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

Patients with severe left ventricular failure generally have both reduced cardiac output and increased pulmonary and systemic venous pressures. A study was therefore made of the use of combined vasodilator therapy with nonparenterally administered nitrates, which act primarily on venous capacitance vessels and thus reduce preload, and orally administered hydralazine, which acts on arteriolar resistance vessels and thus reduces afterload. Twelve patients with chronic refractory heart failure were given these drugs individually and in combination during continuous hemodynamic monitoring. Heart rate and arterial pressure did not change significantly. Nitrates significantly reduced filling pressures of both ventricles without affecting cardiac index. Hydralazine did not alter filling pressures but dramatically increased cardiac index. The hemodynamic effects of each drug were additive during combined therapy, resulting in a 36 percent (28 to 18 mm Hg) mean decrease in left ventricular filling pressure and a 58 percent (2.1 to 3.3 liters/min per m(2)) mean increase in cardiac index. The seven patients who have continued to receive combined therapy for 3 to 10 months have shown sustained clinical improvement.
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PMID:Hemodynamic advantage of combined administration of hydralazine orally and nitrates nonparenterally in the vasodilator therapy of chronic heart failure. 41 64

Changes in left ventricular performance were evaluated in 14 patients with functional New York Heart Association class III or IV chronic heart failure before and after the addition of oral hydralazine to conventional therapy. With conventional therapy, cardiac output increased from 3.4 +/- 0.8 (mean +/- 1 standard deviation) at rest to 4.7 +/- 1.4 liters/min during exercise. This increase in cardiac output on exercise during conventional therapy was mainly due to an increase in heart rate. After the addition of hydralazine, cardiac output at rest increased to 5.0 +/- 1.4 liters/min. The increase in cardiac output was essentially due to an increase in stroke volume. This enhanced stroke volume after hydralazine therapy was maintained during exercise. Hydralazine therapy did not change either the left ventricular filling pressure at rest or the magnitude of increase in left ventricular filling pressure during exercise. Nevertheless, increased cardiac output and stroke volume with similar changes in left ventricular filling pressure during exercise indicated improved left ventricular performance after hydralazine therapy. After short-term hydralazine therapy, symptom-limited peak exercise work load, duration of exercise and maximal oxygen consumption during exercise did not increase. Clinical follow-up at 2 months after long-term therapy revealed subjective improvement in exercise tolerance in 13 of the 14 patients.
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PMID:Influence of short-term oral hydralazine therapy on exercise hemodynamics in patients with severe chronic heart failure. 49 13

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

Vasodilators acutely reduce afterload and improve hemodynamics in congestive heart failure. Intravenous nitroprusside reduces left ventricular filling pressure and increases cardiac output while modestly reducing blood pressure and not changing heart rate in patients with heart failure in whom this response is characteristic. Comparably reduced blood pressure during nitroprusside infusion in normal subjects or hypertensive patients without failure results in a decrease in cardiac output and tachycardia. Long-acting vasodilators are also effective in patients with congestive heart failure. Nitrates, predominant venodilators, decrease left ventricular filling pressure as much as nitroprusside does, but increase cardiac output less. Hydralazine, an arterial dilator, increases cardiac output similarly to nitroprusside but decreases filling pressure less. Combining hydralazine with nitrates results in hemodynamic effects almost identical to those of nitroprusside. The quinazoline derivatives, trimazosin and prazosin, are also effective vasodilators, which act on both arteries and veins in patients with congestive heart failure. The hemodynamic response to vasodilators is influenced by the underlying hemodynamic status, as the change in cardiac output is directly related to base line ventricular filling pressure as well as systemic vascular resistance, and inversely related to the base line cardiac output. Response to vasodilators does not appear to be altered by age, diabetes, acute myocardial infarction or the cause of congestive myocardiopathy.
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PMID:Hemodynamic responsiveness to short- and long-acting vasodilators in left ventricular failure. 68 86

Vasodilator and inotropic drugs work through independent mechanisms in augmenting left ventricular pump function in patients with heart failure. The selection between these two classes of pharmacologic agents for an individual patient may be based on the control blood pressure as well as the underlying disease. Although vasodilator drugs are easiest and safest to employ in patients with normal or high arterial presure levels, even in relatively hypotensive subjects (systolic arterial pressure less than 105 mm Hg), a salutary hemodynamic effect can be achieved without an undue decrease in pressure. Inotropic drugs may be safest to administer to patients without coronary artery disease, but the oxygen-consuming effect of these drugs need not necessarily have an adverse effect on patients with ischemic heart disease. Combined vasodilator and inotropic drug therapy is the most potent pharmacologic means of restoring pump function in patients with severe heart failure. The long-term use of vasodilator and inotropic drugs in the treatment of heart failure is dependent on the availability of agents that will produce a sustained hemodynamic effect. Hydralazine, nitrates and prazosin have been employed alone or in combination and provide a promising approach to vasodilator treatment of heart failure. Better and more selective oral inotropic agents are needed to allow this therapeutic modality to be employed optimally.
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PMID:Selection of vasodilator, inotropic or combined therapy for the management of heart failure. 68 92

1. We investigated the haemodynamic effects of intravenously administered hydrallazine, diazoxide and nitroprusside and orally administered minoxidil to determine whether vasodilators (such as nitroprusside) which do not increase cardiac output might be better treatment for hypertensive complications associated with, or caused by, myocardial failure than those that do. 2. Hydrallazine and diazoxide caused increases in heart rate, cardiac output, cardiopulmonary blood volume, the ratio of cardiac output to cardiopulmonary volume, and pulmonary artery pressure. Nitroprusside, although decreasing pressure and vascular resistance, caused no significant change in the other functions except for reducing pulmonary artery pressure. Minoxidil, when given orally, had the potential for causing pulmonary hypertension. This seemed explained by increased flow (hyperdynamic type) in some but by congestive cardiac failure in others; the latter condition was probably intensified by the marked fluid retention that the drug can cause. 3. On the basis of these results a classification of vasodilators was constructed which depends on the presence or absence of a venodilating effect. Vasodilators which produce no (or little) venodilatation, increase heart rate, cardiac output, cardiopulmonary blood volume and pulmonary artery pressure. In this class are diazoxide, hydrallazine and minoxidil. Those that cause venodilatation do not stimulate the heart nor do they cause pulmonary hypertension. Nitroprusside and nitroglycerine are drugs of this type. 4. These results suggest that drugs producing both venodilatation and arteriolar dilatation may be more specific therapy for hypertensive complications associated with cardiac failure than those that cause only arteriolar dilatation.
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PMID:Vasodilating drugs: contrasting haemodynamic effects. 107 83

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

V-HeFT, the first mortality trial in patients with heart failure, has provided important insights regarding trial design, including patient selection and efficacy criteria. Planning of V-HeFT II, the trial comparing hydralazine-isosorbide dinitrate and enalapril, has raised additional issues regarding the power to detect mortality effects and the relative value of non-mortality endpoints for efficacy. V-HeFT has demonstrated that some vasodilator regimens can prolong life in heart failure. Hydralazine + isosorbide dinitrate reduced mortality by 27% compared to placebo in patients treated with digoxin and diuretics. The possibility of a non-vasodilator mechanism for long-term benefit of these interventions is raised by the apparently poor relationship between the magnitude of vasodilation and the favorable long-term effects. These issues need to be explored in subsequent trials. In future long-term trials, however, the need for background therapy with drugs that have been effective in reducing mortality will make the identification of life prolongation from new therapies more difficult to demonstrate.
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PMID:Lessons from V-HeFT: questions for V-HeFT II and the future therapy of heart failure. 182 Feb 92

Hydralazine (1-hydrazinophthalazine) has been used extensively in the treatment of hypertension and congestive heart failure and produces arteriolar vasodilation, in part, mediated by prostaglandins. Its associated reflex baroreceptor-mediated responses of tachycardia and increased ejection velocity are attenuated in congestive heart failure. A direct inotropic effect has been attributed to the drug. Pharmacokinetic data indicate hydralazine is absorbed well from the gastrointestinal tract, and has an extensive and complex metabolism depending on acetylator status: slow acetylators undergo primary oxidative metabolism, while rapid acetylators are acetylated. Half-lives, clearances and bioavailability of the drug are not significantly altered in congestive heart failure compared with hypertensive patients. A wide range of dosages in heart failure has been noted (150 to 3000 mg/24h), and may related to a saturation of the first-pass effect. Hydralazine improves haemodynamics in the short term in patients with increased peripheral vascular resistance, and has variable effects on pulmonary capillary wedge and left ventricular filling pressures. Prediction of the short term clinical response is difficult and appears to be independent of pharmacokinetics. A meta analysis did not demonstrate long term efficacy of hydralazine alone in heart failure, but combination therapy with nitrates has been shown to improve survival and exercise performance in patients with mild to moderate heart failure. Side effects are common and are dependent on dose, duration and acetylator status.
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PMID:Clinical pharmacokinetics and therapeutic use of hydralazine in congestive heart failure. 265 46

We evaluated the effects of intravenous hydralazine (5 to 30 mg) and oral nifedipine (20 to 80 mg) on plasma catecholamines, renin, and aldosterone in 18 patients with severe chronic heart failure. Both drugs resulted in a significant decrease in systemic vascular resistance and mean systemic blood pressure, and led to an increase in cardiac output. Baseline plasma norepinephrine concentration was elevated in most patients; however, augmentation of cardiac output with both drugs did not decrease the values of this hormone (from 870 +/- 128 to 946 +/- 161 pg/ml with hydralazine and from 1088 +/- 260 to 1106 +/- 187 pg/ml with nifedipine). Plasma epinephrine level was also elevated at baseline and did not change significantly following nifedipine therapy (164 +/- 44 vs 199 +/- 54 pg/ml), but increased in most patients following the administration of hydralazine (from 105 +/- 45 to 153 +/- 27 pg/ml, p less than 0.01). The renin-aldosterone system was activated in our patients and also demonstrated a different response to both drugs. Hydralazine therapy did not change either the plasma renin concentration (30 +/- 7 vs 28 +/- 7 ng/ml/hr) or the aldosterone level (24 +/- 7 vs 22 +/- 5 ng/dl). In contrast, nifedipine increased the plasma renin concentration (22 +/- 7 to 29 +/- 8 ng/ml/hr, p less than 0.05). This change did not correlate with changes in systemic blood pressure (r = 0.03) and was probably the result of previously shown calcium blockade-mediated stimulation of renin release from the juxtaglomerular cells of the kidney.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neurohumoral consequences of vasodilator therapy with hydralazine and nifedipine in severe congestive heart failure. 287 93


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