Influence of Subclinical Atherosclerosis Burden and Progression on Mortality.

BACKGROUND

Atherosclerosis is a dynamic process. There is little evidence regarding whether quantification of atherosclerosis extent and progression, particularly in the carotid artery, in asymptomatic individuals predicts all-cause mortality.

OBJECTIVES

This study sought to evaluate the independent predictive value (beyond cardiovascular risk factors) of subclinical atherosclerosis burden and progression and all-cause mortality.

METHODS

A population of 5,716 asymptomatic U.S. adults (mean age 68.9 years, 56.7% female) enrolled between 2008 and 2009 in the BioImage (A Clinical Study of Burden of Atherosclerotic Disease in an At Risk Population) study underwent examination by vascular ultrasound to quantify carotid plaque burden (cPB) (the sum of right and left carotid plaque areas) and by computed tomography for coronary artery calcium (CAC). Follow-up carotid vascular ultrasound was performed on 732 participants a median of 8.9 years after the baseline exam. All participants were followed up for all-cause mortality, the primary outcome. Trend HRs are the per-tertile increase in each variable.

RESULTS

Over a median 12.4 years' follow-up, 901 (16%) participants died. After adjustment for cardiovascular risk factors and background medication, baseline cPB and CAC score were both significantly associated with all-cause mortality (fully adjusted trend HR: 1.23; 95% CI: 1.16-1.32; and HR: 1.15; 95% CI: 1.08-1.23), respectively (both P < 0.001), thus providing additional prognostic value. cPB performed better than CAC score. In participants with a second vascular ultrasound evaluation, median cPB progressed from 29.2 to 91.3 mm

CONCLUSIONS

Subclinical atherosclerosis burden (cPB and CAC) in asymptomatic individuals was independently associated with all-cause mortality. Moreover, atherosclerosis progression was independently associated with all-cause mortality.

Informations de copyright

Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Funding Support and Author Disclosures The High-Risk Plaque BioImage initiative was a precompetitive industry collaboration funded by BG Medicine, Abbott Vascular, AstraZeneca, Merck & Co., Philips, and Takeda. These funders had no role in the present study. Dr Ibanez was supported by the European Commission (grant numbers H2020-HEALTH 945118 and ERC-CoG 819775), La Caixa Foundation (HR22-00533, DIREQT2Heart), the Spanish Ministry of Science and Innovation (PID2022-140176OB-I00), and the Red Madrileña de Nanomedicina en Imagen Molecular–Comunidad de Madrid (2022/BMD-7403 RENIM-CM). Dr García-Álvarez was supported by the Instituto de Salud Carlos III (PI20/00742 and PI23/01341) and La Fundació la Marató TV3 (202314-30/31). Dr Devesa is an Alfonso Martin Escudero fellow and was scientifically supported by la La Caixa Foundation. The CNIC is supported by the Instituto de Salud Carlos III (ISCIII), the Ministerio de Ciencia, Innovación y Universidades (MICIU) and the Pro CNIC Foundation, and is a Severo Ochoa Center of Excellence (grant CEX2020-001041-S funded by MICIU/AEI/10.13039/501100011033). Dr Sánchez-González is an employee of Philips. Dr Muntendam is CEO of SQ innovation. Philips and SQ innovation had no role in the present study. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.