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局部动作电位持续时间和复极时间子间期的心电图估计显示,急性冠状动脉综合征中缺血诱导的异常从整体QT间期无法明显看出。

Electrocardiographic estimates of regional action potential durations and repolarization time subintervals reveal ischemia-induced abnormalities in acute coronary syndrome not evident from global QT.

作者信息

Rautaharju Pentti M, Gregg Richard E, Zhou Sophia H, Startt-Selvester Ron H

机构信息

Division of Public Health Sciences, Wake Forest University School of Medicine, Winston-Salem, NC, USA.

出版信息

J Electrocardiol. 2011 Nov-Dec;44(6):718-24. doi: 10.1016/j.jelectrocard.2011.08.007.

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 (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.

摘要

我们分别评估了5376名健康男性和女性参考组以及125名急性冠状动脉综合征患者(其中657名无诊断性ST段抬高,分别为非ST段抬高型心肌梗死[NSTEMI]和ST段抬高型心肌梗死[STEMI])初始和终末复极期的复极时间(RTs)和动作电位时程(APD)的心电图估计值。该模型中的两个关键协变量是速率校正QT峰间期(QT(pa)),指定为最早的心外膜RT(RT(epi)),以及(T(p)-T(xd)),即从T波下降支的T(p)到拐点(T(xd))的速率不变间期。(T(p)-T(xd))定义了跨壁RT梯度(XMRT(grad))。跨壁RT梯度(TMRT(grad))通过CosΘ(R(max)|T(max))*XMRT(grad)获得,其中Θ是最大QRS向量和T向量之间的空间角度。推导的心内膜变量为XMRT(endo),等于QT(pa)+XMRT(grad),以及TMRT(endo),等于QT(pa)+TMRT(grad)。注意到激动时间(ET)和RT定义了APD,V6导联中APD(epi)=RT(epi)-QR(p),TMAPD(endo)=TMRT(endo)-10毫秒。与参考组相比,STEMI组中APD(epi)和TMAPD(endo)的估计值分别缩短了20毫秒和31毫秒(两者p<0.001),表明存在透壁性缺血。相比之下,在NSTEMI组中,TMAPD(endo)缩短了28毫秒(P<0.001),APD(epi)缩短较少,为5毫秒,表明存在心内膜下缺血。STEMI组中QT延长了6毫秒(P<0.05),NSTEMI组中QT延长了8毫秒(P<0.001)。QT延长而APD(epi)缩短表明,终末可能非缺血区域的复极延长是两个心肌梗死组QT延长的原因。复极模型揭示的缺血诱导的复极异常区域表现的这些显著差异,从整体QT评估中并不明显。

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