This study investigates the long-term effects of lipoprotein(a) (Lp(a)) on coronary artery plaque progression, high-risk plaque formation, and pericoronary adipose tissue inflammation. The study included 267 patients with suspected coronary artery disease who underwent repeated coronary computed tomography angiography (CCTA) imaging over a 10-year period. Lp(a) levels were measured using an isoform-insensitive assay, and CCTA scans were analyzed using an artificial intelligence-based algorithm. Key findings include: - Patients with Lp(a) levels of 125 nmol/L or higher had significantly higher percent atheroma volume (PAV) and percent noncalcified plaque volume compared to those with lower Lp(a) levels. - Every doubling of Lp(a) levels resulted in an additional 0.32% increase in PAV during the 10-year follow-up. - Patients with higher Lp(a) levels had an increased prevalence of low-density noncalcified plaque and pericoronary adipose tissue inflammation. - The association between Lp(a) and plaque progression was adjusted for clinical risk factors, including age, sex, and other cardiovascular risk factors. The study concludes that elevated Lp(a) levels are associated with increased coronary plaque burden, more rapid progression of coronary plaque, and higher rates of low-density noncalcified plaque and pericoronary inflammation. These findings suggest that Lp(a) plays a significant role in the development of high-risk, inflammatory, and rupture-prone plaques, which may explain the increased risk of myocardial infarction observed in previous studies.This study investigates the long-term effects of lipoprotein(a) (Lp(a)) on coronary artery plaque progression, high-risk plaque formation, and pericoronary adipose tissue inflammation. The study included 267 patients with suspected coronary artery disease who underwent repeated coronary computed tomography angiography (CCTA) imaging over a 10-year period. Lp(a) levels were measured using an isoform-insensitive assay, and CCTA scans were analyzed using an artificial intelligence-based algorithm. Key findings include: - Patients with Lp(a) levels of 125 nmol/L or higher had significantly higher percent atheroma volume (PAV) and percent noncalcified plaque volume compared to those with lower Lp(a) levels. - Every doubling of Lp(a) levels resulted in an additional 0.32% increase in PAV during the 10-year follow-up. - Patients with higher Lp(a) levels had an increased prevalence of low-density noncalcified plaque and pericoronary adipose tissue inflammation. - The association between Lp(a) and plaque progression was adjusted for clinical risk factors, including age, sex, and other cardiovascular risk factors. The study concludes that elevated Lp(a) levels are associated with increased coronary plaque burden, more rapid progression of coronary plaque, and higher rates of low-density noncalcified plaque and pericoronary inflammation. These findings suggest that Lp(a) plays a significant role in the development of high-risk, inflammatory, and rupture-prone plaques, which may explain the increased risk of myocardial infarction observed in previous studies.