THE INFLUENCE OF MYOCARDIAL SYSTOLIC SHORTENING ON ACTION-POTENTIAL DURATION FOLLOWING CHANGES IN LEFT-VENTRICULAR END-DIASTOLIC PRESSURE

Introduction: Contraction-excitation feedback may be an important fact or in arrhythmogenesis in patients with heart failure. We have previou sly demonstrated the contrasting effects of raising left ventricular e nd-diastolic pressure on action potential duration in dog and guinea p ig hearts. The current study was undertaken to assess whether these di ffering effects might reflect differences in the effect of varying lef t ventricular end-diastolic pressure on systolic shortening in the two models. Methods and Results: Two models were studied and compared. In open chest dog hearts and isolated guinea pig hearts, measurements of myocardial segment length were made while left ventricular end-diasto lic pressure was raised and lowered at constant left ventricular peak systolic pressure. Action potentials were also recorded while left ven tricular end-diastolic pressure was changed. The dog hearts were studi ed further in a manner aimed at reproducing the contraction pattern of the guinea pig hearts. In the in situ dog heart, elevation of left ve ntricular end-diastolic pressure, and the consequent increase in end-d iastolic segment length, was accompanied by a marked increase in systo lic shortening, such that minimum systolic segment length remained unc hanged. Elevation of left ventricular end-diastolic pressure was accom panied by a prolongation of action potential duration. In the in vitro guinea pig model, elevation of left ventricular end-diastolic pressur e was accompanied by more modest changes in systolic shortening, which were not sufficient to compensate for increased diastolic segment len gth. Consequently, minimum systolic segment length increased as the he arts dilated. Elevation of left ventricular end-diastolic pressure was accompanied by a shortening of action potential duration. In a furthe r series of experiments, the effects of increased left ventricular end -diastolic pressure were studied in the dog model while allowing aorti c pressure to rise, thereby restricting systolic shortening. Under the se circumstances, the dog model was similar to the guinea pig model, w ith an increase in left ventricular end-diastolic pressure causing a s hortening of action potential duration. Conclusion: Our results sugges t that the effects of preload changes on action potential duration dep end on accompanying changes in systolic shortening. This suggests a po ssible role for contraction-excitation feedback in arrhythmogenesis in patients with regional wall-motion abnormalities.