Key result
Elevated lipoprotein(a) levels were significantly associated with left ventricular systolic dysfunction in patients with chronic total occlusion of the coronary artery (OR 1.149 per 100 mg/L increase).
Why the study?
Although lipoprotein(a) is an established prognostic marker in coronary chronic total occlusion and left ventricular systolic dysfunction is a common complication, the relationship between them required exploration.
Are elevated lipoprotein(a) levels associated with left ventricular systolic dysfunction in patients with chronic total occlusion of the coronary artery?
Cohort (n=309)
No
Are elevated lipoprotein(a) levels associated with left ventricular systolic dysfunction in patients with chronic total occlusion of the coronary artery?
Odds Ratio: 1.149 (95% CI 1.042–1.267)
p-value: p=0.005
Elevated Lipoprotein(a) levels are independently associated with left ventricular systolic dysfunction in patients with chronic total occlusion, and adding Lp(a) to traditional risk models improves risk discrimination.
Lipoprotein(a) [Lp(a)] has been established as a significant prognostic marker in patients with chronic total occlusion (CTO) of the coronary artery. Left ventricular systolic dysfunction (LVSD) is a common and serious complication associated with CTO. This study aimed to explore the relationship between Lp(a) and LVSD in patients with CTO. A total of 309 patients with CTO who underwent elective percutaneous coronary intervention were consecutively enrolled in the study. The patients were stratified by left ventricular ejection fraction (LVEF) into the LVSD group (LVEF < 50%, n = 80) and preserved systolic function group (LVEF ≥ 50%, n = 229). The mean age of the cohort was 61.5 ± 11.3 years, 83.8% were males, and the prevalence of LVSD was 25.9%. Compared with patients with preserved systolic function, those with LVSD tended to be older, had a higher prevalence of arrhythmia, a history of myocardial infarction, and multivessel CTO disease, and exhibited more severe calcified lesions, while having a lower prevalence of hypertension. They also exhibited higher levels of Lp(a), NT-proBNP, and neutrophils, but had a lower body mass index, lower albumin levels, and a reduced LVEF (all P < 0.05). Multivariate regression analysis revealed that Lp(a) was significantly associated with LVSD, with an odds ratio (OR) per 100 mg/L of 1.149 (95% CI: 1.042–1.267; P = 0.005) after adjusting for potential confounding factors. Furthermore, incorporating Lp(a) into a model based on traditional risk factors significantly improved its discriminatory ability for LVSD (AUC = 0.839, 95% CI: 0.786–0.891, P < 0.001). Subgroup analysis indicated that the association between Lp(a) and LVSD was more pronounced in patients with multivessel CTO disease (P for interaction = 0.034). Elevated Lp(a) levels were significantly associated with LVSD in patients with CTO of the coronary artery.
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Xu et al. (2026) conducted a cohort in Chronic total occlusion of the coronary artery (n=309). Lipoprotein(a) vs. Lower Lipoprotein(a) levels was evaluated on Left ventricular systolic dysfunction (LVEF < 50%) (OR 1.149, 95% CI 1.042-1.267, p=0.005). Elevated lipoprotein(a) levels were significantly associated with left ventricular systolic dysfunction in patients with chronic total occlusion of the coronary artery (OR 1.149 per 100 mg/L increase).
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