Demidova Marina M, van der Pals Jesper, Ubachs Joey F A, Kanski Mikael, Engblom Henrik, Erlinge David, Tichonenko Victor M, Platonov Pyotr G
Federal Centre of Heart, Blood and Endocrinology, Akkuratova 2, St. Petersburg, Russian Federation.
J Electrocardiol. 2011 Jan-Feb;44(1):74-81. doi: 10.1016/j.jelectrocard.2010.10.035.
Exacerbation of ST elevation associated with reperfusion has been reported in patients with myocardial infarction. However, the cause of the "reperfusion peak" and relation of its magnitude to the size of myocardial damage has not been explored. The aim of our study was to assess the correlation between the ST-dynamics during reperfusion, the myocardium at risk (MaR), and the infarct size (IS).
Infarction was induced in 15 pigs by a 40-minute-long balloon inflation in the left anterior descending coronary artery. Tetrofosmin Tc 99m was given intravenously after 20 minutes of occlusion, and ex vivo single photon emission computed tomography was performed to assess MaR. Maximal ST elevation in a single lead and maximal sum of ST deviations in 12 leads were measured before, during, and after occlusion from continuous 12-lead electrocardiographic monitoring. A gadolinium-based contrast agent was given intravenously 30 minutes before explantation of the heart. Final IS was estimated using ex vivo cardiac magnetic resonance imaging.
All pigs developed an anteroseptal infarct with MaR = 42% ± 9% and IS = 26% ± 7% of left ventricle. In all pigs, reperfusion was accompanied by transitory exacerbation of ST elevation that measured 1300 ± 500 μV as maximum in a single lead compared with 570 ± 220 μV at the end of occlusion (P < .001). The transitory exacerbation of ST elevation exceeded the maximal ST elevation during occlusion (920 ± 420 μV, P < .05). The ST elevation resolved by the end of the reperfusion period (90 ± 30 μV, P < .001). Exacerbation of ST elevation after reperfusion correlated with the final IS (r = 0.64, P = .025 for maximal ST elevation in a single lead and r = 0.80, P = .002 for sum of ST deviations) but not with MaR (r = 0.43, P = .17 for maximal ST elevation in a single lead and r = 0.49, P = .11 for sum of ST deviations). The maximal ST elevation in a single lead and the sum of ST deviations during occlusion did not correlate with either MaR or final IS.
In the experiment, exacerbation of ST elevation is common during restoration of blood flow in the occluded coronary artery. The magnitude of the exacerbation of ST elevation after reperfusion in experimentally induced myocardial infarction in pigs is associated with infarct size but not with MaR.
心肌梗死患者中已报道了与再灌注相关的ST段抬高加重情况。然而，“再灌注峰值”的原因及其幅度与心肌损伤大小的关系尚未得到探究。我们研究的目的是评估再灌注期间ST段动态变化、危险心肌（MaR）和梗死面积（IS）之间的相关性。
通过在左前降支冠状动脉中进行40分钟的球囊充盈，诱导15头猪发生梗死。闭塞20分钟后静脉注射锝99m替曲膦，并进行离体单光子发射计算机断层扫描以评估MaR。通过连续12导联心电图监测，在闭塞前、闭塞期间和闭塞后测量单导联最大ST段抬高以及12导联ST段偏移总和。在心脏取出前30分钟静脉注射钆基造影剂。使用离体心脏磁共振成像估计最终梗死面积。
所有猪均发生前间壁梗死，MaR为左心室的42%±9%，IS为左心室的26%±7%。在所有猪中，再灌注伴随着ST段抬高的短暂加重，单导联最大ST段抬高为1300±500μV，而闭塞结束时为570±220μV（P<.001）。ST段抬高的短暂加重超过了闭塞期间的最大ST段抬高（920±420μV，P<.05）。ST段抬高在再灌注期结束时恢复（90±30μV，P<.001）。再灌注后ST段抬高加重与最终梗死面积相关（单导联最大ST段抬高时r = 0.64，P = 0.025；ST段偏移总和时r = 0.80，P = 0.002），但与MaR无关（单导联最大ST段抬高时r = 0.43，P = 0.17；ST段偏移总和时r = 0.49，P =
