title: Energetic consequences of substances currently used or recommended for long-term treatment of chronic heart failure.
abstract: 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 effects of vasodilators and inotropic agents on myocardial mechanics and energetics in patients with congestive heart failure New York Heart Association (NYHA) classes II-III. In these patients, who underwent routine heart catheterization, myocardial oxygen consumption was measured using the argon method, and LV pressure and geometry were obtained from LV angiography using a Millar microtipped catheter. 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 LV pressure, LV wall thickness, and LV 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, beta 1-agonists and phosphodiesterase inhibitors increased myocardial oxygen consumption independently of changes in the stress-time integral. In conclusion, vasodilators decrease LV 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 inotropic substances, especially beta 1-agonists, increase myocardial oxygen consumption with only minor changes of systolic stress-time integral.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Cardiology, Medizinische Universitätsklinik Freiburg.
authors.forename: C
authors.initials: C
authors.lastname: Holubarsch
authors.forename: G
authors.initials: G
authors.lastname: Hasenfuss
authors.forename: L
authors.initials: L
authors.lastname: Thierfelder
authors.forename: H
authors.initials: H
authors.lastname: Just
mesh_terms: D001552:Benzazepines / Q000494:pharmacology; D002316:Cardiotonic Agents / Q000494:pharmacology*; D004734:Energy Metabolism / Q000187:drug effects; D017335:Enoximone; D006333:Heart Failure / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology; D009206:Myocardium / Q000378:metabolism; D009599:Nitroprusside / Q000494:pharmacology; D010101:Oxygen Consumption / Q000187:drug effects; D011412:Propanolamines / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology*; D017307:Xamoterol
chemical_list: D001552:Benzazepines; D002316:Cardiotonic Agents; D007093:Imidazoles; D011412:Propanolamines; D014665:Vasodilator Agents; D009599:Nitroprusside; D017307:Xamoterol; D017335:Enoximone; C044946:benazepril