Myocardial perfusion and oxygen consumption in reperfused noninfarcted dysfunctional myocardium after unstable angina - Direct evidence for myocardial stunning in humans

OBJECTIVES To positively establish the diagnosis of myocardial stunning in patients with unstable angina and persistent wall motion abnormalities afte r reperfusion by coronary angioplasty. BACKGROUND Although myocardial stunning is thought to occur in several clin ical conditions, definite proof of its existence in humans is still lacking , owing to the difficulty of measuring myocardial blood flow (MBF) in absol ute terms. METHODS We studied 14 patients with unstable angina due to proximal left an terior descending coronary artery disease who presented persistent anterior wall motion abnormalities despite revascularization of the culprit lesion by percutaneous coronary angioplasty (PTCA) and who did not have clinical e vidence of necrosis. Dynamic positron emission tomography (PET) with [N-13] -ammonia and [C-11]-acetate was performed 48 h after PTCA to determine abso lute MBF and oxygen consumption (MVO2). Regional wall thickening and region al cardiac work were determined using two-dimensional echocardiography. Imp rovement of segmental wall motion abnormalities nas followed for a median o f 4 months (1.5 to 14 months). RESULTS As judged from the changes in segmental wall motion score, regional dysfunction was spontaneously reversible in 12/14 patients and improved fr om 2.2 +/- 0.3 to 1.2 +/- 0.3 at late follow-up (p < 0.001). With PET, [13N ]-ammonia MBF was similar among dysfunctional and remote normally contracti ng segments (85 +/- 29 vs. 99 +/- 20 ml.min(-1).100g(-1), p = not significa nt [n.s.]), thus demonstrating a perfusion-contraction mismatch. Despite th e reduced contractile function, dysfunctional myocardium presented near nor mal levels of MVO2, (6.5 +/- 4.2 vs. 8.0 +/- 1.9 ml.min(-1).100g(-1), p = n .s.). Consequently, the regional myocardial efficiency (regional work divid ed by MVO2) of the dysfunctional myocardium was found to be markedly decrea sed as compared with normally contracting myocardium (6 +/- 6% vs. 26 +/- 6 %, p < 0.001). CONCLUSIONS This study demonstrates that human dysfunctional myocardium cap able of spontaneously recovering contractile function after unstable angina endures a state of perfusion-contraction mismatch. These data for the firs t time provide unequivocal direct evidence for the existence of acute myoca rdial stunning in humans. (C) 1999 by the American College of Cardiology.