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

Nitrate derivatives are venous vasodilators which are effective in reducing the symptoms of pulmonary congestion. The beneficial action on exercise capacity was recently demonstrated in the Veterans II Study in association with Hydralazine and has also been suggested by other trials. The reduction in mortality from cardiac failure was demonstrated in the Veterans I Study in association with Hydralazine compared to conventional digitalo-diuretic therapy but seems less important than that obtained by angiotensin converting enzyme inhibitors. The phenomenon of tolerance seems to be related to the use of high doses in continuous therapy and may be countered by discontinuous use of the drug during the 24 hour period. Tolerance seems to be related to neuro-hormonal factors and perhaps to depletion of SH groups. Simultaneous use of nitrates and ACE inhibitors seems to be an interesting therapeutic concept.
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PMID:[Nitrate derivatives and cardiac insufficiency]. 153 Apr 25

Nitrates have been used for the last 130 years to treat and control the symptoms of angina pectoris. Within the last 15 years, nitrates also have been shown to limit infarct size and to be beneficial in the treatment of patients with severe intractable heart failure, cardiogenic shock, severe mitral and aortic regurgitation, hypertensive episodes, and portal hypertension. The adequate use of nitrates to treat these disorders requires the ability to document a hemodynamic response and to closely monitor the adverse consequences of this therapy. Nitrates work by directly relaxing smooth muscle in resistance and capacitance vessels, thereby causing generalized dilation. Nitrates reduce preload and, at higher doses, reduce systemic vascular resistance and afterload. This chapter reviews the physiologic mechanisms that underlie nitrate therapy, the appropriate indications for nitrate use, the usefulness of specific agents, and their appropriate nursing implications.
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PMID:Nitrates. 157 38

1. Seven randomized controlled trials of intravenous nitroglycerin in a total of about 850 patients have been reported. Overall, there were 51 deaths (12.5%) in the nitroglycerin group and 87 (20%) in the control group. This indicates a 48% reduction in the odds of death (P less than 0.001, 95% confidence limits (25% to 64%)). 2. There are five randomized trials of oral nitrates after acute myocardial infarction. In these trials, 11.8% of the patients in the nitrate group compared with 13.3% in the control group died. This indicates a nonsignificant 12% reduction in the odds of death but the 95% confidence interval overlaps widely with the i.v. trials. If all trials of i.v. or oral nitrates are considered the reduction in the odds of death is 32% (P less than 0.01). 3. Nitrates have a beneficial effect on haemodynamics in heart failure but the data on mortality effects are sparse. In combination with hydralazine, however, long-term mortality was reduced in the V-HEFT trial of chronic heart failure.
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PMID:Effects of nitrates on mortality in acute myocardial infarction and in heart failure. 163 75

Nitrates are drugs of first choice in patients with acute heart failure. Acute pulmonary edema can be successfully treated with single or repeated doses of sublingual nitroglycerin. In cases of prolonged acute heart failure, e.g. in the setting of acute myocardial infarction, nitroglycerin or isosorbide dinitrate can be given by the intravenous route for up to 24 h. Patients with acute myocardial infarction usually benefit from nitrate therapy if filling pressures are high and/or left ventricular function is compromised. Nitrate therapy can be considered safe if arterial blood pressure is maintained above 95 mm Hg. With these precautions nitrates can reduce infarct size and the incidence of complications as well as improve long-term prognosis. In the chronic treatment concern has risen with regard to possible nitrate tolerance. Thus, therapy schedules allowing for nitrate-poor phases are generally recommended. Therapy schedules with constant-rate delivery of drugs achieved with patches or intravenous administration of nitrates should be used with caution.
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PMID:Nitrate therapy in heart failure. 176 Aug 30

The geometry of both the infarcted and non-infarcted zone of the left ventricle changes after myocardial infarction. Two mechanisms are involved: expansion of the infarcted zone and secondary dilatation of the non-infarcted zone. The necrosed area undergoes an inflammatory reaction followed by fibrosis which end up as a sca within a period of a few days to a few weeks. During this period if fibrous scarring the infarcted, thinned myocardium undergoes progressive expansion which starts in the first hours of the myocardial infarction. The loss of left ventricular systolic function related to the infarct and volumic overload created by expansion of the infarct influence the secondary development of dilatation of the non-infarcted zones. This dilatation results in restoration of left ventricular stroke volume but at the price of increased wall stress, which itself induces compensatory wall hypertrophy. These phenomena are more pronounced when the initial infarction is extensive and if they are sustained, they result in definitive myocardial failure. Several factors influence remodeling: the size of the infarct, arterial patency, wall stress and the quality of the scarring process itself. Therapeutic interventions of each of these factors can influence the remodeling. Limitation of infarct size by thrombolytic therapy, arterial revascularisation, even when performed late, seem capable of limiting expansion of the necrosed zone. Pharmacodynamic intervention of left ventricular afterload also affects ventricular remodeling. Nitrate derivatives, vasodilator therapy in general and converting enzyme inhibitors have been shown to be effective.
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PMID:[Physiopathology of left ventricular remodeling after myocardial infarction]. 183 20

Left ventricular failure is a common complication of the acute phase of myocardial infarction. The most appropriate current treatment, when an increase in preload is the predominant or sole feature, involves nitroglycerin by infusion combined in varying degrees with diuretics. The aim of this study was to assess the value of maintenance treatment following intravenous nitroglycerin based upon a long acting nitrate derivative designed to achieve a hemodynamic result. Twenty patients with a mean age of 62 and with left ventricular failure during the acute phase of a myocardial infarction were studied. They were all treated with IV nitroglycerin using an automatic pump syringe. Pulmonary artery diastolic pressure, cardiac output, blood pressure and heart rate were measured hourly for six hours then every 6 hours. When PADP fell to below 18 mmHg, maintenance treatment with placebo or long acting nitroglycerin was given double-blind (10 patients were given long acting nitroglycerin and 10 patients the placebo). Pulmonary artery pressures, blood pressure and heart rate were measured every 2 hours for 8 hours, then at 12 and 24 hours. No significant difference was found in heart rate, blood pressure, cardiac output nor PADP (10 +/- 3.5 mmHg cf. 12 +/- 2.8 mmHg; NS) between the two groups. In total, maintenance treatment with long acting nitrate derivatives following IV nitroglycerin for hemodynamic purposes in patients with an acute myocardial infarction complicated by regressive cardiac failure would no appear to be necessary.
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PMID:[Value of the replacement of intravenous trinitrin by oral trinitrin in the acute phase of myocardial infarction complicated by regressive left ventricular insufficiency]. 195 77

Isosorbit 5-mononitrate is useful in ischaemic heart disease and in cardiac failure because of its favourable pharmacokinetic properties, in particular the absence of the so-called first pass effect, the great biological availability and long elimination time. The authors demonstrated on the preparation Elentan long, Schwarz Monheim GFR, which contains 50 mg isosorbit 5-mononitrate the improved efficiency of the left ventricle after three months administration to 15 patients with confirmed ischaemic heart disease, by exerting a favourable effect on the diastolic, systolic and global left ventricular function. Nitrates are drugs of first choice in some forms of ischaemic heart disease and are also effective in cardiac failure because they exert a marked effect on some cardiac functions on which the efficiency of the left ventricle depends. Elentan long proved, while using simple dosage, a preparation with favourable characteristics as regards biological availability and nitrate tolerance.
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PMID:[Effectiveness of the delayed-action form of isosorbide 5-mononitrate in ischemic heart disease]. 203 13

Organic nitrates were the first peripherally-active vasodilators to be used for the treatment of heart failure. Currently, three nitrate derivatives, glycerol trinitrate, isosorbide dinitrate and isosorbide 5-mononitrate as well as the nitrate-like substance molsidomine are employed clinically. For treatment of heart failure, the decisive hemodynamic effect is a meaningful reduction in ventricular filling pressures with maintenance or even a slight increase in cardiac output. The individual response to nitrates is variable. An important indicator for the effect achievable for a certain dose or for the necessary dosage to affect a defined reduction in ventricular filling pressures, is the magnitude of right atrial pressure. It can be assumed that the latter statement is also valid for the nitrate-like substance molsidomine. An inherent problem with any long-term treatment with nitrates is the incurrence of tolerance. This can be expected with any dosing regimen which leads to nitrate cumulation in the plasma or to nearly-constant, high, plasma concentrations as rendered by multiple daily administration of orally-active nitrates or with continuous transdermal or intravenous nitrate administration. The cause of nitrate tolerance is regarded as an insufficient or absent stimulation of guanylate cyclase and, consequently, inadequate generation of cyclic GMP due to availability of thiol substrate. Since the nitrate-like substance molsidomine appears to be able to stimulate guanylate cyclase independent of thiol groups, tolerance development may not be a limiting factor with this agent. Comparable reduction of diastolic pulmonary artery pressure after acute administration and at the end of one week of treatment with 4 mg molsidomine four times daily has been reported.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Nitrates in the treatment of heart failure]. 211 55

To determine whether a 72-hour infusion of nitroglycerin produces hemodynamic improvement in patients with severe congestive heart failure and to assess the contributing role of various possible causes of hemodynamic tolerance to nitroglycerin, 19 patients received an infusion of nitroglycerin 1.5 micrograms/kg/min for 72 hours. In a subgroup of patients (n = 10), there was an increase in stroke work index and a decrease in ventricular filling pressures throughout the infusion and even after it was discontinued. Tolerance to the hemodynamic effects of nitroglycerin was partially reversed 8 hours after the infusion was stopped. Neurohumoral changes occurred but appeared to play only a minor role in the development of nitroglycerin tolerance. However, hematocrit fell 9 +/- 5%, which suggests that an increased intravascular volume contributed to tolerance. In summary: (1) a 72-hour infusion of nitroglycerin improves ventricular function in some patients with severe heart failure; (2) volume shifts from the extravascular to the intravascular compartments may, at least in part, be responsible for nitroglycerin tolerance; and (3) reflex neurohumoral activation may also play a small role in nitrate tolerance.
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PMID:Sustained beneficial effect of a seventy-two hour intravenous infusion of nitroglycerin in patients with severe chronic congestive heart failure. 211 45

Over 30 per cent of coronary patients die of cardiac failure excluding the acute phase of myocardial infarction. With the exception of preexisting hypertension, there is no compensatory hypertrophy in ischemic heart disease. However, hypertrophy is a costly adaptation in terms of myocardial oxygen demand and, therefore, coronary flow. Fibrous zones are unresponsive to inotropic drugs and so the treatment of cardiac failure due to ischemic heart disease consists in limiting or preventing episodes of ischemia. Each mechanism of ischemia has an appropriate treatment: the preload is reduced by trinitrin and its derivatives and by molsidomine; the after-load by calcium antagonists and angiotensin converting enzyme inhibitors; tachycardia and hypercontractile states by betablockers. The risk of arrhythmia, aggravated by many inotropic therapies, constitutes the major danger to ischemic heart failure; amiodarone, betablockers and preventive nitrate therapy are the most effective and least dangerous antiarrhythmics. Revascularisation is effective for permanently ischemic segments or for ischemia on effort but does not improve large plaques of fibrosis which sometimes require surgical ablation or plastic procedures. But these measures are incomplete if all aspects of the disease are not taken in consideration: loss of excessive body weight, exercise rehabilitation by modern techniques, limitation of bed rest at the ultimate stage of the disease allowing patients with ischemic cardiac failure a better quality of life without aggravating the prognosis.
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PMID:[Treatment of cardiac insufficiency in ischemic heart disease]. 212 13


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