ABSTRACTDespite 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 201TI defects in the infarct zone (0.9 vs 1.9; p = .0001). Patientswith NQMI also had more patent infarct-related vessels (54% vs 25%; p < .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 201T1 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 followup, cardiac mortality was low, 8.4% in the QMI group and 9.2% in the NQMI group (p = NS). However, patients with NQMI had a higher reinfarction rate (18.4% vs 6.5%; p = .009), a higher rate of unstable angina necessitating hospitalization (36% vs 22%; p = .034), and had a greater incidence of subsequent bypass surgery or angioplasty (33% vs 19%; p = .018). Moreover, 88% of the recurrent infarctions in the NQMI group involved the same area as the original infarction compared with only 20% in the QMI group (p < .01). Thus, in a consecutive series of patients with uncomplicated myocardial infarction who were eligible for predischarge exercise testing, NQMI was characterized by: (1) similar long-term mortality despite a smaller infarct size and better left ventricular function, (2) a higher rate of reinfarction and incidence of angina and bypass surgery at 30 months, and (3) more evidence of residual infarct zone ischemia as compared to patients with QMI. Our data also suggest that the pathogenesis of NQMI may involve spontaneous reperfusion, since 47% of our patients had ST segment elevation on their admission electrocardiograms, the time to peak creatine kinase level was shorter than that in patients with QMI, and 54% of our patients with NQMI had patent infarct-related vessels during predischarge angiography.