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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Besides the characteristic disturbances of the motor nervous system symptoms indicating an overactivity of the sympathetic nervous system can complicate the course of severe cases of tetanus. These symptoms include fluctuating tachycardia and hypertension, electrocardiographic changes, sweating, constipation with development of paralytic ileus and metabolic disorders. These symptoms are comparable to these developing in patients with phaeochromocytoma. Elevated catecholamine levels in plasma and urine have been found in several patients with tetanus who developed these symptoms. The prolonged over-activity of the sympathetic nervous system is thought to contribute to the still considerably high mortality rate. Myocardial lesions observed at necropsy are comparable to those found in patients dying of phaeochromocytoma. These lesions are suggested to be associated with sudden death from arrhythmias or cardiac failure in patients with tetanus. For the protection of the organism against the overactivity of the sympathetic nervous system a treatment using the combination of beta-adrenergic receptor blocking agents and adrenergic neuron blocking agents has been introduced. A reduction of the mortality rate was achievable by this treatment. Experimental evidence is accumulating that the tetanus toxin affects not only the motor, but also the sympathetic and sensory neurons.
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PMID:The involvement of the sympathetic nervous system in tetanus. 3 68

Trimipramine and clozapine show some similarities in their receptor binding profiles. Since both have the same affinity for the D2 receptor and since the affinity for this receptor correlates closely with the antipsychotic potency of a drug, an antipsychotic efficacy of trimipramine in acute schizophrenia could be expected. Therefore 28 schizophrenic patients in an acute phase were treated with trimipramine up to 400 mg/d in an open clinical trial. For the whole group of patients the BPRS total score changed from 58 +/- 5 before treatment to 46 +/- 18 at the last rating (p less than 0.05). According to our clinical judgement the patients were divided into three subgroups. Thirteen patients showed a good remission under trimipramine so that they could be discharged on a trimipramine maintenance treatment. They improved on the BPRS from 58 +/- 6 before treatment to 32 +/- 8 at endpoint. Six patients deteriorated during the first week of treatment and had to be withdrawn from the study. Nine patients showed insufficient improvement or became worse after an initial improvement. The observed side-effects (dry mouth, sedation, sweating, increased appetite, constipation, tremor, vertigo) are well known under trimipramine and were therefore expected. Beyond these, one patient developed a cardiac insufficiency. No clinical relevant extrapyramidal side-effects occurred. Since the improvement of florid psychotic symptoms seems to be markedly higher under trimipramine than the one reported under placebo, our results indicate that trimipramine may have an antipsychotic potency.
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PMID:Trimipramine--an atypical neuroleptic? 180 21

Analysis of 14 cases of stercoral ulcer showed that they tended to occur in patients over 70 years of age and associated diseases included heart failure under hemodialysis, cerebral hemorrhage, and postoperative states requiring bet rest for long duration. Constipation is always preceded the occurrence of the disease, and the initial symptoms was generally massive hematochezia of sudden onset. Massive blood transfusion was often required, however, heater probe hemostasis was effective. The most common site of involvement was the rectum, and the shape of ulcer was irregular or round. Measurement of the mucosal blood flow in the rectum revealed that blood perfusion was markedly reduced immediately after the occurrence, and that it recovered with healing of ulcer. Ischemia was considered to participate in the pathogenesis of the disease.
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PMID:[Clinical investigation of stercoral ulcer]. 207 57

The major antihypertensive mechanism of calcium antagonists is by decreasing the systemic vascular resistance, modified by the counter-regulatory responses of the baroreflexes and the renin-angiotensin-aldosterone system. In severe hypertension, the concept that calcium overload of the vascular myocyte could precipitate or aggravate peripheral vasoconstriction provides a logical basis for the use of these agents as first choice therapy; nifedipine, especially, has been well tested. As monotherapy for mild to moderate hypertension each of the three first-generation agents compares well with beta-blockers. Calcium antagonists may have a special role in the therapy of certain patient groups (elderly, black) or in those subjects whose life style involves intense physical or mental exertion (hemodynamics better maintained than with beta-blockade) or in patients with early end-organ damage such as left ventricular hypertrophy or renal insufficiency. However, the goal blood pressure may not be reached during monotherapy so that drug combinations may be required. Further indications for these compounds are as follows. Verapamil and diltiazem are frequently used in supraventricular tachycardias including acute and chronic atrial fibrillation. In the arrhythmias of the Wolff-Parkinson-White syndrome, there is the potential danger of provocation of anterograde conduction. Further indications for calcium antagonists, still under evaluation, include congestive heart failure (controversial), hypertrophic cardiomyopathy (verapamil), primary pulmonary hypertension (high doses required), Raynaud's phenomenon (nifedipine and diltiazem effective), peripheral vascular disease (proof not yet documented), cerebral insufficiency and subarachnoid hemorrhage (nimodipine promising), migraine, exertional bronchospasm, renal disease, atherosclerosis (experimental), and primary aldosteronism (nifedipine inhibits aldosterone release). Second-generation agents include dihydropyridines, such as nitrendipine, nicardipine, felodipine, amlodipine, nisoldipine, nimodipine, and isradipine. From these will be selected agents that are longer acting and provide higher vascular selectivity. New preparations of existing agents include slow-release formulations of nifedipine, verapamil, and diltiazem. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine. Yet caution is required when calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Calcium channel antagonists. Part III: Use and comparative efficacy in hypertension and supraventricular arrhythmias. Minor indications. 315 29

With the correct selection of drug and patient, the calcium antagonists as a group can be remarkably effective at relatively low cost of serious side effects. Almost all side effects are dose related. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil (or diltiazem) is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine which actually has the most marked negative inotropic effect. Yet caution is required when even calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide. The most marked interaction with digoxin is that with verapamil, which may raise digoxin levels by over 50%. Combination therapy of calcium antagonists with beta-blockers is increasingly common, and is probably safest in the case of dihydropyridines. Other combinations being explored are those with angiotensin-converting enzyme inhibitors and diuretics.
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PMID:Calcium channel antagonists. Part IV: Side effects and contraindications drug interactions and combinations. 315 4

Calcium channel blocking drugs are a chemically heterogenous group, so it might be expected that their effects on vascular smooth muscle, cardiac contractility, and conduction tissue may differ. However, the majority of adverse reactions are predictable from their pharmacological actions and may be conveniently grouped in the following categories: 1) vasodilatation, 2) negative inotropic effects, 3) conduction disturbances, 4) gastrointestinal effects, 5) metabolic effects, and 6) drug interactions. Vasodilatory symptoms, namely, dizziness, headaches, flushing sensation, and palpitation, are more likely with nifedipine. Peripheral edema is also common with nifedipine, but the mechanism is uncertain. For a given degree of vasodilation, the greatest negative inotropic effect is seen with verapamil first, diltiazem second, and nifedipine last. Calcium channel blocking drugs are contraindicated in hypertensive patients with second and third degree heart block, sick sinus syndrome, and severe heart failure. Verapamil and diltiazem have a significant effect on cardiac conduction, whereas nifedipine, in therapeutic doses, does not. Local gastrointestinal symptoms, such as nausea and constipation, are common with verapamil. None of the calcium channel blocking drugs have been reported to adversely affect lipid or protein metabolism. However, nifedipine, verapamil, and diltiazem in high doses may inhibit liberation of insulin. The significance of this finding needs to be explored further in hypertensive diabetics. Serum digoxin levels have been shown to increase after administration of verapamil and nifedipine, but there is no evidence that this change has any clinical relevance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Side effects of calcium channel blockers. 328 Apr 92

The long-term antianginal effect of orally administered verapamil over 1 year of continuous treatment was assessed in 11 patients with effort-induced angina. In the short-term phase of the study, patients were given, in random order, placebo and verapamil (360 mg/day). The tolerated work load during a bicycle exercise test was 531.8 +/- 123.0 kg/min on placebo and 763.6 +/- 124.7 kg/min on verapamil (p less than 0.001). Subsequently all patients entered a long-term study of 1-year continuous treatment with 120 mg t.i.d. verapamil. The tolerated work load at 8-week (736.4 +/- 105.1 kg/min) and 1-year (804.6 +/- 101.1 kg/min) tests did not significantly differ from the results in the short-term study. The average verapamil plasma level was 138.5 +/- 90.6 ng/ml before and 357.8 +/- 199.2 ng/ml 90 min after drug administration; the average norverapamil plasma levels were, respectively, 248.0 +/- 84.4 and 368.0 +/- 135.9 ng/ml. There was no correlation between verapamil or norverapamil plasma concentrations and the antianginal effect. No patient developed signs of heart failure during the treatment. Two patients had mild constipation. The average P-R interval was slightly, although significantly (p less than 0.01) prolonged, but no patient developed first-degree atrioventricular block. We conclude that verapamil proves an effective and safe drug in the treatment of effort-induced angina; the beneficial effects of the short-term treatment are sustained during 1 year of continuous treatment.
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PMID:Long-term persistence of antianginal effect of oral verapamil in chronic stable angina. 620 67

Verapamil hydrochloride, a prototype calcium antagonist, is now marketed in the United States for the acute treatment of supraventricular tachyarrhythmias and for chronic management of vasospastic and chronic stable angina. It inhibits the slow inward channel in in the heart and blocks calcium influx in smooth muscle. Its intrinsic negative inotropic action, which is apparent in isolated tissues, is offset in vivo by peripheral vasodilation. It has a mild, noncompetitive sympathetic antagonist effect; its most important electrophysiologic action is a depression of AV nodal conduction, accounting for its effect in supraventricular tachyarrhythmias. Its hemodynamic actions are characterized by a complex interplay of changes in preload, afterload, contractility, heart rate, and coronary blood flow. It does not depress cardiac function, except in severe heart failure. The drug has a mild dilator action on coronary arteries and reverses ergonovine-induced vasoconstriction. Controlled trials have established its role in Prinzmetal's variant angina, unstable angina, and chronic stable angina. It has also been found to be effective in obstructive cardiomyopathies. The potential role of verapamil in such conditions as hypertension, cardioprotection, and Raynaud's phenomenon needs further evaluation; at present these indications have not been approved by the Food and Drug Administration. The most common side effects include constipation, skin rash, and dizziness; AV block, heart failure, and sinus arrest may occasionally be encountered, especially when ventricular function is compromised or conduction system disease is present.
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PMID:Verapamil hydrochloride: pharmacological properties and role in cardiovascular therapeutics. 676 30

The long-term efficacy of verapamil in a dose of 360 mg daily in patients with chronic stable angina pectoris was assessed by quantitated serial treadmill exercise tests. Twenty-eight patients were investigated with a placebo-controlled, double-blind, crossover protocol of 2 weeks each and afterward all patients were put on long-term therapy. Exercise tests were performed at the end of the placebo period and after 2, 4, 8, 16, 24 and 52 weeks of verapamil therapy. All 28 experienced angina during treadmill tests on placebo and the mean (+/- standard error of the mean) exercise time was 6.6 +/- 0.5 minutes. This increased to 9.2 +/- 0.8 minutes at 2 weeks and 50 11.2 +/- 0.8 minutes at 4 weeks. Fifteen and 20 of the 28 patients became angina-free during treadmill exercise at 2 and 4 weeks, respectively. The consumption of nitroglycerin showed a similar improvement. The improvement was maintained at 1 year of follow-up. The on-line computer-analyzed S-T segment changes showed a statistically significant improvement at all follow-up periods. Withdrawal of verapamil produced a return to pretreatment levels. The adverse effects noted were constipation in seven patients and reversible P-R interval prolongation in two. No heart failure occurred in any patient. These findings suggest that verapamil possesses a powerful and sustained antianginal action and, in a dose of 360 mg daily, merits a place as a primary therapeutic agent in the management of chronic stable angina.
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PMID:Long-term antianginal action of verapamil assessed with quantitated serial treadmill stress testing. 679 87

1. The efficacy of verapamil in a dose of 360 mg daily in patients with chronic stable angina pectoris was assessed by quantitative serial treadmill exercise tests and trinitrin consumption. Twenty-eight patients were investigated in a placebo-controlled, double-blind cross-over comparison of 2 weeks each, after which all were put on long-term verapamil treatment. Exercise tests were done at the end of the placebo period and after 2 and 4 weeks on verapamil. 2. On placebo, all twenty-eight patients developed angina during treadmill tests and the mean exercise time was 6.6 min (s.e.m. = 0.5 min). On verapamil, this increased to 9.2 min (s.e.m. = 0.8 min) at 2 weeks and to 11.2 (s.e.m. = 0.8 min) at 4 weeks, respectively. Trinitrin consumption showed a similar improvement. The double product and ST segment changes, analysed by on-line computer, showed a statistically significant improvement. The only side effects were constipation (in seven patients) and reversible PR-interval prolongation (in two patients). There was no clinical evidence of heart failure in any of the patients. 3. These findings suggest that verapamil has a powerful antianginal action and, in a dose of 360 mg daily, may have a place as a primary agent in the management of chronic stable angina.
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PMID:An objective comparison of verapamil and placebo in chronic stable angina. 681 Nov 77


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