Acute non-Q wave myocardial infarction associated with early ST segment elevation: Evidence for spontaneous coronary reperfusion and implications for thrombolytic trials

The clinical significance of early ST segment elevation in patients with non-Q wave infarction is unknown. Therefore, 150 consecutive patients with creatine kinase isoenzyme-confirmed acute uncomplicated myocardial infarction who had ST segment elevation of 1 mm or more in at least two contiguous leads on the admission electrocardiogram were analyzed. None received thrombolytic therapy or acute coronary angioplasty. Predis-charge angiography, radionuclide ventriculography and exercise thallium-201 scintigraphy were performed 10 ± 3 days after myocardial infarction. Based on serial electrocardiograms (on days 1, 2, 3 and 10), all 150 infarcts were classified as Q wave (n = 115 [77%]) or non-Q wave (ri = 35 [23%]). Although patients with Q wave infarction exhibited greater ST elevation, the amount observed in the non-Q wave group was appreciable, as reflected by the number of leads with ST elevation (3.8 ±1.8 versus 3.1 ± 1.2, p = 0.007) and the sum of the ST elevation (9.6 ± 7.4 versus 6.2 ± 6.2 mm, p = 0.016). When compared with the Q wave group, patients with non-Q wave infarction had a shorter time to peak creatine kinase (23.0 ± 9.1 versus 15.8 ± 7.9 hours, p = 0.0001), a higher infarct vessel patency rate (24 versus 57%, p = 0.001), lower peak creatine kinase values based on 4 hour sampling (1,372 ± 964 versus 664 ± 924 IU/liter, p = 0.0002) and a higher left ventricular ejection fraction (46 ± 12% versus 54 ± 9%, p = 0.0003). Among all admission historic and electrocardiographic data available for the 95 patients without pathologic Q waves on the admission electrocardiogram, two variables were found to be independent predictors of infarct type: a history of prior infarction and ST segment elevation between 1 and 2 mm. The presence of these two variables correctly identified 24 (69%) of 35 patients with non-Q wave infarction, whereas their absence identified, 43 (72%) of 60 patients with Q waves. In summary, the pathogenesis Of non-Q wave myocardial infarction in some patients may involve spontaneous coronary reperfusion characterized by early peaking of serum enzyme levels and a high prevalence of patent infarct vessels, which results in better left ventricular function and regional perfusion. These results may have implications for the design of thrombolytic trials because 23% of all patients with early ST elevation evolved non-Q wave infarction with a late infarct vessel patency rate approaching that seen in patients treated with thrombolytic agents.