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

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

A haemodynamic study was conducted in 96 patients with acute myocardial infarction. The method of right heart catheterization at the bedside using the Swan-Ganz floating balloon-tipped catheter is safe and feisible. An elevation of pressure in the pulmonary circulation was revealed in patients with transmural myocardial infarction and in those without clinical signs of heart failure. The pressure elevation is detected the more often the sooner after the onset of infarction the examination is conducted. To evaluate fast pressure changes heart catheterization is essential and cannot be substituted by any other technique of examination Digoxin administration during the acute phase of myocardial infarction fails to produce any significant reduction of the pulmonary circulation pressure, but a prompt reduction of the pulmonary circulation pressure can be achieved by way of Phentolamine infusion. The pulmonary circulation pressure measurements during the acute phase of myocardial infarction are believed to be an indispensable component of examinations for the heart failure therapy.
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PMID:[Hemodynamic observations in acute myocardial infarct]. 85 47

Vasodilative treatment of severe heart failure with infusions of phentolamine leads to ventricular unloading and in many cases brings about a dramatic improvement of the patient's condition. Phentolamine is the only one of the vasodilators so far used in the treatment of heart failure that has a positively inotropic effect. In contrast to sodium nitroprusside and nitroglycerin, it also increases stroke volume at normal filling pressures. Although vasodilative therapy has resulted in a notable decline in the mortality from severe heart failure among hospitalized patients, the long-term prognosis after discharge remains poor. One of the chief reasons is that there has hitherto been no effective orally administrable drug suitable for protracted therapy. Initial clinical studies with a newly developed slow-release formulation of phentolamine have shown that the preparation produces remarkably good effects in patients with chronic heart failure: systolic pressure rises, the amplitude of the blood pressure is augmented and there is an increase in urinary excretion accompanied with a corresponding reduction in weight. In practically all cases, there is a distinct decrease in the size of the heart and in pulmonary congestion.
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PMID:[Treatment of heart failure with phentolamine (Regitin)]. 89 48

During exercise in subjects with congestive heart failure and mitral regurgitation the rise in systemic arterial pressure is usually accompanied by increase in systemic vascular resistance. That could cause decrease of cardiac output not only because of a lack of myocardial reserve, but also because of an increase of mitral regurgitant volume. In such situation decrease in left ventricular preload could further increase the regurgitant volume and cardiac output. Whether changes in pre-or afterload can cause significant changes in mitral regurgitation, nitroglycerin and phentolamine was assessed in that group of patients. 22 patients with significant mitral regurgitation (3+,4+) was randomly divided into two groups. The first one received short intravenous infusion of nitroglycerin at a rate of 170 micrograms/min. The second one received phentolamine intravenously 1-1,5 mg/min. Patients underwent right heart catheterization with Swan-Ganz thermodilution catheter. Mean pulmonary, pulmonary capillary wedge, and right atrial pressure were monitored and recorded. Cardiac output was determined by thermodilution technique using iced 5% dextrose. If there were no contraindications (PWP greater than 30 mm Hg) an effort test was performed (cycloergometer, supine position). The same protocol was repeated during administration of nitroglycerin and phentolamine. Nitroglycerin significantly decreased right atrial and capillary wedge pressure (from 22.9 to 15.6 mm Hg). There were no significant differences in cardiac output, pulmonary and systemic vascular resistance. Pulmonary artery pressure decreased after nitroglycerin but the difference was not significant. All above effects of nitroglycerin persisted during effort. Phentolamine decreased significantly right atrial, pulmonary and capillary wedge pressure with simultaneous increase of cardiac output (30%) and decrease of pulmonary and systemic vascular resistance. In summary, nitroglycerin decreases only symptoms and theoretically could worsen forward flow in patients with mitral regurgitation and heart failure, especially in subjects with a significant increase of systemic vascular resistance during effort.
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PMID:[Effect of intravenous administration of nitroglycerin and regitine on hemodynamics in mitral valve insufficiency]. 212 94

Six clinically stable patients with cystic fibrosis (24 to 31 yr of age) and severe pulmonary impairment, right ventricular hypertrophy, and previous right-sided heart failure underwent cardiac catheterization to assess the hemodynamic effects of oxygen (fraction of inspired O2, 0.31, 0.50), phentolamine (5 mg intravenously), hydralazine (0.33 mg/kg intravenously), and nifedipine (20 mg sublingually). Measurements during dynamic exercise were also obtained before and after hydralazine therapy. Studies after 5 to 8 wk of continuous, orally administered hydralazine therapy were performed in 3 patients. The resting mean pulmonary artery pressure was 31 +/- 4 mmHg. At rest, only oxygen was a selective pulmonary vasodilator, decreasing pulmonary artery pressure and pulmonary vascular resistance in all patients. Systemic arterial pressure and resistance were not significantly changed. Phentolamine, hydralazine, and nifedipine did not alter pulmonary artery pressure or selectively affect the pulmonary vascular bed, reducing both calculated pulmonary and systemic vascular resistance, the latter to a similar or greater degree. Hydralazine and nifedipine significantly increased cardiac index and decreased systemic arterial pressure. Nifedipine mildly decreased systemic oxygenation. During exercise, the mean pulmonary artery pressure increased to 51 +/- 15 mmHg. Hydralazine increased systemic and mixed venous oxygenation both at rest and during exercise but did not alter the elevation in pulmonary artery pressure observed during exercise. After orally administered hydralazine therapy, oxygen delivery and cardiac index remained increased in 2 patients. These data support the use of oxygen but not of the other agents in patients with cystic fibrosis and chronic cor pulmonale unless the ability of hydralazine to increase oxygen delivery is determined to improve prognosis.
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PMID:Effect of vasodilators at rest and during exercise in young adults with cystic fibrosis and chronic cor pulmonale. 399 48

We described recently that systemic hypoxia provokes vasoconstriction in heart failure (HF) patients. We hypothesized that either the exaggerated muscle sympathetic nerve activity and/or endothelial dysfunction mediate the blunted vasodilatation during hypoxia in HF patients. Twenty-seven HF patients and 23 age-matched controls were studied. Muscle sympathetic nerve activity was assessed by microneurography and forearm blood flow (FBF) by venous occlusion plethysmography. Peripheral chemoreflex control was evaluated through the inhaling of a hypoxic gas mixture (10% O(2) and 90% N(2)). Basal muscle sympathetic nerve activity was greater and basal FBF was lower in HF patients versus controls. During hypoxia, muscle sympathetic nerve activity responses were greater in HF patients, and forearm vasodilatation in HF was blunted versus controls. Phentolamine increased FBF responses in both groups, but the increase was lower in HF patients. Phentolamine and N(G)-monomethyl-l-arginine infusion did not change FBF responses in HF but markedly blunted the vasodilatation in controls. FBF responses to hypoxia in the presence of vitamin C were unchanged and remained lower in HF patients versus controls. In conclusion, muscle vasoconstriction in response to hypoxia in HF patients is attributed to exaggerated reflex sympathetic nerve activation and blunted endothelial function (NO activity). We were unable to identify a role for oxidative stress in these studies.
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PMID:Mechanisms of blunted muscle vasodilation during peripheral chemoreceptor stimulation in heart failure patients. 2280 26