Oliva P B, Hammill S C, Edwards W D
Heart Research and Education Association of Colorado, Rose Medical Center, Denver 80220.
Circulation. 1993 Sep;88(3):896-904. doi: 10.1161/01.cir.88.3.896.
The ECG recognition of diffuse pericarditis following acute myocardial infarction has been based on changes of the ST segment and, to a lesser extent, alterations of the PQ segment. No ECG criteria exist for the diagnosis of postinfarction regional pericarditis. Recently, it was observed that the T wave evolution follows an atypical pattern before fatal free wall rupture and that this pattern is due to the associated pericarditis. Therefore, this study was conducted on 200 patients with acute myocardial infarction to further elucidate the sensitivity and specificity of the atypical T wave changes in patients with regional postinfarction pericarditis without rupture and to assess the affect of lytic treatment on the rapidity and amplitude of postinfarction T wave evolution.
An analysis of the clinical courses and serial ECGs of 200 consecutive patients with acute myocardial infarction was performed. Among 43 patients with postinfarction pericarditis, the pattern of T wave evolution consistently differed from the customary postinfarction pattern of T wave evolution. This unusual evolutionary course was expressed as either persistently positive T waves 48 or more hours after infarction (67%) or premature, gradual reversal of inverted T waves to positive deflections (33%). The sensitivity and specificity of these T wave alterations were 100% and 77%, respectively. The only other processes identified that caused this type of postinfarction T wave evolution were cardiopulmonary resuscitation, reinfarction, and very small infarcts. Both reperfusion, as judged by the creatine kinase-MB curve, and patency, as assessed by the angiogram, were correlated with the rapidity and depth of T wave inversion. Ninety percent of patients with reperfusion attained a maximum T wave negativity of 3 mm or more within 48 hours after the onset of chest pain in the lead that initially displayed the greatest ST segment elevation. Seventy-six percent of patients without reperfusion attained a maximum negativity of 2 mm or less within 72 hours. Thus, like the ST segment, accelerated evolution and deepening of the T wave may be noninvasive markers of reperfusion.
First, premature reconcordancy of the ST segment and T wave after acute myocardial infarction is a sensitive, reasonably specific, and easily recognizable ECG manifestation of postinfarction regional pericarditis. Second, reperfusion is associated with accelerated evolution and deepening of the T waves following acute myocardial infarction.
急性心肌梗死后弥漫性心包炎的心电图识别一直基于ST段改变，在较小程度上还基于PQ段改变。目前尚无诊断心肌梗死后局限性心包炎的心电图标准。最近观察到，在致命性游离壁破裂前T波演变呈非典型模式，且这种模式是由相关的心包炎所致。因此，本研究对200例急性心肌梗死患者进行，以进一步阐明非典型T波改变在无破裂的心肌梗死后局限性心包炎患者中的敏感性和特异性，并评估溶栓治疗对心肌梗死后T波演变速度和幅度的影响。
对200例连续的急性心肌梗死患者的临床病程和系列心电图进行分析。在43例心肌梗死后心包炎患者中，T波演变模式始终不同于心肌梗死后T波演变的常规模式。这种异常演变过程表现为梗死48小时或更长时间后T波持续正向（67%），或倒置T波过早、逐渐转为正向波（33%）。这些T波改变的敏感性和特异性分别为100%和77%。确定的导致这种心肌梗死后T波演变的其他唯一过程是心肺复苏、再梗死和非常小的梗死灶。根据肌酸激酶-MB曲线判断的再灌注以及根据血管造影评估的通畅情况均与T波倒置的速度和深度相关。90%的再灌注患者在胸痛发作后48小时内，在最初ST段抬高最明显的导联中T波最大负向幅度达到3mm或更大。76%的未再灌注患者在72小时内最大负向幅度达到2mm或更小。因此，与ST段一样，T波加速演变和加深可能是再灌注的无创性标志。
第一，急性心肌梗死后ST段和T波过早一致是心肌梗死后局限性心包炎敏感、特异性尚可且易于识别的心电图表现。第二，再灌注与急性心肌梗死后T波加速演变和加深相关。
