Abstract 1605: High Lipoprotein(a) Level Promotes Both Coronary Atherosclerosis and Myocardial Infarction: A Path Analysis Using a Large Number of Autopsy Cases
[Objective] Lipoprotein(a) [Lp(a)] has two different molecular characteristics: a LDL-like lipoprotein and an anti-plasminogen molecule. We investigated whether hyper-Lp(a) promotes coronary atherosclerosis, acute thrombosis resulting in myocardial infarction (MI), or both.
[Methods] The subjects were 1,062 consecutive autopsy cases (609 men and 453 women) performed at a community-based general geriatric hospital. The mean age at the time of death was 80 years. The coronary stenosis on cut sections was semiquantitatively evaluated. Lp(a) levels of fresh serum taken antemortem were measured by a latex-enhanced turbidimetric immunoassay.
[Results] The prevalence of severe coronary stenosis and MI increased linearly with increasing Lp(a) levels with no apparent threshold. The odds ratios (95% C.I.) of hyper-Lp(a) [2.99 (1.70 –5.28) for 200 –299 mg/L or 3.25 (1.90 –5.54) for ≥ 300 mg/L] for severe coronary stenosis were larger than those of hypertension (2.61), diabetes mellitus (2.09), and hypercholesteremia (2.05). The severe coronary sclerosis was much stronger risk of MI [6.28 (4.33–9.11)] than hyper-Lp(a), hypertension, and diabetes mellitus. A path analysis showed that the Lp(a) levels affected both coronary sclerosis and MI with path coefficients of 0.15 and 0.07 (direct effect), respectively. In cases with severe coronary sclerosis, Lp(a) affected MI (0.15) more than it affected coronary sclerosis (0.10).
[Conclusions] Lp(a) levels have distinct effects on coronary sclerosis and MI with about half of the overall effect on MI being via coronary sclerosis. This result supports the prothrombotic and a probable proinflammatory role of Lp(a) in coronary events.