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Serum lipoprotein(a) and its relation to left ventricular thrombus in patients with acute myocardial infarction
Insights
Lipoprotein(a) does not appear to be a risk factor for left ventricular (LV) thrombus formation in patients with acute myocardial infarction (AMI). Peak creatine kinase levels and LV wall motion score index are the best predictors of LV thrombus after AMI.
Area of Science:
- Cardiology
- Biochemistry
- Thrombosis
Background:
- Left ventricular (LV) thrombosis is common in acute myocardial infarction (AMI).
- Lipoprotein(a) (Lp(a)), due to its structural similarity to plasminogen, may influence fibrinolysis and thrombosis.
- The specific role of Lp(a) levels in LV thrombus formation post-AMI remains understudied.
Purpose of the Study:
- To investigate whether Lp(a) levels are a risk factor for LV thrombus development in patients experiencing their first anterior AMI.
- To identify independent predictors of LV thrombus formation in this patient cohort.
Main Methods:
- Analysis of clinical, echocardiographic, and biochemical data from 102 patients with first anterior AMI.
- Echocardiography performed serially on days 1, 3, 7, 15, and 30 post-AMI.
- Plasma Lp(a) and fibrinogen levels measured via enzyme-linked immunosorbent assay and immunonephelometry, respectively, within 12 hours of symptom onset.
Main Results:
- LV thrombus was detected in 20.3% of patients.
- No significant difference in admission Lp(a) levels was observed between patients with and without LV thrombus (30.5±17.2 vs 32.3±22.4 mg/dl, p=0.7).
- Independent predictors for LV thrombus formation identified through multivariate analysis were higher peak creatine kinase levels (p=0.04) and higher LV wall motion score index (p=0.002).
Conclusions:
- Lp(a) is not identified as a risk factor for LV thrombus formation in patients with AMI.
- Elevated peak creatine kinase levels and impaired LV wall motion are significant predictors of LV thrombus development following AMI.
Abstract:
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.
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