Hemodynamic effects of vasodilators and long-term response in heart failure

• Published in: Journal of the American College of Cardiology 1984-06, Vol.3 (6), p.1521-1530
• Main Authors: Franciosa, Joseph A., Dunkman, W. Bruce, Leddy, Cheryl L.
• Format: Article
• Language: English
• Subjects: Antihypertensive Agents - therapeutic use; Biological and medical sciences; Captopril - therapeutic use; Cardiovascular system; Dipeptides - therapeutic use; Enalapril; Exercise Test; Heart Failure - drug therapy; Hemodynamics - drug effects; Humans; Isosorbide Dinitrate - therapeutic use; Male; Medical sciences; Middle Aged; Minoxidil - therapeutic use; Oxygen Consumption - drug effects; Pharmacology. Drug treatments; Pulmonary Wedge Pressure - drug effects; Stroke Volume - drug effects; Vascular Resistance - drug effects; Vasodilator Agents - therapeutic use; Vasodilator agents. Cerebral vasodilators
• ISSN: 0735-1097; 1558-3597
• DOI: 10.1016/S0735-1097(84)80292-2

Hemodynamic responses to vasodilators are commonly assessed when starting long-term vasodilator treatment in patients with chronic left ventricular failure, although the relation between short- and long-term responses is not established. Thus, short- and long-term hemodynamic responses to placebo and vasodilators (isosorbide dinitrate, minoxidil and enalapril or captopril) were measured and long-term clinical efficacy was assessed by changes in exercise capacity after 1 to 5 months of vasodilator administration (plus digitalis and diuretic agents) in 46 patients with New York Heart Association functional class II to IV heart failure caused by cardiomyopathy. There were no significant changes in hemodynamics or exercise capacity during placebo treatment. After initial doses and during long-term administration of vasodilator drugs, hemodynamics were significantly improved. After long-term vasodilator treatment, maximal oxygen uptake during exercise increased by 2.9 ± 5.7 ml/min per kg from a control value of 14.1 ± 5.6 ml/min per kg (p < 0.01), and exercise duration also increased by 1.8 ± 3.5 minutes (p < 0.01). Changes in maximal oxygen uptake, however, did not correlate with short-term changes in pulmonary wedge pressure (correlation coefficient [r] = -0.14), cardiac index (r = -0.01) or systemic vascular resistance (r = -0.20). Long-term hemodynamic changes also failed to correlate with changes in exercise capacity. Baseline hemodynamics, cardiac dimensions and left ventricular ejection fraction before vasodilator administration all failed to correlate with baseline exercise capacity or with longterm changes in exercise capacity. Thus, hemodynamic measurements at initiation or during follow-up of vasodilator therapy do not relate to long-term clinical efficacy assessed by exercise capacity in patients with chronic left ventricular failure. Therefore, the rationale for making invasive hemodynamic measurements before initiating long-term vasodilator therapy for heart failure is questioned.