Relation of plasma lipoprotein(a) with myocardial viability and left ventricular performance in survivors of myocardial infarction

Abstract

Previous studies have reported that high serum lipoprotein(a) levels may be responsible for total occlusion of the infarct-related artery via inhibition of intrinsic fibrinolysis during acute myocardial infarction. We evaluated whether this would result in a greater extent of myocardial necrosis and impaired left ventricular function in patients with high lipoprotein(a) levels. Sixty-eight patients with prior myocardial infarction, who were not receiving thrombolytic therapy underwent coronary angiography and stress-redistribution-reinjection T1-201 scintigraphy. Antegrade TIMI flow in the infarct-related artery was lower (1.54 ± 1.14 vs 2.15 ± 1.05; p = 0.03) and the collateral index was higher (1.3 ± 1.0 vs 0.8 ± 0.9; p = 0.07) in patients with high lipoprotein(a) levels (> 30 mg/dl) compared to those with low lipoprotein(a) levels (≤ 30 mg/dl). Regional wall motion score index was lower (0.8 ± 0.8 vs 1.4 + 0.5; P = 0.008) and global ejection fraction was higher (46 ± 10% vs 40 ± 11%; p = 0.03) in patients with low lipoprotein(a) levels. On SPECT images, the number of nonviable defects was higher in patients with high lipoprotein(a) levels (4.0 ± 2.5 vs 1.9 ± 1.3; p = 0.0002), whereas the number of viable defects was higher in those with low lipoprotein(a) levels (2.5 ± 1.8 vs 1.5 ± 1.3; p = 0.02). We conclude that high lipoprotein(a) levels may prolong the occlusion of infarct-related artery during acute myocardial infarction and lead to a greater extent of myocardial necrosis and impaired left ventricular function.