We evaluated electrocardiogram estimates of repolarization times (RTs) and action potential durations (APD) separately for initial and terminal repolarization periods in a reference group of 5376 healthy men and women and in 125 acute coronary syndrome patients with and 657 without diagnostic ST elevation (ST-elevation myocardial infarction [STEMI] and non-STEMI [NSTEMI], respectively). Two key covariates in the model are the rate-adjusted QT peak interval (QT(pa)), assigned to earliest epicardial RT (RT(epi)), and (T(p)-T(xd)), the rate-invariant interval from T(p) to the inflection point (T(xd)) at T wave downstroke. (T(p)-T(xd)) defines the crossmural RT gradient (XMRT(grad)). Transmural RT(grad) (TMRT(grad)) is obtained as CosΘ(R(max)|T(max))*XMRT(grad), where Θ is the spatial angle between the maximal QRS and T vectors. Derived endocardial variables are the XMRT(endo), equal to QT(pa) + XMRT(grad) and TMRT(endo), equal to QT(pa) + TMRT(grad). Noting that excitation time (ET) and RT define APD, APD(epi) = RT(epi) - QR(p) in V6 and TMAPD(endo) = TMRT(endo)--10 milliseconds. Compared to the reference group, the estimates for APD(epi) and TMAPD(endo) were shortened in STEMI by 20 and 31 milliseconds, respectively, (p < 0.001 for both) signifying transmural ischemia. In contrast, in NSTEMI, TMAPD(endo) was shortened by 28 milliseconds (P < 0.001) with a lesser, 5 millisecond shortening of APD(epi), signifying subendocardial ischemia. QT was prolonged by 6 milliseconds in STEMI (P < 0.05) and by 8 milliseconds in NSTEMI (P < 0.001). Prolonged QT with shortened APD(epi) suggests that prolonged repolarization in terminal possibly non-ischemic regions accounts for QT prolongation in both myocardial infarction groups. These substantial differences in ischemia-induced regional manifestations of repolarization abnormalities revealed by the repolarization model were not evident from evaluation of the global QT.
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