Detection of latent function in acutely ischemic myocardium in the dog: comparison of pharmacologic inotropic stimulation and postextrasystolic potentiation.

Abstract

In poorly perfused myocardium with resultant ischemic dysfunction, augmentation of contractility can, under certain conditions, be used to detect viable but ordinarily noncontracting muscle. Two methods of inotropic augmentation, pharmacologic inotropic stimulation and postextrasystolic potentiation (PESP), were studied in acutely ischemic canine myocardium with controlled coronary blood flow. A caliper length gauge to record segmental shortening and left ventricular pressure was used to construct pressure-length loops. Acute regional ischemia depressed segmental function: early segmental shortening decreased (-20 ± 0.02% [SE]) and frequent dyskinesia occurred. Restoring coronary blood flow corrected segmental shortening to control levels. During acute regional ischemia, PESP consistently augmented segmental function (+49 ± 0.03%) and abolished dyskinesia. Pharmacologic inotropic stimulation with isoproterenol or calcium administered into the coronary arteries did not produce a comparable improvement in segmental function (+9 ± 0.05%). Although early shortening markedly increased with pharmacologic stimulation, there was no consistent change in total shortening, and the area of the pressure-length loop decreased. Due to late dyskinesia, there was a decrease in injection shortening. Systemically administered pharmacologic agents accentuated early dyskinesia but caused no consistent change in total shortening. Unlike PESP, pharmacologic agents either worsened segmental function or caused responses that were minimum and inconsistent; such responses clearly cannot be used to identify viable ischemic myocardium. KEY WORDS

Quantification of synchronous contraction of left ventricle in normal subjects using ECG-gated-SPECT images

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The effect of verapamil on mechanical performance of acutely ischemic and reperfused myocardium in the conscious dog.

“…It is well recognized that segmental systolic shortening is impaired promptly and markedly in ischemic zones of myocardium following coronary occlusion. Postextrasystolic potentiation of systolic shortening still may be elicited for a short time (Dyke et al, 1975;Crozatier et al, 1977;Boden et al, 1978) but, within 10 minutes, this is also abolished in the subendocardium (Crozatier et al, 1977). Studies using length gauges attached to the epicardium indicate that stable postextrasystolic potentiation may persist in this location for up to two hours (Boden et al, 1980), perhaps due to better perfusion known to exist in the epicardial myocardium.…”

Effects of nitroglycerin, postextrasystolic potentiation, and pacing-induced ischaemia on wall motion in patients with ischaemic heart disease.

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