Abstract
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 (QTpa), assigned to earliest epicardial RT (RTepi), and (Tp-Txd), the rate-invariant interval from Tp to the inflection point (Txd) at T wave downstroke. (Tp-Txd) defines the crossmural RT gradient (XMRTgrad). Transmural RTgrad (TMRTgrad) is obtained as CosΘ(Rmax|Tmax)*XMRTgrad, where Θ is the spatial angle between the maximal QRS and T vectors. Derived endocardial variables are the XMRTendo, equal to QTpa + XMRTgrad and TMRTendo, equal to QTpa + TMRTgrad. Noting that excitation time (ET) and RT define APD, APDepi = RTepi - QRp in V6 and TMAPDendo = TMRTendo - 10 milliseconds. Compared to the reference group, the estimates for APDepi and TMAPDendo were shortened in STEMI by 20 and 31 milliseconds, respectively, (p <0.001 for both) signifying transmural ischemia. In contrast, in NSTEMI, TMAPDendo was shortened by 28 milliseconds (P <0.001) with a lesser, 5 millisecond shortening of APDepi, 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 APDepi 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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