Lipoprotein(a) and Long-Term Plaque Progression, Low-Density Plaque, and Pericoronary Inflammation.

Autor:	Nurmohamed NS; Department of Cardiology, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands.; Department of Vascular Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.; Division of Cardiology, The George Washington University School of Medicine, Washington, DC., Gaillard EL; Department of Cardiology, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands.; Department of Vascular Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands., Malkasian S; Department of Radiological Sciences, Medical Sciences I, University of California, Irvine, California., de Groot RJ; Department of Cardiology, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands., Ibrahim S; Department of Vascular Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands., Bom MJ; Department of Cardiology, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands., Kaiser Y; Department of Vascular Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands., Earls JP; Division of Cardiology, The George Washington University School of Medicine, Washington, DC.; Cleerly, Denver, Colorado., Min JK; Cleerly, Denver, Colorado., Kroon J; Department of Experimental Vascular Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.; Laboratory of Angiogenesis and Vascular Metabolism, VIB-KU Leuven Center for Cancer Biology, Leuven, Belgium., Planken RN; Department of Radiology and Nuclear Medicine, Amsterdam UMC, Universiteit van Amsterdam, Amsterdam, the Netherlands., Danad I; Department of Cardiology, University Medical Center Utrecht, Utrecht, the Netherlands., van Rosendael AR; Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands., Choi AD; Division of Cardiology, The George Washington University School of Medicine, Washington, DC., Stroes ESG; Department of Vascular Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands., Knaapen P; Department of Cardiology, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands.
Jazyk:	angličtina
Zdroj:	JAMA cardiology [JAMA Cardiol] 2024 Sep 01; Vol. 9 (9), pp. 826-834.
DOI:	10.1001/jamacardio.2024.1874
Abstrakt:	Importance: Lipoprotein(a) (Lp[a]) is a causal risk factor for cardiovascular disease; however, long-term effects on coronary atherosclerotic plaque phenotype, high-risk plaque formation, and pericoronary adipose tissue inflammation remain unknown. Objective: To investigate the association of Lp(a) levels with long-term coronary artery plaque progression, high-risk plaque, and pericoronary adipose tissue inflammation. Design, Setting, and Participants: This single-center prospective cohort study included 299 patients with suspected coronary artery disease (CAD) who underwent per-protocol repeated coronary computed tomography angiography (CCTA) imaging with an interscan interval of 10 years. Thirty-two patients were excluded because of coronary artery bypass grafting, resulting in a study population of 267 patients. Data for this study were collected from October 2008 to October 2022 and analyzed from March 2023 to March 2024. Exposures: The median scan interval was 10.2 years. Lp(a) was measured at follow-up using an isoform-insensitive assay. CCTA scans were analyzed with a previously validated artificial intelligence-based algorithm (atherosclerosis imaging-quantitative computed tomography). Main Outcome and Measures: The association between Lp(a) and change in percent plaque volumes was investigated in linear mixed-effects models adjusted for clinical risk factors. Secondary outcomes were presence of low-density plaque and presence of increased pericoronary adipose tissue attenuation at baseline and follow-up CCTA imaging. Results: The 267 included patients had a mean age of 57.1 (SD, 7.3) years and 153 were male (57%). Patients with Lp(a) levels of 125 nmol/L or higher had twice as high percent atheroma volume (6.9% vs 3.0%; P = .01) compared with patients with Lp(a) levels less than 125 nmol/L. Adjusted for other risk factors, every doubling of Lp(a) resulted in an additional 0.32% (95% CI, 0.04-0.60) increment in percent atheroma volume during the 10 years of follow-up. Every doubling of Lp(a) resulted in an odds ratio of 1.23 (95% CI, 1.00-1.51) and 1.21 (95% CI, 1.01-1.45) for the presence of low-density plaque at baseline and follow-up, respectively. Patients with higher Lp(a) levels had increased pericoronary adipose tissue attenuation around both the right coronary artery and left anterior descending at baseline and follow-up. Conclusions and Relevance: In this long-term prospective serial CCTA imaging study, higher Lp(a) levels were associated with increased progression of coronary plaque burden and increased presence of low-density noncalcified plaque and pericoronary adipose tissue inflammation. These data suggest an impact of elevated Lp(a) levels on coronary atherogenesis of high-risk, inflammatory, rupture-prone plaques over the long term.
Databáze:	MEDLINE
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