Abstract Body (Do not enter title and authors here): Background: Elevated lipoprotein(a) (Lp[a]) is an independent, causal, genetic risk factor for CVD. While increasing infarct size corresponds with poor outcomes, it is unknown whether Lp(a) is associated with infarct size.
Objective: To understand if elevated Lp(a), including intermediate risk (30–50 mg/dL) is associated with increasing infarct size, especially in patients (pts) with premature atherosclerosis (<55 and <65 years in men and women, respectively).
Methods: Data from pts referred for coronary computed tomography angiography (CCTA) and enrolled in the Lp(a) subanalysis of the Genetic Loci and the Burden of Atherosclerotic Lesions (GLOBAL) study (NCT01738828) were analyzed. Lp(a) was measured at the time of CCTA between 2012–2014; Lp(a) data were later validated. Cases were defined by history of myocardial infarction. Infarct size was measured by contrast-enhanced CT and analyzed in a core laboratory. The left ventricle was analyzed visually based on a 17-segment model; infarct size was determined as the number of segments with discernible infarct. Lp(a) (mg/dL) was measured by latex-enhanced immunoturbidimetric assay; apolipoprotein B (apoB; mg/dL) was measured by antigen–antibody turbidimetric assay. The association between Lp(a) and infarct size was determined by Spearman’s correlation, and the independent association of Lp(a) measurements across the apoB range was determined by generalized covariance. Data were adjusted for age, sex, and apoB.
Results: Overall, 800 pts were included: 74.8% male; median (range) age: 61.0 (55.0–68.0) and 57.0 (52.0–65.0) years for cases and controls, respectively (both n=400). Median Lp(a) mass: 11.1 (IQR 41.1; upper limit of Q1, Q3: 5.3, 46.4) mg/dL. Circulating Lp(a) levels and lifetime cumulative exposure to Lp(a) (age multiplied by Lp[a]) correlated with infarct size (rho=0.07 and 0.09, respectively; Fig A, B). Higher Lp(a) levels were associated with significantly larger infarct size vs lower Lp(a) levels (P=0.014; Fig C). Infarct size was significantly larger in pts with Lp(a) levels >30 mg/dL or >50 mg/dL and premature atherosclerosis (P=0.016 and P=0.035, respectively; Fig D, E), but not in pts with nonpremature atherosclerosis. When conditioned on apoB, increasing Lp(a) was associated with increasing infarct size (rho=0.487; Fig F).
Conclusions: Our findings suggest that elevated Lp(a) >30 mg/dL is independently associated with increasing infarct size, particularly in pts with premature atherosclerosis.