Lipoprotein(a) (Lp(a)) is a major risk factor for atherosclerotic cardiovascular disease. A study of 267 patients with suspected coronary artery disease who underwent serial coronary computed tomography angiography (CCTA) over 10 years found that higher Lp(a) levels were associated with increased coronary plaque burden, more rapid plaque progression, and increased presence of low-density noncalcified plaque and pericoronary adipose tissue inflammation. Patients with Lp(a) levels of 125 nmol/L or higher had twice the percent atheroma volume compared to those with lower levels. Adjusted for other risk factors, every doubling of Lp(a) levels was linked to an additional 0.32% increase in atheroma volume over 10 years. Higher Lp(a) levels were also associated with increased odds of low-density plaque at baseline and follow-up, as well as increased pericoronary adipose tissue attenuation. These findings suggest that elevated Lp(a) levels contribute to the development of high-risk, inflammatory, rupture-prone plaques over the long term. The study highlights the importance of Lp(a) in coronary atherogenesis and suggests that Lp(a)-lowering therapies may be beneficial for patients with high Lp(a) levels. The results emphasize the need for further research into the effects of Lp(a)-lowering therapies on plaque burden and pericoronary inflammation. The study also notes that Lp(a) levels are largely genetically determined and stable over time, which supports their use as a risk factor for cardiovascular disease. The findings have important implications for clinical practice, as they suggest that Lp(a) levels should be considered in the management of patients at risk for atherosclerotic cardiovascular disease.Lipoprotein(a) (Lp(a)) is a major risk factor for atherosclerotic cardiovascular disease. A study of 267 patients with suspected coronary artery disease who underwent serial coronary computed tomography angiography (CCTA) over 10 years found that higher Lp(a) levels were associated with increased coronary plaque burden, more rapid plaque progression, and increased presence of low-density noncalcified plaque and pericoronary adipose tissue inflammation. Patients with Lp(a) levels of 125 nmol/L or higher had twice the percent atheroma volume compared to those with lower levels. Adjusted for other risk factors, every doubling of Lp(a) levels was linked to an additional 0.32% increase in atheroma volume over 10 years. Higher Lp(a) levels were also associated with increased odds of low-density plaque at baseline and follow-up, as well as increased pericoronary adipose tissue attenuation. These findings suggest that elevated Lp(a) levels contribute to the development of high-risk, inflammatory, rupture-prone plaques over the long term. The study highlights the importance of Lp(a) in coronary atherogenesis and suggests that Lp(a)-lowering therapies may be beneficial for patients with high Lp(a) levels. The results emphasize the need for further research into the effects of Lp(a)-lowering therapies on plaque burden and pericoronary inflammation. The study also notes that Lp(a) levels are largely genetically determined and stable over time, which supports their use as a risk factor for cardiovascular disease. The findings have important implications for clinical practice, as they suggest that Lp(a) levels should be considered in the management of patients at risk for atherosclerotic cardiovascular disease.