HUMAN VENTRICULAR ACTION-POTENTIAL DURATION DURING SHORT AND LONG CYCLES - RAPID MODULATION BY ISCHEMIA

Background Mechanisms underlying the initiation of ventricular arrhyth mias in ischemia by a premature beat or after a pause remain unclear. The kinetics of electrical restitution, which is the modulation of act ion potential duration (APD) by an abrupt alteration in cycle length, may be important. Methods and Results We recorded one or two simultane ous monophasic action potentials (MAPs) from the right ventricular sep tum during balloon occlusion of the left anterior descending coronary artery (LAD) (14 patients), which is expected to induce ischemia at th e recording site, and during occlusion of the right coronary artery (R CA) (7 patients), which is not expected to induce ischemia at the reco rding area. The latter acted as a control. A test pulse sequence was i ncorporated whereby during steady-state pacing, test beats of altered cycle length were interposed. During LAD occlusion, APD for basic beat s shortened from 260+/-4 to 236+/-4 ms (P<.0001), whereas the control group (RCA occlusion) showed no significant change (251+/-7 to 249+/-9 ms; P=NS). LAD occlusion resulted in flattening of the slope relating APD of test beats to diastolic interval (P=.001), whereas in the cont rol group (RCA occlusion) the slope remained unchanged. Similar result s were obtained during a second occlusion. Conclusions LAD occlusion i n patients during balloon angioplasty shortened MAP duration of basic beats and minimized, abolished, or reversed the normal APD/diastolic-i nterval relation of test beats of altered cycle length at sites served by the occluded vessel. The results suggest that ischemia flattens th e electrical restitution curve in the human endocardium. These finding s may have important implications in arrhythmogenesis.