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

In an attempt to study the possible mechanism(s) by which captopril controls resistant heart failure, sequential haemodynamic studies (radioisotope technique) and humoral measurements (plasma renin activity, plasma aldosterone and plasma catecholamines) were obtained in 11 such patients. The studies were made at the time patients became unresponsive to other vasodilators (hydralazine or prazosin); the vasodilator drug was then discontinued and five days later, the 'no-vasodilator' studies were obtained. Captopril therapy was then started. Optimum daily maintenance dose of captopril varied from 75 to 200 mg in different patients. Studies were again repeated after a period of time equal to the duration of the previous vasodilator therapy. Digitalis and diuretic doses were kept constant throughout. Captopril improved effort tolerance in ten patients. Haemodynamically, mean blood pressure and peripheral resistance were lower than during vasodilator therapy (85 +/- 3.1 v. 92 +/- 3.3 mmHg and 47 +/- 4.4 v. 59 +/- 4.4 U.M2, respectively; p less than 0.05 for both). Cardiac index was higher during captopril treatment (1.95 +/- 0.15 v. 1.63 +/- 0.10 l/m2, p less than 0.01) and pulmonary mean transit was normalized by captopril (14.6 +/- 1.7 v. 18.4 +/- 1.3 s, p less than 0.05). Humoral indices revealed a significant (p less than 0.05) reduction in plasma aldosterone during captopril therapy (25.9 +/- 5.6 ng/dl during captopril, v. 62 +/- 22 ng/dl with no vasodilators and 50.9 +/- 6.1 ng/dl with other vasodilators). Moreover, there was a decrease in circulating plasma catecholamines during captopril treatment, but differences between the three treatment periods were not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Captopril in congestive heart failure resistant to other vasodilators. 636 32

The narrow therapeutic range of digitalis glycosides and the danger of intoxication has prompted a search for alternative medication in recent years. Substances reducing the pre- and afterload of the heart are suitable therapeutic agents and vasodilators are, therefore, used as adjuvant or alternative therapy. Of all positive inotropic substances only the catecholamines play an established part in the treatment of acute myocardial failure. Pilot studies testing orally administrable positive inotropic substances are being conducted, but for the moment no such drugs are available for routine use. Digitalis still remains the drug of choice for all forms of primary impairment of contractility and/or supraventricular tachyarrhythmias. The appropriate dosage has to be adapted to the estimated lean body mass and, if necessary, reduced in a thin person, Digitoxin is preferentially used in cases with suspected renal insufficiency (especially in elderly patients).
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PMID:[Alternatives to glycoside therapy?]. 664 45

Digitalis causes vasoconstriction of peripheral vasculature and has been shown to markedly decrease splanchnic blood flow in experimental animals in doses that are comparable to therapeutic doses in man. The effect of digitalis on splanchnic blood flow in heart failure in experimental animals and in man has been controversial. We found that i.v. ouabin reduced ESBF by 30% to 40% (p less than 0.001) in normal volunteer human subjects, that i.v. digoxin reduced ESBF by 15% to 25% (p less than 0.01) in normal subjects, and that oral digoxin had no discernible effect on ESBF in normal subjects. The difference between the effects of i.v. and oral administration appeared to be due to differences in peak blood levels, which were almost 10 times higher after i.v. administration. Glucagon prevented the effect of i.v. digoxin on ESBF in normal subjects. For patients in heart failure, the effect of i.v. digoxin on ESBF was variable: some patients had decreased ESBF but two had increased ESBF that seemed to be associated with a greater increase in cardiac output.
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PMID:Effect of digitalis on estimated splanchnic blood flow. 705 51

Digitalis constricts the peripheral vasculature. When digitalis is administered to patients whose mesenteric blood flow is reduced secondary to heart failure, the vasoconstrictor action coupled to reduced mesenteric flow may result in mesenteric ischemia or hemorrhagic bowel necrosis. The clinical syndrome of mesenteric ischemia secondary to heart failure and excess digitalis developed in a patient. Splanchnic vasoconstriction was proved angiographically. Both the vasospasm and clinical evidence of mesenteric ischemia were promptly reversed by sodium nitroprusside.
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PMID:Reversal of digitalis-induced mesenteric vasospasm by sodium nitroprusside. 705 69

During the last years as a result of improved diagnostic methods and new developed drugs with different mechanism of action the therapy of congestive heart failure has become more differentiated. Digitalis and diuretics constitute conventional therapy, but systemic vasodilators offer an innovative approach in acute and chronic heart failure. The vasodilators produce disparate modifications of cardiac function depending upon their differing alterations of preload and afterload. Nitrates principally cause vasodilation, nitroprusside, phentolamine and prazosin produce balanced arterial and venous dilation, whereas hydralazine predominantly causes arteriolar dilation. New positive inotropic agents like dopamine and dobutamine are still restricted to parenteral use.
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PMID:[Differential therapy of heart insufficiency]. 715 35

Digitalis therapy in cardiac failure is used by physicians according to conventional dosages; we call this type of digitalization "empiric". With this method digitalis intoxication in hospitalized patients is likely to occur in 8 to 20% of the cases. Another method of digitalization which we call "rational" is based upon an initial dosage of 0.015 mg per Kilo of digoxin, followed by a maintenance dosage determined by the relationship between initial dosage and daily rate of elimination. The latter depends upon the individual value of endogenous creatinine clearance (determined by age, weight and sex). Blood level of digoxin during steady state was measured in 454 patients divided randomly in four groups, each of whom following a different protocol of digitalization: 31 patients were treated with the rapid "empiric" digitalization (group I), 249 patients with the slow "empiric" digitalization (group II), 81 patients with the "rational" digitalization (group III), and 93 patients after a initial "empiric" dosage were treated with a maintenance dosage calculated by the "rational" method. An excessive initial dosage (blood level of digoxin > 2 ng/ml) was observed in 47.9% of patients of group I, in 15.9% of patients in group II, in 9.8% of patients of group III and in 14.7% of patients of group IV. manifestations of digitalis intoxication occurred in 30% patients of group I, in 10% of patients of group II, in 4.9% of patients of group III, and in 2.1% of group IV. Blood value of digoxin below therapeutic levels (under 0.5 ng/ml) was observed in only 13.1% of patients of group II, in 8.6% of patients of group III, and in 8% of patients of group IV. The lower percentage of digitalis intoxication observed in patients treated with "rational" method of digitalization is highly significant if compared with that observed in patients treated with empiric digitalization. The use of the "Lanoxin-rulex" makes the rational digitalization easier to handle, and gives the physicians the habit of considering the more important determinants of digoxin blood level. Conditions more likely to determine a wrong digitalis dosage are discussed in detail.
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PMID:[Digitalis therapy used according to the "rational" method. Techniques of application and clinical advantages (author's transl)]. 746 30

The aims of treatment of chronic heart failure are to improve the symptoms and the quality of life, reduce mortality and prevent left ventricular dysfunction. Before the first symptom occurs, neurohormonal activation takes place (increased catecholamines and atrial natriuretic peptide levels). Diuretics improve symptoms and are irreplaceable for the elimination of salt and water overload. Loop diuretics are used more often than the thiazides. Their deleterious effects on electrolyte balance are well known. The fact that they activate the renin angiotensin system is a more recent acquisition; the increase in plasma renin activity is a poor prognostic factor. Diuretics potentialize the vasodilator effect of angiotensin converting enzyme inhibitors which inhibit the neurohumoral activation induced by the diuretics. This therapeutic association is very logical, effective and allows reduction in the dosage of the diuretic. To date, there are no large scale controlled studies of the effects of diuretics on mortality. Spironolactone corrects hypokalaemia and hypomagnesaemia induced by loop diuretics. Moreover, it has been shown experimentally in renovascular hypertension and in hyperaldosteronism, that this molecule can prevent myocardial fibrosis, a factor which leads to ventricular dysfunction. The RALES study will analyse the effect of associating spironolactone to diuretic and ACE inhibitor therapy on the mortality of patients in NYHA classes III-IV. The value of digitalis in heart failure patients with sinus rhythm is a classical controversy. Digitalis has a positive inotropic effect (inhibition of NaK-dependent ATPase). More recently, a favourable neurohormonal effect has been reported; digitalis decreases the activation of the sympathetic and renin-angiotensin systems.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Classic treatment of chronic heart insufficiency. What if new?]. 748 8

Heart failure is accompanied by sympathetic over-activity, which contributes to the pathophysiology and to poor prognosis. This paper reviews the mechanisms and potential therapy for sympathetic dysregulation in heart failure (HF). Several points are emphasized: (1) There is increased sympathetic activity to skeletal muscle, kidney, and heart, but not to skin, in HF. This information challenges the concept of generalized sympathetic activation in HF and suggests that the factors responsible for sympathetic activation result in a partitioning of excess sympathetic outflow to some but not all tissues and organs. (2) The sympathetic dysregulation appears to result from impairment in cardiac and arterial baroreceptor restraint on sympathetic activity, but this abnormality in baroreceptor function may result from abnormal humoral and/or ionic influences acting on baroreceptor endings or in the central nervous system and not from intrinsic structural abnormalities in baroreceptors. This distinction has potential therapeutic importance because abnormalities in humoral or ionic mechanisms would more likely lend themselves to therapeutic modulation. (3) Digitalis sensitizes cardiac and arterial baroreceptors and inhibits sympathetic nerve activity in patients with HF. This sympathoinhibitory influence of digitalis is maintained during chronic therapy. These observations support the concept that the therapeutic effects of digitalis include autonomic modulation in addition to positive inotropism. In a broader concept, these observations suggest that sympathetic modulation may represent an important target for drugs for treatment of heart failure.
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PMID:Sympathetic dysregulation in heart failure: mechanisms and therapy. 774 96

Digitalis, diuretics and vasodilators are considered the standard therapy for patients with congestive heart failure, for which treatment is tailored according to the severity of the syndrome and the patient profile. Apart from the clinical seriousness, heart failure is always characterized by an energy depletion status, as indicated by low intramyocardial ATP and coenzyme Q10 levels. We investigated safety and clinical efficacy of Coenzyme Q10 (CoQ10) adjunctive treatment in congestive heart failure which had been diagnosed at least 6 months previously and treated with standard therapy. A total of 2664 patients in NYHA classes II and III were enrolled in this open noncomparative 3-month postmarketing study in 173 Italian centers. The daily dosage of CoQ10 was 50-150 mg orally, with the majority of patients (78%) receiving 100 mg/day. Clinical and laboratory parameters were evaluated at the entry into the study and on day 90; the assessment of clinical signs and symptoms was made using from two-to seven-point scales. The results show a low incidence of side effects: 38 adverse effects were reported in 36 patients (1.5%) of which 22 events were considered as correlated to the test treatment. After three months of test treatment the proportions of patients with improvement in clinical signs and symptoms were as follows: cyanosis 78.1%, oedema 78.6%, pulmonary rales 77.8%, enlargement of liver area 49.3%, jugular reflux 71.81%, dyspnoea 52.7%, palpitations 75.4%, sweating 79.8%, subjective arrhytmia 63.4%, insomnia 662.8%, vertigo 73.1% and nocturia 53.6%. Moreover we observed a contemporary improvement of at least three symptoms in 54% of patients; this could be interpreted as an index of improved quality of life.
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PMID:Italian multicenter study on the safety and efficacy of coenzyme Q10 as adjunctive therapy in heart failure. CoQ10 Drug Surveillance Investigators. 775 41

The essential goal of medical treatment following myocardial infarction with left ventricular dysfunction must be the prevention of secondary cardiac failure. The existence of left ventricular dysfunction, in particular when it is not accompanied by clinical cardiac failure, is a virtually formal indication for beta-blocker treatment after an infarction. Beta-blockers with intrinsic sympathomimetic activity (ISA) are possibly better tolerated in this context. However, experience shows that cardiologists and general practitioners often remain reluctant to prescribe beta-blockers whenever left ventricular function is impaired. Converting enzyme inhibitors decrease the risk of onset of secondary cardiac failure, reduce sudden deaths by ventricular arrhythmias, reduce recurrences of myocardial infarction or unstable coronary insufficiency, and more generally reduce overall and cardiovascular mortality. This is a class effect. While there is no urgency to prescribe them during the acute phase, it is generally considered that it is extremely useful to give them fairly quickly, i.e. during the first 72 hours. At the end of the hospital phase, around two weeks, it is desirable, whenever possible, to prescribe a dose of the order of 75 mg/day of captopril or 2.5 mg/day of ramipril. The administration of aspirin can be considered virtually routine. Oral anticoagulants are desirable in the presence of a large akinetic pocket, a frequent starting point of thrombosis and/or systemic emboli, or in the presence of atrial fibrillation. Digitalis/diuretic treatment does not appear to be indicated at this stage. Other types of anti-ischemic treatment are not theoretically indicated as a matter of principle at this stage in the absence of residual ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[What is the appropriate treatment for myocardial infarction with left ventricular dysfunction?]. 786 55


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