It is well known that the incidence of left ventricular (LV) thrombosis is high in patients with acute myocardial infarction (AMI). Due to the high degree of structural homology with plasminogen, lipoprotein(a) may produce thrombogenic effects by modulating the fibrinolytic system. However, the role of Lp(a) level in the formation of LV thrombus has not been studied. This study sought to determine whether Lp(a) is a risk factor for LV thrombus in patients with AMI.
We have analyzed clinical, echocardiographic and biochemical data in 102 consecutive patients (aged 58 ± 12 years; 92 men / 10 women) with first anterior AMI. Two-dimensional examination was performed on days 1, 3, 7, 15, and 30. Blood samples were obtained within 12 h after the onset of symptoms and before beginning the therapy. Plasma levels of fibrinogen and Lp(a) were measured using enzyme-linked immunosorbent assay and immunonephelometric methods, respectively. LV thrombus was detected in 20 (20.3 %) patients. No significant difference was found for admission Lp(a) levels between patients with or without thrombus (30.5 ± 17.2 vs 32.3 ± 22.4 mg / dl, p = 0.7). Univariate analysis showed that patients with LV thrombus had a higher wall motion score index (1.8 ± 0.3 vs 1.4 ± 0.3, p = 0.002), a higher peak creatine kinase level (2945 ± 898 vs 1805 ± 1336, I / U p = 0.004), a larger end-diastolic volume (139.7 ± 38.6 vs 114.1 ± 41.8 ml, p = 0.04), a larger end-systolic volume (83.1 ± 34.3 vs 59.2 ± 30.6 ml, p = 0.02 ), and a lower ejection fraction (38 ± 12 vs 47 ± 11, p = 0.04). In multivariate analyses, only peak creatine kinase level (p = 0.04) and LV wall motion score index (p = 0.002) were independent predictors of left ventricular thrombus formation.
These results suggest that Lp (a) is not a risk factor for LV thrombus in patients with AMI. Our data demonstrate that the best predictors of LV thrombus formation after AMI are a high peak creatine kinase level and a high LV wall motion score index.