Postischemic functional recovery and BMIPP uptake after primary percutaneous transluminal coronary angioplasty in acute myocardial infarction.

To correlate asynergic wall motion after primary percutaneous transluminal coronary angioplasty with myocardial perfusion and fatty acid metabolism, quantitative tomographies using thallium and radioiodinated 15-(p-iodophenyl)-3-R,S-methylpentadecanoic acid (BMIPP) were performed during the acute and recovery stages in 56 consecutive patients with acute myocardial infarction, of whom 32 underwent primary percutaneous transluminal coronary angioplasty (group A) and 24 were conservatively treated (group B); 44 patients (79%) had 1-vessel disease. Reduced myocardial uptakes of thallium and BMIPP and regional wall motion were quantified with a bull's eye technique and a centerline method using contrast left ventriculography, respectively. BMIPP activity was significantly lower than that of thallium at an acute stage in both groups. Abnormal BMIPP activities and the difference in thallium and BMIPP abnormalities (perfusion metabolism mismatch) at an acute stage decreased significantly during follow-up in group A (111 +/- 13 to 99 +/- 12 and 30 +/- 10 to 15 +/- 10, respectively), and not in group B (129 +/- 31 vs 118 +/- 29 and 29 +/- 13 vs 30 +/- 10, respectively). Improvement in regional wall motion abnormality correlated closely with the improved uptakes of thallium and BMIPP (y = 0.64x + 26.4, r = 0.56, p < 0.05; y = 1.1x + 11.1, r = 0.81, p < 0.001; respectively). The mismatched uptake of both tracers at an acute stage was significantly related to recovery from asynergic wall motion during follow-up in group A (y = 0.45x + 13.9, r = 0.65, p < 0.005). In conclusion, despite restored myocardial perfusion by primary coronary angioplasty, BMIPP uptake is impaired in salvaged myocardium at an acute stage of infarction. However, the degree and improvement of perfusion metabolism mismatch in acute myocardial infarction may reflect subsequent recovery from postischemic wall motion abnormality in metabolically impaired but viable myocardium after coronary reperfusion.