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

Digitalis and diuretics constitute conventional therapy of congestive heart failure, but systemic vasodilators offer an innovative approach in acute and chronic heart failure of decreasing increased left ventricular systolic wall tension (ventricular afterload) by reducing aortic impedance and/or by reducing cardiac venous return. Thus, vasodilators increase cardiac output (CO) by diminishing peripheral vascular resistance (PVR) and/or decrease increased left ventricular end-diastolic pressure (LVEDP) (ventricular preload) by diminishing venous tone. Concomitantly, there is reduction of myocardial oxygen demand, thereby reliably reducing angina pectoris in coronary disease, and potentially limiting infarct size and ischemia provided systemic arterial pressure remains normal. The vasodilators produce disparate modifications of cardiac function depending upon their differing alterations of preload versus impedance: nitrates principally cause venodilation (decrease LVEDP); nitroprusside, phentolamine and prazosin produce balanced arterial and venous dilation (decrease LVEDP and increase CO) provided left ventricular filling pressure is maintained at the upper limit of normal; whereas hydralazine predominantly effects arteriolar dilation (increases CO). With depressed CO plus highly increased LVEDP and increased PVR, nitrates also induce some increase of CO by reducing PVR. Combined nitroprusside and dopamine synergistically enhance CO and decrease LVEDP. Mechanical counterpulsation aids nitroprusside in acute myocardial infarction. The 30-minute venodilator action of sublingual nitroglycerin is extended for 4 to 6 hours by cutaneous nitroglycerin ointment, by sublingual and oral isosorbide dintrate, and by oral pentaerythritol tetranitrate and sustained-release nitroglycerin capsules. Ambulatory oral vasodilator therapy is provided by long-acting nitrates (relieve pulmonary congestion); hydralazine (improves fatigue); prazosin alone, combined nitrate-hydralazine combined prazosin-hydralazine (improve both dyspnea and fatigue).
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PMID:Afterload reduction and cardiac performance. Physiologic basis of systemic vasodilators as a new approach in treatment of congestive heart failure. 9 30

The method of radionuclide cardangiography (RNCA) has become a well-established method amongst non-invasive assessments in coronary heart disease (CHD). By means of RNCA the most important parameters of left ventricular function, viz. ejection fraction (EF) and wall motion (WM), can be determined very exactly. The first bolus pass method (FBP), which allows satisfactory separation between right and left heart, enables the additional determination of EF distribution, stroke volume (SV) and SV distribution. This method requires the technical necessity of a multicrystal gamma camera. Special nuclear medicine characteristics have been worked out for different groups of CHD. EF and WM show typical signs of angina pectoris, caused by exercise correlating with reduced perfusion in the referring section of WM. While these changes may be reversible after nitrate administration, pathological myocardial function caused by acute myocardial infarction (AMI) or manifest heart failure is not reversed by nitroglycerine. Typical findings were seen in the course of AMI: initial decrease in global EF and diffuse (multilocated) asynergies in the left ventricular wall; in the second week possible start of recovery, including regression of dyskinesia to akinesia at the end of hospitalization. Especially in the early phase of AMI it was demonstrated that FBP--as a non-invasive technique--gives high information quality which is unequalled by other comparable methods. Therefore, the described method of FBP should be classified as very useful and effective in clinical cardiology.
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PMID:[Radionuclide cardangiography as non-invasive assessment in coronary heart disease (author's transl)]. 39 49

Furosemide was administered intravenously to 11 patients with cardiac failure after acute myocardial infarction. After an initial loading dose furosemide was given four-hourly if the pulmonary capillary wedge pressure (PCW) was not normalized, i.e. less than or equal to 15 mm Hg. The comparison of the hemodynamic results with the results of a previous study with nitrates was as follows: like the nitrates furosemide lowered the PCW early, i.e. within 15 minutes from 22 +/- 3 to 18 +/- 5 mm Hg, but the therapeutic objective (PCW less than or equal to 15 mm Hg) was reached later than with nitrates. During the 24-hour observation period PCW and total peripheral resistance decreased steadily. The decrease of cardiac index to critical low values in some patients after a mean of 7.5 hours of therapy, and of the mean arterial pressure from 100 +/- 13 to 91 +/- 14 mm Hg, may limit the use of furosemide alone in these patients. During nitrate therapy PCW started to rise again after 12 hours in some patients, necessitating higher doses of nitrates with a corresponding decrease of diuresis. A combination of both forms of therapy may be of value and needs further investigation.
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PMID:[Hemodynamic consequences of the furosemide treatment of cardiac insufficiency in recent myocardial infarct]. 53 59

The use of vasodilators represents a new approach to the treatment of cardiac insufficiency, either chronic or acute. Their field of action is venous, arterial or mixed. Decreasing the pre-load, the "venous" vasodilators lighten the congestive symptoms of cardiac insufficiency. By decreasing the post-load, the "arterial" vasodilation increases the cardiac output. Some vasodilators, venously administered, imply a continuous hemodynamic checking (Sodium Nitroprussiate, Phentolamine, injectable Trinitrine). Others are active orally (Trinitrine, Isosorbide Dinitrate, Hydralazine, etc.). Vasodilating treatment is recommended for acute cardiac insufficiency, particularly during myocardium infarct and some acute valvular insufficiencies. It is also successfully used in acute lung edema. Finally it takes an increasing importance in the treatment of chronic cardiac insufficiency.
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PMID:[Vasodilators in the treatment of cardiac insufficiency (author's transl)]. 53 77

Severe tachycardia, ventricular ectopy, and sodium retention manifested by hemodynamic deterioration developed with hydralazine hydrochloride therapy in chronic coronary heart disease with congestive failure refractory to digitalis, diuretics, and nitrates. Coronary care unit admission with Swan-Ganz catheterization corrected hemodynamics by sodium nitroprusside treatment after hydralazine withdrawal. Satisfactory cardiac performance with oral long-acting nitrates were unsuccessful. However, the new oral vasocilator, prazosin hydrochloride, achieved considerable hemodynamic benefit by greatly reducing elevated left ventricular filling pressure and increasing severely depressed cardiac index to normal, accompanied by striking symptomatic improvement. Furthermore, long-term enhancement of cardiac dynamics and salutary functional status was maintained by ambulatory oral prazosin therapy for several months. This experience demonstrates the favorable alternative of prazosin nitroprusside-like actions over hydralazine-nitrate therapy in heart failure therapy and emphasizes prazosin's utility when untoward side effects to hydralazine develop.
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PMID:Hydralazine-induced tachycardia and sodium retention in heart failure. Hemodynamic and symptomatic correction by prazosin therapy. 64 47

Vasodilators are known to be effective in improving the hemodynamics of congestive heart failure by increasing cardiac output and reducing left ventricular filling pressure (LVFP). Long acting agents are needed to augment the practicality and availability of chronic vasodilator therapy. In the present study the vascular effects of chewable isosorbide dinitrate (CHIS), sublingual nitroglycerin (NTG) and placebo (P) were compared in eight patients with high LVFP due to heart failure. Patients with LVFP (pulmonary wedge pressure) over 14 mm Hg were given CHIS, 10 mg, NTG, 0.6 mg, and P, two chewable tablets, in random fashion. Heart rate (HR), blood pressure (BP) and LVFP were monitored for three hours after each drug. HR was not significantly affected by any drug, although it rose slightly after NTG and fell after CHIS. Significant reduction of BP occurred only after NTG, with peak effect at five minutes, but lasting only 15 minutes. NTG reduced LVFP 5.1 mm Hg (19.5%, P, less than 0.05), at peak effect, but LVFP was no longer significantly lower by 20 minutes after NTG. After CHIS, LVFP fell significantly within five minutes, reached a peak reduction of 8.6 mm Hg (32;7%, P less than 0.01) at 15 minutes, and remained significantly lower through three hours. Thus CHIS provides a nitrate action of rapid onset and sustained effect that may be useful for chronic vasodilator therapy of heart failure.
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PMID:Comparative hemodynamic effects of chewable isosorbide dinitrate and nitroglycerin in patients with congestive heart failure. 80 59

Isotopic study of pulmonary and ventricular blood volumes after the ingestion of 5 mg of isosorbide dinitrate showed that cardio-pulmonary blood volume decreased by 380 ml without any change in total circulating blood volume. The demonstration of this effective "internal venesection" explains the fall in capillary pressure seen after the administration of nitrate derivatives. It justifies their use in the treatment of acute pulmonary oedema or refractory cardiac failure and explains the results observed.
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PMID:[Isotope study of the effects of a nitrate derivative on pulmonary blood volume. Application in the treatment of cardiogenic pulmonary edema]. 98 Jul 11

After myocardial infarction, calcium channel blockers are the most prescribed anti-ischemic drugs followed by nitrate derivatives and beta blockers. In order to assess whether this attitude is justified by published data on their efficacy, a meta-analysis of trials of anti-ischemic drugs in myocardial infarction was performed. The early mortality was 13.3% in the group treated by IV nitrates in the acute phase of myocardial infarction and 17.2% in control groups, reducing the risk by a quarter (95% confidence interval of the odds ratio (CI): 0.55-0.95). When all nitrate derivative trials were grouped together, the reduction in the risk of death of 21% was significant (from 15% to 11.8%) (CI: 0.59-0.94). Although oral nitrate derivatives introduced during the acute phase and continued for several weeks induced a non-significant reduction in mortality of 16%, when given intravenously, the benefits on early and longer term mortality were unquestionable. The mortality was 9.8% in the groups treated by calcium channel blockers and 9.3% in control groups (NS); the recurrent infarct rate was 4.8% and 5.4% respectively (NS). In this family of drugs, there was no product which distinguished itself from the others with regard to beneficial or adverse effects. The early mortality decreased from 9.2% to 8.2% in the groups treated by oral beta-blockade--a risk reduction of 10% (NS) and from 4.2% to 3.7% with intravenous beta-blockers--a risk reduction of 12% (p = 0.03). Late mortality decreased from 9.4% to 7.6%, a reduction of 20% (p < 0.00001) in long term trials.2+ contraindication of betablockers in patients without cardiac failure.
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PMID:[Which anti-ischemic treatment can be prescribed during and after the acute phase of myocardial infarction?]. 136 72

The effect of enoximone was assessed by a randomised double blind trial versus placebo. The clinical status of the patients was evaluated by the NYHA classification and quality of life score. Inotropic state was estimated from the maximum acceleration of aortic and pulmonary blood flow recorded by Doppler echocardiography. Thirty patients with severe cardiac failure, aged 66.4 +/- 14 years, symptomatic despite maximal therapy associating diuretics, digitalis, nitrate derivatives and angiotensin converting enzyme inhibitors, were included. Fifteen patients were given enoximone 100 mg three times a day orally (Group E) and the other 15 were given a placebo (Group P). The NYHA class and quality of life scores were assessed at D0, D4 and D31. Doppler echocardiography and Holter recordings were performed on D0 and D31. The two groups were comparable at D0. Ten patients abandoned the trial, 3 from Group E (including 1 death) and 7 from Group P (including 3 deaths). At D4, 13 patients from Group E and 8 from Group P were clinically improved (p < 0.05). At D31, the clinical state was stable or improved in 10 of the 12 patients in Group E and 6 of the 8 patients in Group P (NS). No secondary effects were severe enough to warrant the withdrawal of treatment: the frequency of ventricular extrasystoles was comparable in the two groups at D0 and D31. At D31 the maximal aortic acceleration had increased by 20% compared with D0 (p < 0.05) and the maximal pulmonary acceleration by 31% (p < 0.05) in Group E. The same parameters showed no significant change in Group P (-6% and +5% respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Double-blind clinical and echocardiographic study of oral enoximone versus placebo in severe cardiac insufficiency]. 144 35

The organic nitrates have remarkably diverse actions that are or should be beneficial in patients with ischemic heart disease. These drugs are effective in all the important ischemic syndromes. Preliminary data in patients with acute infarction suggest that the drugs may be truly cardioprotective, resulting in improved mortality. This review has not discussed the role of nitrates in congestive heart failure or LV dysfunction, a subject of great importance. The nitrates are useful adjunctive agents in these syndromes, and the two VeHfT trials support the concept that long-term nitrate administration, in conjunction with hydralazine, may favorably alter the natural history of heart failure. This cardioprotective effect is similar to that suggested for the post-MI patient. The data are not strong enough for definitive conclusions at this time. The clinical benefits of nitrates in decreasing subjective (angina) and objective indices of ischemia in stable and unstable angina, as well as limited data in asymptomatic myocardial ischemia, are unequivocal and are as favorable as those for beta blockers or calcium antagonists. Tolerance is an important problem that unfavorably influences the potential benefits of nitrate therapy. I believe that this problem can be avoided with well-designed dosing regimens. Current research into endothelial biology in health and disease has further supported a physiologic role for the organic nitrates in patients with ischemic heart disease. The nitrate-platelet story, while controversial, is promising and offers another positive rationale for nitrate administration. The concept of nitrates replenishing disordered EDRF release or action is an exciting one. Physicians should feel fortunate to have such a remarkable group of drugs available for their patients.
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PMID:Use of nitrates in ischemic heart disease. 151 14


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