Gibson R S, Beller G A, Gheorghiade M, Nygaard T W, Watson D D, Huey B L, Sayre S L, Kaiser D L
Circulation. 1986 Jun;73(6):1186-98. doi: 10.1161/01.cir.73.6.1186.
Despite having smaller infarct size and better left ventricular function, patients with non-Q wave myocardial infarction (NQMI) appear to have an unexpectedly high long-term mortality that is ultimately comparable to that of patients with Q-wave myocardial infarction (QMI). Patients with NQMI may lose their initial prognostic advantage because there is more viable tissue in the perfusion zone of the infarct-related vessel, rendering myocardium more prone to reinfarction. We tested this hypothesis in a prospective study of 241 consecutive patients 65 years of age or younger with acute uncomplicated myocardial infarction confirmed by creatine kinase levels (MB fraction). All patients received customary care and none underwent thrombolytic therapy or emergency angioplasty. Predischarge coronary angiography, radionuclide ventriculography, 24 hr Holter monitoring, and quantitative thallium-201 (201T1) scintigraphy during treadmill exercise were performed 10 +/- 3 days after infarction. Infarcts were designated as QMI (n = 154) or NQMI (n = 87) by accepted criteria applied to serial electrocardiograms obtained on days 1, 2, 3, and 10. The baseline Norris coronary prognostic index, angiographic jeopardy scores, and prevalence of Lown grade ventricular arrhythmias were similar between groups despite evidence for less necrosis with NQMI vs QMI, reflected by lower peak creatine kinase levels (520 vs 1334 IU/liter; p = .0001, 4 hr sampling), higher resting left ventricular ejection fraction (53% vs 46%; p = .0001), fewer akinetic or dyskinetic segments (1.2 vs 2.4; p = .0001), and fewer persistent 201Tl defects in the infarct zone (0.9 vs 1.9; p = .0001). Patients with NQMI also had more patent infarct-related vessels (54% vs 25%; p less than .0001) and a shorter time from onset of infarction to peak creatine kinase level (16.9 vs 22.5 hr; p = .0001). Importantly, the prevalence and extent of quantitatively determined 201Tl redistribution within the infarct zone on exercise scintigraphy was greater in patients with NQMI vs those with QMI (60% vs 36%, p = .007; and 0.98 vs 0.53 myocardial segments, p = .0003); when the two groups were stratified on the basis of the infarct-related vessel, subset analysis revealed the same findings. During 30 months median follow-up, cardiac mortality was low, 8.4% in the QMI group and 9.2% in the NQMI group (p = NS).(ABSTRACT TRUNCATED AT 400 WORDS)
尽管非Q波心肌梗死(NQMI)患者的梗死面积较小,左心室功能较好,但其长期死亡率却出人意料地高,最终与Q波心肌梗死(QMI)患者相当。NQMI患者可能会失去其最初的预后优势,因为梗死相关血管灌注区内有更多存活组织,使心肌更容易再次梗死。我们在一项前瞻性研究中对241例年龄在65岁及以下、经肌酸激酶水平(MB组分)确诊为急性非复杂性心肌梗死的连续患者进行了验证。所有患者均接受常规治疗,无人接受溶栓治疗或急诊血管成形术。在梗死后10±3天进行出院前冠状动脉造影、放射性核素心室造影、24小时动态心电图监测以及运动平板试验期间的定量铊-201(201Tl)闪烁显像。根据第1、2、3和10天获得的系列心电图采用公认标准将梗死分为QMI(n = 154)或NQMI(n = 87)。尽管与QMI相比,NQMI的坏死证据较少(通过较低的肌酸激酶峰值水平反映,520 vs 1334 IU/L;p = 0.0001,4小时采样)、静息左心室射血分数较高(53% vs 46%;p = 0.0001)、运动减弱或运动障碍节段较少(1.2 vs 2.4;p = 0.0001)以及梗死区持续性201Tl缺损较少(0.9 vs 1.9;p = 0.0001),但两组间的基线诺里斯冠状动脉预后指数、血管造影危险评分以及洛恩分级室性心律失常的患病率相似。NQMI患者梗死相关血管通畅的也更多(54% vs 25%;p < 0.0001),从梗死发作到肌酸激酶峰值水平的时间更短(16.9 vs 22.5小时;p = 0.0001)。重要的是,运动闪烁显像时NQMI患者梗死区内定量测定的201Tl再分布的患病率和范围高于QMI患者(60% vs 36%,p = 0.007;以及0.98 vs 0.53个心肌节段,p = 0.0003);当两组根据梗死相关血管进行分层时,亚组分析显示了相同的结果。在30个月的中位随访期内,心脏死亡率较低,QMI组为8.4%,NQMI组为9.2%(p = 无显著差异)。(摘要截断于400字)