PMID- 1827977 OWN - NLM STAT- MEDLINE DCOM- 19910625 LR - 20131121 IS - 0300-8428 (Print) IS - 0300-8428 (Linking) VI - 86 Suppl 1 DP - 1991 TI - Energetic consequences of substances currently used or recommended for long-term treatment of chronic heart failure. PG - 107-12 AB - 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) FAU - Holubarsch, C AU - Holubarsch C AD - Department of Cardiology, Medizinische Universitatsklinik Freiburg. FAU - Hasenfuss, G AU - Hasenfuss G FAU - Thierfelder, L AU - Thierfelder L FAU - Just, H AU - Just H LA - eng PT - Journal Article PL - Germany TA - Basic Res Cardiol JT - Basic research in cardiology JID - 0360342 RN - 0 (Benzazepines) RN - 0 (Cardiotonic Agents) RN - 0 (Imidazoles) RN - 0 (Propanolamines) RN - 0 (Vasodilator Agents) RN - 169D1260KM (Nitroprusside) RN - 7HE0JQL703 (Xamoterol) RN - C7Z4ITI7L7 (Enoximone) RN - UDM7Q7QWP8 (benazepril) SB - IM MH - Benzazepines/pharmacology MH - Cardiotonic Agents/*pharmacology MH - Energy Metabolism/drug effects MH - Enoximone MH - Heart Failure/*drug therapy/metabolism/physiopathology MH - Hemodynamics/drug effects MH - Humans MH - Imidazoles/pharmacology MH - Myocardium/metabolism MH - Nitroprusside/pharmacology MH - Oxygen Consumption/drug effects MH - Propanolamines/pharmacology MH - Vasodilator Agents/*pharmacology MH - Xamoterol EDAT- 1991/01/01 00:00 MHDA- 1991/01/01 00:01 CRDT- 1991/01/01 00:00 PHST- 1991/01/01 00:00 [pubmed] PHST- 1991/01/01 00:01 [medline] PHST- 1991/01/01 00:00 [entrez] PST - ppublish SO - Basic Res Cardiol. 1991;86 Suppl 1:107-12.