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

B. L. Huey, M. Gheorghiade, R. S. Crampton, G. A. Beller, D. L. Kaiser, D. D. Watson, T. W. Nygaard, G. B. Craddock, S. L. Sayre, R. S. Gibson

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69 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)18-25
Number of pages8
JournalJournal of the American College of Cardiology
Volume9
Issue number1
DOIs
StatePublished - Jan 1 1987

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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    Huey, B. L., Gheorghiade, M., Crampton, R. S., Beller, G. A., Kaiser, D. L., Watson, D. D., Nygaard, T. W., Craddock, G. B., Sayre, S. L., & Gibson, R. S. (1987). Acute non-Q wave myocardial infarction associated with early ST segment elevation: Evidence for spontaneous coronary reperfusion and implications for thrombolytic trials. Journal of the American College of Cardiology, 9(1), 18-25. https://doi.org/10.1016/S0735-1097(87)80076-1