Left ventricular geometry, myocardial function and energetics of the dilated left ventricle. Influence of vasodilators and positive inotropic substances.
Vasodilators have been shown to improve hemodynamics of the failing heart as a short-term effect and to decrease mortality as a long-term result. We therefore studied the effect of different vasodilators on myocardial mechanics and energetics in patients with idiopathic dilated cardiomyopathy (IDC) NYHA II to III. In these patients undergoing routine heart catheterization myocardial oxygen consumption was measured using the argon method, and left ventricular pressure and geometry were obtained from left ventricular angiography using a Millar tip microcatheter. All data were analyzed for one single heart beat. The best correlation was found between MVO2/beat and the systolic stress-time integral which considers left ventricular pressure, wall thickness, and geometry. The relation between MVO2/beat and peak systolic wall stress was less relevant. No correlation was found between MVO2/beat and pressure-volume work, dP/dtmax, and mean velocity of circumferential fiber shortening. The intravenous application of nitroprusside and the ACE-inhibitor benazepril decreased both the systolic stress-time integral and the myocardial oxygen consumption in proportion to each other indicating unchanged economy of myocardial contraction. In contrast to other vasodilators, beta 1-agonists and phosphodiesterase inhibitors increase myocardial oxygen consumption independently of changes in the stress-time integral. In conclusion, vasodilators decrease left ventricular pressure and chamber size and thereby proportionally reduce MVO2/beat. The reduction of energy needed for myocardial contraction may partially explain the long-term effects of the ACE-inhibitors and combinations of vasodilators. Pure positive inotropic substances, especially beta 1-agonists, increase myocardial oxygen consumption with minor changes of systolic stress-time integral.(ABSTRACT TRUNCATED AT 250 WORDS)
Holubarsch
C
C
Department of Cardiology, Medizinische Universitätsklinik Freiburg.
Hasenfuss
G
G
Thierfelder
L
L
Just
H
H
D002306:Cardiac Volume / Q000187:drug effects* / Q000502:physiology; D002311:Cardiomyopathy, Dilated / Q000188:drug therapy* / Q000503:physiopathology; D002316:Cardiotonic Agents / Q000627:therapeutic use*; D004734:Energy Metabolism / Q000187:drug effects* / Q000502:physiology; D006333:Heart Failure / Q000188:drug therapy* / Q000503:physiopathology; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D006801:Humans; D009200:Myocardial Contraction / Q000187:drug effects* / Q000502:physiology; D014665:Vasodilator Agents / Q000627:therapeutic use*; D016277:Ventricular Function, Left / Q000187:drug effects* / Q000502:physiology
D002316:Cardiotonic Agents; D014665:Vasodilator Agents