many new bronchodilatory agents have been studied but none have proved more effective. Clinical evaluation of salbutamol in the treatment of premature labour, hyperkalaemia and cardiac failure awaits further studies, although to date some encouraging results have been reported.
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PMID:Salbutamol in the 1980s. A reappraisal of its clinical efficacy. 267 May 12

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


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