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

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 less than 0.01), and exercise duration also increased by 1.8 +/- 3.5 minutes (p less than 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 long-term 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.

This article has been cited by other articles:

				A Ohlsson, S.H Kubo, D Steinhaus, D.T Connelly, S Adler, C Bitkover, R Nordlander, L Ryden, and T Bennett Continuous ambulatory monitoring of absolute right ventricular pressure and mixed venous oxygen saturation in patients with heart failure using an implantable haemodynamic monitor: results of a 1 year multicentre feasibility study Eur. Heart J., June 1, 2001; 22(11): 942 - 954. [Abstract] [PDF]

				A. E. Steimle, L. W. Stevenson, C. Chelimsky-Fallick, G. C. Fonarow, M. A. Hamilton, J. D. Moriguchi, A. Kartashov, and J. H. Tillisch Sustained Hemodynamic Efficacy of Therapy Tailored to Reduce Filling Pressures in Survivors With Advanced Heart Failure Circulation, August 19, 1997; 96(4): 1165 - 1172. [Abstract] [Full Text]

				J. R. Wilson, G. Rayos, T. K. Yeoh, P. Gothard, and K. Bak Dissociation Between Exertional Symptoms and Circulatory Function in Patients With Heart Failure Circulation, July 1, 1995; 92(1): 47 - 53. [Abstract] [Full Text]

				J. Abrams Vasodilator Therapy for Chronic Congestive Heart Failure JAMA, December 6, 1985; 254(21): 3070 - 3074. [Abstract] [PDF]