Search

Background: Elevated levels of lipoprotein(a) (Lp(a)) are independently associated with an increased risk of atherosclerotic cardiovascular disease events. However, the mechanisms driving this association are poorly understood. We aimed to evaluate the association between Lp(a) and coronary plaque characteristics in a contemporary US cohort without clinical atherosclerotic cardiovascular disease, undergoing coronary computed tomography angiography, the noninvasive gold standard for the assessment of coronary atherosclerosis., Methods: We used baseline data from the Miami Heart Study-a community-based, prospective cohort study-which included asymptomatic adults aged 40 to 65 years evaluated using coronary computed tomography angiography. Those taking any lipid-lowering therapies were excluded. Elevated Lp(a) was defined as ≥125 nmol/L. Outcomes included any plaque, coronary artery calcium score >0, maximal stenosis ≥50%, presence of any high-risk plaque feature (positive remodeling, spotty calcification, low-attenuation plaque, napkin ring), and the presence of ≥2 high-risk plaque features., Results: Among 1795 participants (median age, 52 years; 54.3% women; 49.6% Hispanic), 291 (16.2%) had Lp(a) ≥125 nmol/L. In unadjusted analyses, individuals with Lp(a) ≥125 nmol/L had a higher prevalence of all outcomes compared with Lp(a) <125 nmol/L, although differences were only statistically significant for the presence of any coronary plaque and ≥2 high-risk features. In multivariable models, elevated Lp(a) was independently associated with the presence of any coronary plaque (odds ratio, 1.40, [95% CI, 1.05-1.86]) and with ≥2 high-risk features (odds ratio, 3.94, [95% CI, 1.82-8.52]), although only 35 participants had this finding. Among participants with a coronary artery calcium score of 0 (n=1200), those with Lp(a) ≥125 nmol/L had a significantly higher percentage of any plaque compared with those with Lp(a) <125 nmol/L (24.2% versus 14.2%; P <0.001)., Conclusions: In this contemporary analysis, elevated Lp(a) was independently associated with the presence of coronary plaque. Larger studies are needed to confirm the strong association observed with the presence of multiple high-risk coronary plaque features., Competing Interests: Dr Cainzos-Achirica has received research support from Novo Nordisk and Boehringer Ingelheim, has received travel support from Novartis, and is in the steering committee of the Pak-SEHAT study, partially funded by Getz Pharma. Dr Nasir is on the advisory board of Amgen, Novartis, and Medicine Company, and his research is partly supported by the Jerold B. Katz Academy of Translational Research. Dr Blankstein receives research support from Amgen Inc, and Novartis Inc, and is a consultant to Caristo Diagnostics, Silence Therapeutics, and Roivant Sciences Inc, Dr Shapiro is on the advisory boards of Amgen, Novartis, and Novo Nordisk and is a consultant for Regeneron and Novartis. Dr Cury declares that he is a consultant to GE Healthcare, Covera Health, and Cleerly. Dr Santos declares he has received honoraria related to consulting, speaker activities, and research activities from Abbott, Amgen, Aché, Amryt, Astra Zeneca, Esperion, GETZ Pharma, Kowa, Libbs, Merck, Novo Nordisk, Novartis, PTC Therapeutics, Pfizer, Roche, and Sanofi. Dr Blaha is on the advisory board of Amgen, Novartis, Novo Nordisk, Bayer, Roche, 89Bio, Agepha, Inozyme, and Kaleido; and is a consultant for Emocha Health, Kowa. The rest of the authors declare that they have no conflicts of interest relevant to the content of this article.

Background: The contemporary burden and characteristics of coronary atherosclerosis, assessed using coronary computed tomography angiography (CCTA), is unknown among asymptomatic adults with diabetes and prediabetes in the United States. The pooled cohort equations and coronary artery calcium (CAC) score stratify atherosclerotic cardiovascular disease risk, but their association with CCTA findings across glycemic categories is not well established., Methods: Asymptomatic adults without atherosclerotic cardiovascular disease enrolled in the Miami Heart Study were included. Participants underwent CAC and CCTA testing and were classified into glycemic categories. Prevalence of coronary atherosclerosis (any plaque, noncalcified plaque, plaque with ≥1 high-risk feature, maximal stenosis ≥50%) assessed by CCTA was described across glycemic categories and further stratified by pooled cohort equations-estimated atherosclerotic cardiovascular disease risk and CAC score. Adjusted logistic regression was used to evaluate the associations between glycemic categories and coronary outcomes., Results: Among 2352 participants (49.5% women), the prevalence of euglycemia, prediabetes, and diabetes was 63%, 30%, and 7%, respectively. Coronary plaque was more commonly present across worsening glycemic categories (euglycemia, 43%; prediabetes, 58%; diabetes, 69%), and similar pattern was observed for other coronary outcomes. In adjusted analyses, compared with euglycemia, prediabetes and diabetes were each associated with higher odds of any coronary plaque (OR, 1.30 [95% CI, 1.05-1.60] and 1.75 [1.17-2.61], respectively), noncalcified plaque (OR, 1.47 [1.19-1.81] and 1.99 [1.38-2.87], respectively), and plaque with ≥1 high-risk feature (OR, 1.65 [1.14-2.39] and 2.53 [1.48-4.33], respectively). Diabetes was associated with stenosis ≥50% (OR, 3.01 [1.79-5.08]; reference=euglycemia). Among participants with diabetes and estimated atherosclerotic cardiovascular disease risk <5%, 46% had coronary plaque and 10% had stenosis ≥50%. Among participants with diabetes and CAC=0, 30% had coronary plaque and 3% had stenosis ≥50%., Conclusions: Among asymptomatic adults, worse glycemic status is associated with higher prevalence and extent of coronary atherosclerosis, high-risk plaque, and stenosis. In diabetes, CAC was more closely associated with CCTA findings and informative in a larger population than the pooled cohort equations., Competing Interests: Disclosures Dr Patel has received research support from the National Heart, Lung, and Blood Institute (R21HL169708); has served as a consultant to Novo Nordisk. Dr Blankstein receives research support from Amgen Inc and Novartis Inc and is a consultant to Caristo Diagnostics, Silence Therapeutics, and Roivant Sciences Inc. Dr Shapiro is on the advisory boards of Amgen, Novartis, and Novo Nordisk and is a consultant for Regeneron. Dr. Pandey has received research support from the National Institute on Aging GEMSSTAR Grant (1R03AG067960-01), the National Institute on Minority Health and Disparities (R01MD017529), and the National Institute of Heart, Lung, and Blood Institute (R21HL169708). Dr. Pandey has received grant funding (to the institution) from Applied Therapeutics, Gilead Sciences, Ultromics, Myovista, and Roche; has served as a consultant for and/or received honoraria outside of the present study as an advisor/consultant for Tricog Health Inc, Lilly USA, Rivus, Cytokinetics, Roche Diagnostics, Sarfez Therapeutics, Edwards Lifesciences, Merck, Bayer, Novo Nordisk, Alleviant, Axon Therapies, and has received nonfinancial support from Pfizer and Merck. Dr. Pandey is also a consultant for Palomarin Inc. with stocks compensation. Dr Cury declares that he is a consultant to GE Healthcare, Covera Health, and Cleerly. Dr Nasir is on the advisory board of Amgen, Novartis, Novo Nordisk, and his research is partly supported by the Jerold B. Katz Academy of Translational Research. Dr Cainzos-Achirica and Dr Nasir are part of the steering committee of the PAK-SEHAT study, which is partly funded by Getz Pharma. The other authors report no conflicts.