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

Dobutamine (and dopamine) are potent positive inotropic drugs which are frequently given to treat decompensated congestive heart failure. This study reports on the use of ambulatory dobutamine (and dopamine) infusions in 21 outpatients with advanced congestive heart failure. Each patient was initially hospitalized, and hemodynamic and clinical efficacy to dobutamine (and dopamine) was assessed. These 21 patients were carefully selected from a larger population of approximately 40 patients referred for this therapy. Chronic venous access was established and a drug infusion pump was supplied. Patients and family members were trained in the use of these devices. Eleven patients were treated with intermittent dobutamine infusions for 48 consecutive hours weekly, six patients with continuous (i.e., 24 hours daily) dobutamine infusions, and four patients with continuous, daily dobutamine and dopamine infusions. Significant (p less than 0.001) increases in cardiac index (1.8 +/- 0.6 to 2.7 +/- 0.7 L/min/m2) occurred during the initial dobutamine titrations. Functional classification (3.8 +/- 0.4 to 2.8 +/- 0.7) also improved significantly (p less than 0.01) during the 1.8 to 24 (mean 7.8) months of outpatient infusion therapy with dobutamine (and dopamine). Complications during outpatient therapy included drug tolerance (two instances), infection (two with bacteremias, eight with exit site infections), drug extravasation (three instances), and pump malfunction (two instances). Twenty patients have died: eleven from heart failure, four suddenly (one of them 9 months after dobutamine was stopped), and five from noncardiac causes. Our data suggest that outpatient dobutamine (and dopamine) infusions may be an effective form of therapy for selected patients with severe congestive failure who are refractory to more conventional treatment or who are awaiting cardiac transplantation.
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PMID:Outpatient dobutamine and dopamine infusions in the management of chronic heart failure: clinical experience in 21 patients. 363 Sep

78 patients were treated with dobutamine for a severe episode of heart failure at a mean dose of 9.51 micrograms . kg-1 . min-1 for an average of 5 days. 59 of these patients had ischaemic heart disease, including 34 with recent infarcts. The monitoring of treatment was essentially clinical, consisting of repeated measurement of the heart rate, the systolic and diastolic blood pressure and the diuresis. A haemodynamic survey was performed in only 25 cases. 48 patients were improved. 24 of these patients had no clinical or radiological signs of heart failure at the end of the treatment. Dobutamine significantly increases the blood pressure (97.7 +/- 24.9 to 105.8 +/- 21 mm Hg), the diuresis and the cardiac index (2.02 +/- 0.51 to 2.52 +/- 0.54 l . min-1 . m-2) and it significantly decreases the mean capillary pressure (25.36 +/- 6.20 to 21.03 +/- 6.94 mm Hg). The tolerance was very satisfactory, particularly in terms of the heart rate, ventricular excitability and the progression of the coronary disease. This clinical study confirms the value of dobutamine in the treatment of severe heart failure, either alone or in combination with vasodilators. The authors do not believe tha haemodynamic monitoring is essential at the doses used, which means that dobutamine could be used more widely in these indications.
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PMID:[Clinical study of the action of dobutamine in acute cardiac insufficiency]. 614 16

The impaired cardiac performance in patients with congestive cardiac failure may be improved by the introduction of inotropic therapy. Dopamine and dobutamine are both potent cardiac stimulants although their haemodynamic profile is different. Dobutamine would appear to be the more appropriate choice in cardiac failure because of the additional benefit of preload reduction although in the context of severe hypotension dopamine would be preferred. The need for intravenous administration, however, limits their clinical application. In acute studies, the oral agents prenalterol and pirbuterol, are effective in improving myocardial function; pirbuterol mainly due to peripheral vasodilatation and afterload reduction. There are few chronic studies but confirmation of sustained haemodynamic improvement is lacking. This could be due, either to the inexorable deterioration in cardiac function or to a reduction in the beta receptor population available for catecholamine stimulation.
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PMID:The clinical use of inotropes in cardiac failure: dopamine, dobutamine, prenalterol and pirbuterol. 683 90

Despite the high incidence of sudden death in pregnant patients with primary pulmonary hypertension (PPH) and heart failure, no data are available that thoroughly elucidate the peripartum hemodynamic alterations occurring in these patients. The present report describes the clinical course of a pregnant patient with PPH and provides data regarding peripartum hemodynamic alterations. Hemodynamic parameters were stable during labor and delivery, but pulmonary vascular resistance rose gradually while cardiac output fell after parturition. Dobutamine caused a modest but unsustained increase in cardiac output. Nitroprusside produced a significant sustained augmentation of cardiac output from 3.5 to 5.0 liters/min due to reduction of systemic and pulmonary vascular resistances, and permitted restoration of hemodynamic stability and resolution of heart failure. The authors believe that pregnant patients with PPH and severe heart failure in whom abortion is not possible should have complete hemodynamic monitoring during parturition and for several days thereafter. Segmental epidural anesthesia and lateral positioning of the patient minimize hemodynamic alterations during labor and delivery. Nitroprusside and dobutamine may be effective for treatment of congestive heart failure.
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PMID:Peripartum heart failure due to primary pulmonary hypertension. 687 14

Dopamine is commonly used to improve cardiac output and to maintain peripheral perfusion after myocardial injury. It has several advantages over other catecholamines. At effective inotropic dose levels, dopamine produces less peripheral vasoconstriction than norepinephrine. Dopamine also causes fewer arrhythmias than isoproterenol. This is a case report of a heart transplant patient who began rejecting and developed heart failure. In addition to the immunosuppressive agents, dopamine was used initially as the vasopressor with marked deterioration in the patient's condition. Dobutamine, a new inotropic agent, was substituted for dopamine with subsequent improvement in cardiac function. The authors concluded that dobutamine may be the most appropriate agent to use in the rejecting transplanted heart because of the former's direct action on the heart. Dobutamine may also be preferred for support of the cardiac outputs of patients with chronic heart failure.
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PMID:Dobutamine in the rejecting transplanted heart. 701 1

Heart failure is a syndrome with distinct clinical signs and symptoms. The severity of cardiac failure and a deterioration in functional capacity can be determined by a progressive exercise test and by the noninvasive determination of maximum oxygen uptake. In patients with severe cardiac failure refractory to medica therapy, particularly those with cardiomyopathy or ischemic heart disease, survival is seriously compromised, resembling the most serious malignancy. Cardiotonic agents may be useful in improving the quality of life, provided that they are effective and are given sufficiently early in the course of the disease. Dobutamine given intravenously augments cardiac performance and improves renal function in patients with very advanced disease refractory to multiple diuretics; long-term survival, however, remains dismal. Amrinone appears to be a promising agent for the long-term treatment of chronic cardiac failure; the utility of pirbuterol, an oral catecholamine analog, remains to be determined.
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PMID:Cardiotonic agents in the management of chronic cardiac failure. 706 6

We studied the hemodynamic effects of dobutamine in 10 patients with severe chronic heart failure due to congestive cardiomyopathy in 5, to ischemic heart disease in 4 and to hypertensive cardiomyopathy in 1. Dobutamine was injected during three periods of 30 min each alternated with equal periods of placebo at doses of 2,5-5 and 7,5 mcg/Kg/min respectively. The most favorable hemodynamic effects, obtained at an infusion rate of 5 mcg/Kg/min, was characterized by a significant inn 4 and to hypertensive cardiomyopathy in 1. Dobutamine was injected during three periods of 30 min each alternated with equal periods of placebo at doses of 2,5-5 and 7,5 mcg/Kg/min respectively. The most favorable hemodynamic effects, obtained at an infusion rate of 5 mcg/Kg/min, was characterized by a significant increase of the cardiac index and of the left ventricle stroke work index, accompanied by a significant decrease of the left ventricular filling pressure and of the systemic and pulmonary vascular resistance. The hemodynamic monitoring showed that the pharmacological effects of the drug subsided about 5-10 min after the interruption of infusion. At the infusion rate of 7,5 mcg/Kg/min we observed a significant increase of premature ventricular beats in 3 patients. We conclude that dobutamine at the dose of 5 mcg/Kg/min shows a powerfull positive inotropic action not accompanied by apparent side effects.
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PMID:[Hemodynamic effects of dobutamine in patients with severe low-output heart failure (author's transl)]. 719 52

The hemodynamic effects of dobutamine were compared with those of digoxin in six patients with cardiac failure within 24 hours of onset of acute myocardial infarction. Dobutamine (8.5 microgram per kilogram of body weight per minute) was given intravenously for 30 minutes and then discontinued until hemodynamics returned toward base line. Digoxin (12.5 microgram per kilogram) was then given intravenously, and hemodynamics were recorded for 90 minutes. Dobutamine decreased left ventricular filling pressure (from 22.3 to 9.8 mm Hg, P < 0.02) and systemic vascular resistance (1686 +/- 188 to 1259 +/- 108 dynes . sec . cm-5), and increased cardiac index (from 2.4 to 3.2 liters per minute per square meter of body-surface area, P < 0.005) and stroke work index (from 24.6 to 36.6 g . m per square meter, P < 0.02), without changing heart rate or arterial pressure. In contrast, digoxin had no effect on filling pressure (18.3 versus 17.0) and only a slight effect on cardiac index (2.2 versus 2.4, P < 0.05) and stroke work index (21.9 versus 27.6, P < 0.05). Thus, dobutamine markedly increased cardiac output, decreased filling pressure, and relieved pulmonary congestion. Digoxin, did not affect preload or afterload.
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PMID:A comparison of digoxin and dobutamine in patients with acute infarction and cardiac failure. 741 2

Dobutamine is a new inotropic agent that may induce prolonged clinical improvement in patients with congestive cardiomyopathy. Sixteen patients with severe heart failure but without obstructive coronary disease were studied by serial functional class determinations and by noninvasive measurements of left ventricular function before and after bedrest control period and then after a 3-day infusion of dobutamine. An endomyocardial biopsy procedure was performed on 11 patients before and after the bedrest and on all 16 patients before and after dobutamine. Quantitative ultrastructural analysis of the biopsies was performed on electron micrographs (31,200 X) by a grid technique. The number of electron dense particles per 100 mitochondria did not change after bedrest but there was a significant decrease from 84 +/- 14 to 65 +/- 12 (P < .005) in the pre- to postdobutamine biopsies. The cristae to matrix ratio of the mitochondria did not change with bedrest but improved from 0.37 +/- 0.04 to 0.47 +/- 0.05 (P < .02) after dobutamine. The average mitochondrial size did not change significantly in the bedrest control nor in the dobutamine biopsy samples. However, when the 16 patients were divided into those who had a good clinical response (by functional class and noninvasive measurements of left ventricular function) and those who had no or little response, the 10 responders did decrease their average mitochondria size from 0.26 +/- 0.03 mu 2 to 0.23 +/- 0.02 mu 2 (P < .02). The mechanism by which a 3-day infusion of dobutamine induces a prolonged clinical improvement is not well understood. The use of quantitative ultrastructural technique in this study has demonstrated that there is a morphologic basis to the improvement.
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PMID:Improvement of human myocardial mitochondria after dobutamine: a quantitative ultrastructural study. 744 13

Intravenous inotropic agents promote increased myocardial contractility via elevation of myocyte calcium concentrations, a mechanism that is also known to promote the development of cardiac arrhythmias. The purpose of this article is to review the electrophysiologic effects and relative potential for proarrhythmia associated with dobutamine, dopamine, and the phosphodiesterase inhibitors amrinone and milrinone. Dobutamine increases sinoatrial node automaticity and decreases atrial and atrioventricular (AV) node refractoriness and AV nodal conduction time. The drug also decreases ventricular refractoriness in both healthy and ischemic myocardium. Dobutamine has been shown to increase heart rate in a dose-related fashion in animals and in humans. In humans, dobutamine has been reported to induce ventricular ectopic activity (VEA) in 3% to 15% of patients, although VEAs are often asymptomatic, requiring no intervention. Ventricular tachycardia (VT) associated with dobutamine appears to occur rarely. Patients with underlying arrhythmias or heart failure or those receiving excessive doses of dobutamine are at greatest risk for proarrhythmia. Dopamine increases automaticity in Purkinje fibers and has a biphasic effect on action potential duration. Dopamine has been reported to induce atrial or ventricular arrhythmias in animals. In humans, dopamine may be associated with dose-related sinus tachycardia but has also been reported to cause VEA, which is usually asymptomatic. Dopamine-associated VT appears to occur rarely. Dopamine produces greater elevations in heart rate or frequency of ventricular premature beats at a given value of cardiac index than does dobutamine. The phosphodiesterase inhibitors amrinone and milrinone increase conduction through the AV node and decrease atrial refractoriness. Intravenous administration of these drugs may result in sinus tachycardia in some patients and has been reported to cause VEA, which is often asymptomatic, in up to 17% of patients. VT has also been reported in association with short-term use of intravenous phosphodiesterase inhibitors. In summary, intravenous inotropic agents may be associated with proarrhythmic effects in some patients. The primary arrhythmias reported are sinus tachycardia and VEA, although other supraventricular or ventricular arrhythmias have been reported less commonly. However, clinically significant proarrhythmic effects associated with these agents appear to occur rarely, and, at conventional doses, intravenous inotropic agents are relatively safe with respect to proarrhythmic effects.
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PMID:Electrophysiologic and proarrhythmic effects of intravenous inotropic agents. 756 5


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