Effect of Inotropic Agents on the Localized Dyskinesis of Acutely Ischemic Myocardium
An Experimental Ultrasound Study
The response of the segmental dyskinesis of acutely ischemic myocardium to inotropic agents has not been well characterized. We studied this in detail in open-chest anesthetized dogs. Acute myocardial ischemia was produced by coronary ligation and confirmed by histologic studies. Ultrasound recordings obtained by direct reflection off the ischemic posterior wall revealed characteristic dyskinesis: aneurysmal bulging during isometric contraction and markedly reduced mean posterior wall velocity (PWVm), and excursion during ventricular ejection. Isoproterenol (I), norepinephrine (N), ouabain (O), glucagon (G), and propranolol (P) were then administered intravenously in graded doses. The response to these agents consisted of two discordant elements. There was a significant (P < 0.01) increase in aneurysmal bulging during isometric contraction with isoproterenol (5 ± 0 to 6 ± 0 mm) and ouabain (4 ± 0 to 5 ± 0 mm). However, during the ventricular ejection phase PWVm increased with isoproterenol (12 ± 1 to 26 ± 2 mm/sec), glucagon (12 ± 2 to 22 ± 2 mm/sec), norepinephrine (12 ± 1 to 17 ± 1 mm/sec), and ouabain (8 ± 1 to 12 ± 2 mm/sec). Simultaneous hemodynamic measurements showed the drugs elevated cardiac output (G > I > 0) and left ventricular dp/dt ( I > G > N).
Inotropic agents thus have two opposing effects on the dyskinesis of acutely ischemic myocardium: increased aneurysmal bulging during isometric contraction, but improved wall velocity during ventricular ejection. The latter contributes to the drug-induced improvement in over-all ventricular performance and also indicates that acutely ischemic myocardium retains the capacity to respond to pharmacologic stimuli.
- Coronary artery occlusion
- Ventricular aneurysm
- Segmental motion abnormality
- Posterior wall velocity
- Received September 7, 1973.
- Accepted February 4, 1974.
- © 1974 American Heart Association, Inc.