Very low Lp(a) levels (<75 nmol/L) were associated with worse acute myocardial damage and higher 1-year mortality and recurrent MI rates after STEMI.
Is lipoprotein(a) level associated with myocardial damage and 1-year clinical outcomes in patients with STEMI?
In patients with STEMI, very low Lp(a) levels may be associated with worse acute myocardial damage on CMR, though this does not appear to translate into statistically significant differences in final myocardial damage or 1-year clinical outcomes.
Absolute Event Rate: 0% vs 0%
Abstract Background Lipoprotein(a) Lp(a) is an independent risk factor for ST-segment elevation myocardial infarction (STEMI) and associated with adverse outcomes. However, its direct association with myocardial damage after STEMI is unknown. Purpose We aimed to investigate the association between Lp(a) and myocardial damage and 1-year clinical outcomes in patients with STEMI. Methods This study recruited consecutive patients with STEMI. All patients with plasma Lp(a) level tested since admission were included. Acute and final myocardial damage were assessed with cardiac magnetic resonance (CMR) during index admission and after 90 days. The association between continuous Lp(a) and cardiac damage was analyzed with spearman correlation and logistic regression. The differences in CMR outcomes were then compared among low (75 nmol/L), middle (75-125 nmol/L) and high (125 nmol/L) Lp(a) groups based on Lp(a) threshold consensus. Cox proportional hazards regression was applied to analyze the association between categorical Lp(a) groups and 1-year clinical outcomes including all-cause mortality, cardiovascular mortality, and recurrent myocardial infarction. Results A total of 526 patients had Lp(a) measured since admission. The median of Lp(a) level was 24 nmol/L (interquartile range IQR 20 to 104 nmol/L). When assessing Lp(a) on a continuous scale, lower Lp(a) was associated with worse acute cardiac damage including larger infarct size, lower myocardial salvage index (MSI), and higher prevalence of microvascular obstruction (MVO). A total of 365 (69.4%) had Lp(a) 75 nmol/L, 57 (10.8%) had Lp(a) ranging from 75 to 125 nmol/L, and 104 (19.8%) had Lp(a) 125 nmol/L. There was a trend towards worse acute myocardial damage including larger infarct size (median from 9.5 to 15.1), lower MSI (median from 57 to 49) and higher prevalence of MVO (from 33.7% to 40.5%) presented from high to low Lp(a) groups. The low Lp(a) group had the highest incidence rate of 1-year clinical outcomes (5.5% in all-cause mortality, 3.0% in cardiovascular mortality and 3.6% in recurrent myocardial infarction). Continuous or categorical Lp(a) was not associated with final myocardial damage or 1-year clinical outcomes. Conclusions Very low Lp(a) level may be associated with worse acute myocardial damage and higher incidence rate of 1-year clinical outcomes after STEMI.
Zhou et al. (Sat,) reported a other. Very low Lp(a) levels (<75 nmol/L) were associated with worse acute myocardial damage and higher 1-year mortality and recurrent MI rates after STEMI.