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

The usefulness of vasodilating agents in congestive heart failure depends on their ability to diminish left ventricular afterload; this effect does not necessarily persist with long-term treatment. The present study reports the clinical response of 16 patients in heart failure; the trial was double blind with enalapril and/or placebo during 24 weeks. Diagnoses were dilated cardiomyopathy in six, rheumatic heart disease in five, ischemic heart disease in four und hypertensive heart disease in one. Two patients on enalapril died of non cardiac causes and one was withdrawn from the study due to pregnancy. In those patients treated with enalapril the NYHA functional class improved from 2.9/0.8 to 1.1/0.4 (p less than 0.001), and the effort capacity increased from 545/171 to 888/160 seconds (p less than 0.01). Left ventricular systolic function evaluated by echocardiogram and Tc 99 m ventriculogram, radiologic size of the heart and echocardiographic left ventricular diameters showed no significant changes. There were no adverse clinical effects nor laboratory abnormalities. It is concluded that in this study, enalapril produced sustained clinical improvement in patients with heart failure and it was well tolerated during long-term treatment.
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PMID:[Usefulness of enalapril in congestive heart failure]. 282 38

An abnormal electrocardiographic P wave (AEPW) has been interpreted as indicative of heart failure, hypertrophy or dilatation of left atrium, or diminished left ventricular compliance. In order to determine the significance of this electrocardiographic sign we studied 47 cases of systemic arterial hypertension (SAH) without heart failure or coronary obstruction. Patients were assigned at 2 groups: group A (22 cases with P wave duration greater than 0.11 seg. (LEAD D2); and group B 25 cases with P wave duration less than this. The following data were studied in all cases: left ventricular ejection fraction (LVEF), left ventricular presystolic filling fraction (LVPFF), Sokoloff electrocardiographic index (SEI), final diastolic pressure of LV (FDPLV), and systolic arterial pressure (SAP). Results were: (Table: see text). There were not statistical differences in these values between groups A and B (including the FDPLV value not shown in the table). Correlation coefficient between duration of P wave and the other parameters studied were also no significant. AEPW in SAH is not related to an specifically degree of left ventricular hypertrophy or disfunction; therefore, hypertensive heart disease should not be classified taking in account this electrocardiographic sign.
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PMID:[The P-wave in systemic arterial hypertension]. 294 53

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

This paper discusses the possible pathogenesis of the cerebral atrophy (CA) observed in a large percentage of uraemic patients, taking the form of prevalently cortical damage (cortical atrophy) and/or subcortical enlargement of ventricular cavities (subcortical atrophy). This central nervous system pathology seems to share very little either with the better known 'dialysis encephalopathy' or with the 'acute encephalopathy syndrome', even though sporadic cases of both these forms have shown concomitant CA. Histopathologically it offers the picture of loss of neurons and nerve fibres and can thus be compared with uraemic peripheral nervous system damage. CA is unquestionably important because of its implications in terms of impairment of superior cortical functions, just as in CA of non-uraemic aetiology. A first aetiopathogenic hypothesis might include endogenous uraemic intoxication to the nerve tissue, believed responsible for peripheral uraemic neuropathy, but other possibilities merit consideration: vascular calcification secondary to hyperparathyroidism, blood lipid disorders, and systemic hypertension--factors that contribute to impairing the brain vasculature, with cascade effects on brain tissue oxygenation, neuronal metabolism, and energy exchanges. Tissue oxygenation is already jeopardized in the uraemic patient by the concomitant chronic anaemia and by cardiac insufficiency in cases with hypertensive heart disease. In dialysis patients with volume-dependent hypertension the brain may be further damaged by abrupt pressure changes produced by dialytic ultrafiltration; these constitute a severe challenge to cerebral blood flow autoregulation. Cyclic variations of brain tissue hydration connected with regular dialysis treatment may have adverse effects on neurotransmitter functions, particularly those mediated by neuropeptidergic systems. Chronic intoxication may result from oral Al(OH)3 of phosphorus-chelating agents: in animal studies and clinical observations in non-uraemic populations the neurotoxic potential of Al is indicated by a significant correlation between histological neuronal damage, impaired function, and Al concentration in brain tissues. In addition, a concausal role of malnutrition in central nervous system damage in the uraemic patient cannot be overlooked, since malnutrition is known to give rise to functional and structural alterations in non-uraemic human pathology. In the light of these clinical observations and experimental findings, it would appear that the prevention of CA in uraemia is today feasible.
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PMID:Pathogenesis of cerebral atrophy in uraemia. State of the art. 328 91

To evaluate the therapeutic efficacy of L-carnitine in elderly subjects suffering from heart failure, secondary to ischemic and/or hypertensive heart disease, 38 patients (22 men, 16 women) were studied, aged from 65 to 82 years. In addition to traditional therapy (digitalis, diuretics, antiarrhythmic agents) given in all cases, 21 patients received oral L-carnitine on the basis of a randomized protocol in 1-g doses twice daily for 45 days (the other 17 received placebo). In the group treated with L-carnitine, a distinct improvement was observed in both subjective and objective conditions; reduced heart rate, edema and dyspnea, increased diuresis and a marked reduction in daily digitalis consumption. L-carnitine treatment also induced a significant reduction in serum cholesterol and triglyceride levels. No adverse reactions attributable to L-carnitine administration were observed in any of the patients.
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PMID:Evaluation of the therapeutic efficacy of L-carnitine in congestive heart failure. 340 1

To elucidate recent trends in the mortality and morbidity of myocardial infarction (MI), we investigated death certificates and changes in the survival rate of MI patients at coronary care units (CCUs), which may affect the death rates. For all cases of MI, acute heart failure (AHF), heart failure (HF) as underlying cause, and hypertension as underlying cause with HF or AHF (categorized as hypertensive heart disease) on death certificates in two rural and two urban populations between 1981 and 1984, medical records were reviewed and case histories obtained from interviews with patients' families to validate the diagnosis. The number of MI deaths on the death certificates was not underestimated because some MI deaths were misdiagnosed as AHF, HF and hypertensive heart disease and some MI death certificates were misdiagnosed. Survival of MI patients at CCUs improved in several major cities, Tokyo, Osaka, Wakayama and Asahikawa between 1978 and 1984; a total of 4318 MI deaths were estimated to be averted by CCUs in 1984 compared with the number of deaths in 1978. Therefore, improvement of MI cases at CCUs may be one of the factors attenuating the rise in death rates in all of Japan.
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PMID:Recent morbidity trends in myocardial infarction in Japan: investigation of death certificates and the survival rates at coronary care units. 359 73

The most often causes of cardiac arrhythmias in aged patients are heart failure as a consequence of coronary or of hypertensive heart disease, hypersensitive carotis-sinus, digitalisintoxication and hypokalemia. Out of that, the different tachyarrhythmias and bradyarrhythmias and often also a tachycardia-bradycardia-syndrome may develop. Appropriately it results the most often kinds of antiarrhythmic therapy as the treatment of heart failure with digitalis, diuretics and nitrates, the handling of electrostimulation with pacemakers, the removal of digitalis and the supply of potassium. Beyond of that, there are many antiarrhythmic drugs, selected for therapy of "first choice". These are betablockers in sinustachycardia, ajmaline in supraventricular ectopic beats, verapamile in supraventricular tachycardia, lidoflazine with propafenone in atrial fibrillation, propafenone in ventricular ectopic beats, lidocaine in ventricular tachycardia, electrodefibrillation in ventricular fibrillation, orciprenaline, atropine and electrostimulation in bradyarrhythmias. The relation of advantage and risk of an antiarrhythmic therapy has to be considered carefully, especially in higher decades. Mostly it is already sufficient, to avoid arrhythmias by a critical and controlled prescription of digitalis, diuretics and laxatives.
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PMID:[Treatment of cardiac arrhythmias in aged patients (author's transl)]. 615 69

The spontaneously hypertensive rat (SHR) exhibits both a compensated phase of cardiac hypertrophy in which forward output is maintained despite persistently elevated systemic arterial pressures and a decompensated phase in which cardiac performance has deteriorated in spite of further hypertrophic growth. To determine whether chronic antihypertensive therapy prevents the development of heart failure and the progression of cardiac hypertrophy in SHR with advanced hypertension, captopril (2 g/l of drinking water), a converting enzyme inhibitor, was administered to 14 month old female SHR and normotensive American Wistar rats (NWR) for 10 months. The severe left ventricular hypertrophy of the 24 month old untreated SHR (4.37 +/- 0.2 mg/g v. 2.50 +/- 0.06 mg/g, untreated NWR) was markedly reduced (P less than 0.02) by captopril (3.01 +/- 0.1 mg/g). Chronic therapy prevented the reduction of both baseline and maximal cardiac indices in SHR, but did not alter blood flow in NWR. Left ventricular dilatation was present in 24 month old SHR and, as peak stroke volume index was diminished, the ejection fraction index of the SHR was reduced. Captopril restored this index in SHR to normal. The relation of ejection fraction index and afterload (peak systolic wall stress) was depressed in untreated SHR, but was normal in treated SHR. Thus, chronic therapy with captopril prevented the development of severe cardiac dysfunction and produced a marked regression of cardiac hypertrophy in SHR with advanced hypertensive heart disease.
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PMID:Prevention of the development of heart failure and the regression of cardiac hypertrophy by captopril in the spontaneously hypertensive rat. 622 Aug 93

The hemodynamic and contractile effects of acute cigarette smoking were analyzed in 35 patients with normal cardiac and coronary function as well as with cardiac failure and with coronary artery disease. In normal patients (normal ventricular function, normal coronary arteriogram) cigarette smoking exhibited no contractile depressant effects. Moderate increase in global and in regional wall motion and contractility was found. Likewise, in patients with compensated hypertensive hypertrophy (normal ventriculogram, significant left ventricular hypertrophy, normal coronary arteriogram) cigarette smoking increased global and regional contraction function. In cardiac disease patients (dilatative cardiomyopathy, advanced coronary artery disease, decompensated hypertensive heart disease) cigarette smoking was associated with depression in the overall and regional contraction behavior of the left ventricular myocardium. In patients with coronary artery disease, cigarette smoking was accompanied by marked depression of the regional contraction pattern in hypokinetic, akinetic, and dyskinetic zones. Moreover, contractile depression also occurred in the non-ischemic zones, without pre-existing coronary artery stenoses. In conclusion, acute cigarette smoking may not cause contractile depressant effects in normal patients and patients with compensated hypertensive hypertrophy. However, in coronary patients, significant negative inotropic effects are present not only in the ischemic zones, but also in the non-ischemic myocardium.
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PMID:Global and regional wall motion and contractility of the left ventricle following cigarette smoking. 623 23


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