Lipoprotein(a) is associated with a larger systemic burden of arterial calcification

Author:

Singh Sunny S1ORCID,van der Toorn Janine E23,Sijbrands Eric J G1,de Rijke Yolanda B4,Kavousi Maryam2ORCID,Bos Daniel23ORCID

Affiliation:

1. Department of Internal Medicine, Erasmus MC, University Medical Centre , Rotterdam , The Netherlands

2. Department of Epidemiology, Erasmus MC, University Medical Centre , PO Box 2040, Rotterdam 3000 CA , The Netherlands

3. Department of Radiology and Nuclear Medicine, Erasmus MC, University Medical Centre , PO Box 2040, Rotterdam 3000 CA , The Netherlands

4. Department of Clinical Chemistry, Erasmus MC, University Medical Center , Rotterdam , The Netherlands

Abstract

Abstract Aims Lipoprotein(a) [Lp(a)] is a genetically determined risk factor for cardiovascular disease. However, population-based evidence on the link between Lp(a) and subclinical arteriosclerosis is lacking. We assessed associations of Lp(a) concentrations with arteriosclerosis in multiple arteries. Methods and results From the population-based Rotterdam study, 2354 participants (mean age: 69.5 years, 52.3% women) underwent non-contrast computed tomography to assess arterial calcification as a hallmark of arteriosclerosis. We quantified the volume of coronary artery calcification (CAC), aortic arch calcification (AAC), extracranial (ECAC), and intracranial carotid artery calcification (ICAC). All participants underwent blood sampling, from which plasma Lp(a) concentrations were derived. The association of plasma Lp(a) levels was assessed with calcification volumes and with severe calcification (upper quartile of calcification volume) using sex-stratified multivariable linear and logistic regression models. Higher Lp(a) levels were associated with larger ln-transformed volumes of CAC [fully adjusted beta 95% confidence interval (CI) per 1 standard deviation (SD) in women: 0.09, 95% CI 0.04–0.14, men: 0.09, 95% CI 0.03–0.14], AAC (women: 0.06, 95% CI 0.01–0.11, men: 0.09, 95% CI 0.03–0.14), ECAC (women: 0.07, 95% CI 0.02–0.13, men: 0.08, 95% CI 0.03–0.14), and ICAC (women: 0.09, 95% CI 0.03–0.14, men: 0.05, 95% CI −0.02 to 0.11]. In the highest Lp(a) percentile, severe ICAC was most prevalent in women [fully adjusted odds ratio (OR) 2.41, 95% CI 1.25–4.63] and severe AAC in men (fully adjusted OR 3.29, 95% CI 1.67–6.49). Conclusion Higher Lp(a) was consistently associated with a larger calcification burden in all major arteries. The findings of this study indicate that Lp(a) is a systemic risk factor for arteriosclerosis and thus potentially an effective target for treatment. Lp(a)-reducing therapies may reduce the burden from arteriosclerotic events throughout the arterial system. Translational perspective In 2354 participants from the Rotterdam study, we assessed the link between Lp(a) concentrations and arterial calcifications, as proxy for arteriosclerosis, in major arteries. We found that higher Lp(a) levels were consistently associated with larger volumes of calcification in the coronary arteries, aortic arch, extracranial carotid arteries, and intracranial carotid arteries. The findings of our study indicate that Lp(a) is a systemic risk factor for arteriosclerosis, suggesting that the systemic burden of arteriosclerosis throughout the arterial system could be reduced by targeting Lp(a).

Funder

Erasmus Medical Center and Erasmus University

Organization for Scientific Research

Netherlands Organization for Health Research and Development

Research Institute for Diseases in the Elderly

Netherlands Genomics Initiative

Ministry of Education, Culture, and Science

Ministry of Health, Welfare, and Sports

European Commission

Municipality of Rotterdam

VENI

BrightFocus Foundation

Alzheimer’s Association

Publisher

Oxford University Press (OUP)

Subject

Cardiology and Cardiovascular Medicine,Radiology, Nuclear Medicine and imaging,General Medicine

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