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Improved global or segmental wall motion following revascularization suggests potential reversibility of ischemic left ventricular dysfunction in coronary artery disease (CAD). This study evaluates the effectiveness of post-extra systolic potentiation (PESP) to detect latent residual contractile function. Quantitative left ventriculography was performed in 15 patients with CAD (including seven with significant asynergy) and in three normal controls. During the ventriculogram, a single extra-systole was introduced by an R-wave coupled stimulator (R-stimulus interval averaged 398 msec, with an average mA of 2.4). PESP improved segmental axis shortening in 51 of 55 normal axes and 15 of 17 hypokinetic or akinetic axes. It also increased both ejection fraction and mean rate of circumferential fiber shortening in 17 of 18 patients. No significant arrhythmia occurred with this technique. A single interposed beat with PESP in one ventriculogram is a safe, effective method to detect residual potential contractile function in myocardium that may be hypokinetic or akinetic under conditions of the study.

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

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