Efficacy of prazosin in the management of chronic congestive heart failure: A 6-month randomized, double-blind, placebo-controlled study

Markham, Roy V.; Corbett, James R.; Gilmore, Alyce; Pettinger, William A.; Firth, Brian G.

doi:10.1016/0002-9149(83)90310-7

Cited by 86 publications

(16 citation statements)

References 35 publications

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“…Short-term clinical results have shown that prazosin therapy provides favorable hemodynamic responses such as reduced pulmonary venous congestion, improved end-diastolic and -systolic volumes, increased CBF, CO, and improved New York Heart Association functional class (4,6,9,11,17,22,41,43,57). However, these responses were attenuated in the long-term (11,17), and there was no improvement in mortality (9).…”

Section: Discussionmentioning

confidence: 99%

Muscle metaboreflex-induced coronary vasoconstriction limits ventricular contractility during dynamic exercise in heart failure

Coutsos

Sala‐Mercado

Ichinose

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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Muscle metaboreflex activation (MMA) during dynamic exercise increases cardiac work and myocardial O2 demand via increases in heart rate, ventricular contractility, and afterload. This increase in cardiac work should lead to metabolic coronary vasodilation; however, no change in coronary vascular conductance occurs. This indicates that the MMA-induced increase in sympathetic activity to the heart, which raises heart rate, ventricular contractility, and cardiac output, also elicits coronary vasoconstriction. In heart failure, cardiac output does not increase with MMA presumably due to impaired ability to improve left ventricular contractility. In this setting actual coronary vasoconstriction is observed. We tested whether this coronary vasoconstriction could explain, in part, the reduced ability to increase cardiac performance during MMA. In conscious, chronically instrumented dogs before and after pacing-induced heart failure, MMA responses during mild exercise were observed before and after α1-adrenergic blockade (prazosin 20-50 μg/kg). During MMA, the increases in coronary vascular conductance, coronary blood flow, maximal rate of left ventricular pressure change, and cardiac output were significantly greater after α1-adrenergic blockade. We conclude that in subjects with heart failure, coronary vasoconstriction during MMA limits the ability to increase left ventricular contractility.

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Section: Discussionmentioning

confidence: 99%

Muscle metaboreflex-induced coronary vasoconstriction limits ventricular contractility during dynamic exercise in heart failure

Coutsos

Sala‐Mercado

Ichinose

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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“…The majority of drugs used to treat this condition, including diuretics and most vasodilators, stimulate renin release further (Nicholls et al, 1974(Nicholls et al, , 1976Markham et al, 1983;Pouleur et al, 1983). High circulating levels of angiotensin II are likely to place an added burden on the failing heart by means of a direct constrictor action on arterioles (and perhaps veins), and indirectly through stimulation of aldosterone secretion.…”

Section: Discussionmentioning

confidence: 99%

Enalapril in heart failure.

Nicholls¹,

Ikram²,

Espiner³

et al. 1984

Brit J Clinical Pharma

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Serum MK‐422 and plasma angiotensin converting enzyme activity were measured during the introduction of enalapril therapy in eight patients with heart failure. In a second study of 16 patients, we recorded exercise tolerance, clinical status and haemodynamics before and after 12 weeks of placebo or enalapril treatment. Increasing doses of enalapril gave step‐wise increments in serum MK‐422. Plasma converting enzyme activity remained low for at least 24 h after each dose of enalapril (5, 10 and 20 mg). Compared to placebo patients (n = 8), those receiving enalapril (n = 8) tended to improve their exercise performance and clinical status, and showed a fall in right heart pressures after 12 weeks of treatment.

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“…Vasodilator therapy with prazosin affects neither HR nor mortality, whereas the combination of hydralazine and isosorbide dinitrate reduces mortality without affecting HR [35][36][37].…”

Section: Clinical Studiesmentioning

confidence: 98%

Is Heart Rate Reduction Beneficial to Patients with Chronic Congestive Heart Failure?

Henriksen¹,

Gadsbøll

2002

Heart Drug

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It has been suggested that drugs for the treatment of heart failure which lower heart rate (HR) have a beneficial effect on mortality, whereas the reverse is true for drugs that increase HR. The objective of this review was to examine the relationship between drug-induced changes in HR and prognosis in heart failure. We reviewed the epidemiological, pathophysiological and clinical evidence of a possible relationship between HR and mortality in heart failure patients. Several heart failure drugs improve patient status and survival without affecting HR. However, part of the beneficial effect of beta-blockers must be attributed to their effect of slowing HR.

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Efficacy of prazosin in the management of chronic congestive heart failure: A 6-month randomized, double-blind, placebo-controlled study

Cited by 86 publications

References 35 publications

Muscle metaboreflex-induced coronary vasoconstriction limits ventricular contractility during dynamic exercise in heart failure

Muscle metaboreflex-induced coronary vasoconstriction limits ventricular contractility during dynamic exercise in heart failure

Enalapril in heart failure.

Is Heart Rate Reduction Beneficial to Patients with Chronic Congestive Heart Failure?

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