Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 1980;62:28-34

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Benotti, J. R.
Right arrow Articles by Carabello, B. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Benotti, J. R.
Right arrow Articles by Carabello, B. A.

Circulation, Vol 62, 28-34, Copyright © 1980 by American Heart Association


ARTICLES

Effects of amrinone on myocardial energy metabolism and hemodynamics in patients with severe congestive heart failure due to coronary artery disease

JR Benotti, W Grossman, E Braunwald and BA Carabello

Amrinone has been shown to exhibit a potent inotropic effect in patients with heart failure secondary to congestive cardiomyopathy, but its effects on myocardial oxygen consumption (MVO2) and coronary blood flow (CBF) are unknown. Accordingly, the hemodynamic, myocardial metabolic and ECG responses to amrinone (2.5 mg/kg i.v. over 1 hour) were measured in nine patients with congestive heart failure secondary to coronary artery disease. Increases were observed in cardiac index (1.3 +/- 0.4 to 2.2 +/- 0.7 l/min/m2) and left ventricular stroke work (10.6 +/- 3.0 to 19.2 +/- 6.3 g-m/m2), and decreases in mean pulmonary wedge (31 +/- 5 to 26 +/- 4 mm Hg), mean pulmonary artery (44 +/- 8 to 36 +/- 7 mm Hg) and mean right atrial pressures (18 +/- 4 to 10 +/- 4 mm Hg), myocardial arteriovenous oxygen difference (129 +/- 19 to 109 +/- 17 ml/l), CBF (215 +/- 117 to 178 +/- 84 ml/min) and MVO2 (27 +/- 14 to 19 +/- 9 ml/min). All changes were significant (p less than 0.01). No significant changes occurred in aortic mean pressure, heart rate, myocardial lactate extraction or ECG, and no patient developed angina. In explaining the decline in MVO2, it is possible that the increase in contractility was more than offset by the reductions in preload and afterload. The amrinone-induced hemodynamic improvement in patients with congestive heart failure secondary to coronary artery disease was associated with reductions in MVO2 and CBF and no evidence of myocardial ischemia.


This article has been cited by other articles:


Home page
ANN INTERN MEDHome page
S. M. Hollenberg, C. J. Kavinsky, and J. E. Parrillo
Cardiogenic Shock
Ann Intern Med, July 6, 1999; 131(1): 47 - 59.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
J. C. Sill, B. Bertha, I. Berger, C. Uhl, M. Nugent, and J. Folts
Human Platelet Ca2+ Mobilization, Glycoprotein IIb/IIIa Activation, and Experimental Coronary Thrombosis In Vivo in Dogs Are All Inhibited by the Inotropic Agent Amrinone
Circulation, September 2, 1997; 96(5): 1647 - 1653.
[Abstract] [Full Text]


Home page
Ann. Thorac. Surg.Home page
R. Gitter, J. M. Anderson Jr, and G. K. Jett
Influence of Milrinone and Norepinephrine on Blood Flow in Canine Internal Mammary Artery Grafts
Ann. Thorac. Surg., May 1, 1996; 61(5): 1367 - 1371.
[Abstract] [Full Text]


Home page
ANN INTERN MEDHome page
J. A. FRANCIOSA
Intravenous Amrinone: An Advance or a Wrong Step?
Ann Intern Med, March 1, 1985; 102(3): 399 - 400.
[Abstract] [PDF]


Home page
ANN INTERN MEDHome page
R. E. RUDE, J. E. MULLER, and B. EUGENE
Efforts to Limit the Size of Myocardial Infarcts
Ann Intern Med, December 1, 1981; 95(6): 736 - 761.
[Abstract] [PDF]