Alterations in left ventricular function, coronary hemodynamics and myocardial catecholamine balance with MDL 17043, a new inotropic vasodilator agent, in patients with severe heart failure.
Publication/Presentation Date
2-1-1985
Abstract
To evaluate changes in myocardial energetics and systemic and cardiac sympathetic activity associated with improved left ventricular function after MDL 17043, a new inotropic vasodilator agent, systemic and coronary hemodynamics and myocardial catecholamine balance were determined in 17 patients with severe heart failure. After the administration of MDL 17043, cardiac index increased by 67% and pulmonary capillary wedge pressure decreased (25 +/- 5 to 14 +/- 7 mm Hg, p less than 0.01), indicating improved left ventricular function. Coronary sinus blood flow (75 +/- 29 to 111 +/- 51 ml/min, p less than 0.01) and myocardial oxygen consumption (9.9 +/- 3.3 to 11.8 +/- 5.4 ml/min, p less than 0.05) increased despite decreased myocardial oxygen extraction (11.7 +/- 2 to 10.1 +/- 3.3 vol%, p less than 0.05) and a higher coronary sinus oxygen content. Although transmyocardial lactate extraction remained unchanged, increased myocardial oxygen consumption has potential deleterious effects on myocardial metabolic function. Arterial norepinephrine concentrations and transmyocardial norepinephrine release also remained unchanged. These findings suggest that MDL 17043 improves left ventricular pump function, but produces no detectable change in systemic and cardiac sympathetic activity. Improved left ventricular function is associated with increased myocardial oxygen consumption despite primary coronary vasodilation.
Volume
5
Issue
2 Pt 1
First Page
326
Last Page
332
ISSN
0735-1097
Published In/Presented At
Viquerat, C. E., Kereiakes, D., Morris, D. L., Daly, P. A., Wexman, M., Frank, P., Parmley, W. W., & Chatterjee, K. (1985). Alterations in left ventricular function, coronary hemodynamics and myocardial catecholamine balance with MDL 17043, a new inotropic vasodilator agent, in patients with severe heart failure. Journal of the American College of Cardiology, 5(2 Pt 1), 326–332. https://doi.org/10.1016/s0735-1097(85)80054-1
Disciplines
Medicine and Health Sciences
PubMedID
3155761
Department(s)
Department of Medicine, Cardiology Division
Document Type
Article