Lipoprotein(a) is an important factor to determine coronary artery plaque morphology in patients with acute myocardial infarction

Background Lipoprotein(a) [Lp(a)] can influence the development and disruption of atherosclerotic plaques through its effect on lipid accumulation. The purpose of this study was to evaluate the relationship between serum Lp(a) levels and plaque morphology of an infarct-related lesion and non-infarct-related lesion of the coronary artery in acute myocardial infarction (AMI).Methods and results Coronary plaque morphology was evaluated in 68 patients (age 62.1 +/- 12.1 years, mean +/- SD; men n=58, women n=10) with AMI by intravascular ultrasound with radiofrequency data analysis before coronary intervention and by 64-slice computed tomography angiography within 2 weeks. Patients were divided into a group with an Lp(a) level of 25 mg/dl or more (n=20) and a group with an Lp(a) level of less than 25 mg/dl (n=48). Intravascular ultrasound with radiofrequency data analysis identified four types of plaque components at the infarct-related lesion: fibrous, fibrofatty, dense calcium, and necrotic core. The necrotic core component was significantly larger in the group with an Lp(a) level of 25 mg/dl or more than in the group with an Lp(a) level of less than 25 mg/dl (27.6 +/- 8.0 vs. 15.7 +/- 10.0%, P=0.0001). Coronary plaques were classified as calcified plaques, noncalcified plaques, mixed plaques, and low-attenuation plaques on 64-slice computed tomography angiography. Computed tomography indicated that the group with an Lp(a) level of 25 mg/dl or more had a greater number of total plaques, noncalcified plaques, and low-attenuation plaques in whole coronary arteries than did the group with an Lp(a) level of less than 25 mg/dl (5.3 +/- 1.8 vs. 3.7 +/- 2.2, P=0.0061; 4.0 +/- 2.0 vs. 1.2 +/- 1.3, P=0.0001; 2.2 +/- 2.1 vs. 0.5 +/- 0.7, P=0.0001, respectively).Conclusion Elevated serum Lp(a) levels are associated with the number of plaques and plaque morphology. Patients with a high Lp(a) level during AMI require more intensive treatment for plaque stabilization.