1999 Volume 40 Issue 6 Pages 703-713
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 Tl-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 non-viable 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.
