Preinfarction angina as a major predictor of left ventricular function and long-term prognosis after a first Q wave myocardial infarction.

OBJECTIVES

The purpose of this study was to assess the prognostic significance of preinfarction angina after a first Q wave myocardial infarction. Patients with anterior or inferior myocardial infarction were compared.

BACKGROUND

The effect of preinfarction angina on prognosis after anterior and inferior myocardial infarction remains unclear.

METHODS

A total of 291 patients with a first Q wave anterior (n = 171) or inferior (n = 120) myocardial infarction were examined to assess the effect of preinfarction angina on short- and long-term prognosis. The relation between predischarge left ventriculographic findings and preinfarction angina was also examined.

RESULTS

The presence of preinfarction angina was associated with lower peak creatine kinase activity, a lower in-hospital incidence of sustained ventricular tachycardia and fibrillation and a lower incidence of pump failure and cardiac mortality in patients with either anterior or inferior infarction. Among patients with anterior infarction, preinfarction angina was associated with a lower incidence of cardiac rupture and less need for readmission for heart failure within 1 year after the onset of infarction. In this subgroup it was also associated with a higher ejection fraction, a smaller end-diastolic volume and a lower incidence of aneurysm formation noted on ventriculography during convalescence. In patients with inferior infarction, these variables did not differ significantly in the presence or absence of preinfarction angina. Multivariate analysis confirmed that the presence of preinfarction angina was an independent predictor of development of ventricular aneurysm, late phase heart failure and 1-year cardiac mortality.

CONCLUSIONS

The presence of preinfarction angina has a favorable effect on infarct expansion and late phase left ventricular function, especially in patients with anterior myocardial infarction. The mechanisms responsible for this phenomenon are not known but may be secondary to limitations of infarct size through unidentified mechanisms other than collateralization (e.g., ischemic preconditioning).