Lipoprotein(a)-associated thrombus formation and plaque healing in acute coronary syndromes: insights from optical coherence tomography

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BACKGROUND: Elevated lipoprotein(a) levels are associated with myocardial infarction; however, in-vivo evidence linking lipoprotein(a) to intracoronary thrombosis remains limited. We evaluated phase-specific lipoprotein(a) levels during the hyperacute, acute, and stable phases of acute coronary syndrome and their associations with angiographic and optical coherence tomography findings. METHODS: We analyzed 142 patients with acute coronary syndrome who underwent optical coherence tomography during percutaneous coronary intervention and for whom lipoprotein(a) was measured in the hyperacute (n = 58), acute (n = 125), or stable (n = 51) phases. RESULTS: Baseline demographics, laboratory data, angiographic findings, and optical coherence tomography characteristics were similar across phases. Patients with intracoronary thrombus had significantly higher hyperacute-phase lipoprotein(a) levels than did those without [10.2 (interquartile range: 5.4-18.8) vs. 3.7 (3.0-10.3) mg/dl; P = 0.033]. In addition, a greater increase in lipoprotein(a) from the hyperacute to the acute phase was associated with thrombus presence [12.1 (4.0-18.4) vs. 2.35 (0.0-7.1) mg/dl; P = 0.027]. Conversely, patients with layered plaque on acute-phase optical coherence tomography demonstrated significantly lower stable-phase lipoprotein(a) levels than did those without [4.1 (3.0-7.1) vs. 13.0 (5.7-21.3) mg/dl; P = 0.014]. No significant associations were observed for acute-phase lipoprotein(a) levels. CONCLUSION: Elevated hyperacute-phase lipoprotein(a) levels were associated with intracoronary thrombus, whereas low stable-phase lipoprotein(a) levels were associated with layered plaque. These phase-specific relationships suggest that lipoprotein(a) influences thrombosis and plaque healing in acute coronary syndrome, and that stable-phase lipoprotein(a) levels may better reflect baseline biology and help identify prior subocclusive events.

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