Determinants of Progression and Regression of Subclinical Atherosclerosis Over 6 Years.


Journal

Journal of the American College of Cardiology
ISSN: 1558-3597
Titre abrégé: J Am Coll Cardiol
Pays: United States
ID NLM: 8301365

Informations de publication

Date de publication:
28 Nov 2023
Historique:
received: 25 07 2023
revised: 13 09 2023
accepted: 22 09 2023
medline: 27 11 2023
pubmed: 23 11 2023
entrez: 22 11 2023
Statut: ppublish

Résumé

Atherosclerosis is a systemic disease that frequently begins early in life. However, knowledge about the temporal disease dynamics (ie, progression or regression) of human subclinical atherosclerosis and their determinants is scarce. This study sought to investigate early subclinical atherosclerosis disease dynamics within a cohort of middle-aged, asymptomatic individuals by using multiterritorial 3-dimensional vascular ultrasound (3DVUS) imaging. A total of 3,471 participants from the PESA (Progression of Early Subclinical Atherosclerosis) cohort study (baseline age 40-55 years; 36% female) underwent 3 serial 3DVUS imaging assessments of peripheral arteries at 3-year intervals. Subclinical atherosclerosis was quantified as global plaque volume (mm Baseline to 6-year subclinical atherosclerosis progression occurred in 32.7% of the cohort (17.5% presenting with incident disease and 15.2% progressing from prevalent disease at enrollment). Regression was observed in 8.0% of those patients with baseline disease. The effects of higher low-density lipoprotein cholesterol (LDL-C) and elevated systolic blood pressure (SBP) on 6-year subclinical atherosclerosis progression risk were more pronounced among participants in the youngest age stratum (P Over 6 years, subclinical atherosclerosis progressed in one-third of middle-age asymptomatic subjects. Atherosclerosis regression is possible in early stages of the disease. The impact of LDL-C and SBP on subclinical atherosclerosis progression was more pronounced in younger participants, a finding suggesting that the prevention of atherosclerosis and its progression could be enhanced by tighter risk factor control at younger ages, with a likely long-term impact on reducing the risk of clinical events. (Progression of Early Subclinical Atherosclerosis [PESA; also PESA-CNIC-Santander]; NCT01410318).

Sections du résumé

BACKGROUND BACKGROUND
Atherosclerosis is a systemic disease that frequently begins early in life. However, knowledge about the temporal disease dynamics (ie, progression or regression) of human subclinical atherosclerosis and their determinants is scarce.
OBJECTIVES OBJECTIVE
This study sought to investigate early subclinical atherosclerosis disease dynamics within a cohort of middle-aged, asymptomatic individuals by using multiterritorial 3-dimensional vascular ultrasound (3DVUS) imaging.
METHODS METHODS
A total of 3,471 participants from the PESA (Progression of Early Subclinical Atherosclerosis) cohort study (baseline age 40-55 years; 36% female) underwent 3 serial 3DVUS imaging assessments of peripheral arteries at 3-year intervals. Subclinical atherosclerosis was quantified as global plaque volume (mm
RESULTS RESULTS
Baseline to 6-year subclinical atherosclerosis progression occurred in 32.7% of the cohort (17.5% presenting with incident disease and 15.2% progressing from prevalent disease at enrollment). Regression was observed in 8.0% of those patients with baseline disease. The effects of higher low-density lipoprotein cholesterol (LDL-C) and elevated systolic blood pressure (SBP) on 6-year subclinical atherosclerosis progression risk were more pronounced among participants in the youngest age stratum (P
CONCLUSIONS CONCLUSIONS
Over 6 years, subclinical atherosclerosis progressed in one-third of middle-age asymptomatic subjects. Atherosclerosis regression is possible in early stages of the disease. The impact of LDL-C and SBP on subclinical atherosclerosis progression was more pronounced in younger participants, a finding suggesting that the prevention of atherosclerosis and its progression could be enhanced by tighter risk factor control at younger ages, with a likely long-term impact on reducing the risk of clinical events. (Progression of Early Subclinical Atherosclerosis [PESA; also PESA-CNIC-Santander]; NCT01410318).

Identifiants

pubmed: 37993199
pii: S0735-1097(23)07629-5
doi: 10.1016/j.jacc.2023.09.814
pii:
doi:

Substances chimiques

Cholesterol, LDL 0

Banques de données

ClinicalTrials.gov
['NCT01410318']

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

2069-2083

Informations de copyright

Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Funding Support and Author Disclosures The PESA study is funded by the National Center for Cardiovascular Investigations (CNIC) and Santander Bank. The CNIC is supported by the Carlos III Institute of Health (ISCIII), the Ministry of Science and Innovation, and the Pro CNIC Foundation. CNIC is a Severo Ochoa Center of Excellence (grant CEX2020-001041-S funded by MICIN/AEI/10.13039/501100011033). Dr Sánchez-González is an employee of Philips. Dr Ibáñez has received support from the European Commission (ERC-CoG 819775, and H2020-HEALTH 945118), the Spanish Ministry of Science and Innovation (PID2019-110369RB-I00), and the Community of Madrid (P2022/BMD-7403, RENIM-CM). Dr Mendieta was recipient of the 2020 “CardioJoven” Fellowship funded by the Spanish Society of Cardiology and the Centro Nacional de Investigaciones Cardiovasculares. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Auteurs

Guiomar Mendieta (G)

National Center of Cardiovascular Investigations (CNIC), Madrid, Spain; Cardiology Service, Clínic Cardiovascular Institute, Hospital Clínic of Barcelona, Barcelona, Spain; August Pi i Sunyer Institute of Biomedical Research (IDIBAPS), Barcelona, Spain.

Stuart Pocock (S)

National Center of Cardiovascular Investigations (CNIC), Madrid, Spain; Department of Medical Statistics, London School of Hygiene & Tropical Medicine, London, United Kingdom.

Virginia Mass (V)

National Center of Cardiovascular Investigations (CNIC), Madrid, Spain.

Andrea Moreno (A)

National Center of Cardiovascular Investigations (CNIC), Madrid, Spain.

Ruth Owen (R)

National Center of Cardiovascular Investigations (CNIC), Madrid, Spain; Department of Medical Statistics, London School of Hygiene & Tropical Medicine, London, United Kingdom.

Inés García-Lunar (I)

National Center of Cardiovascular Investigations (CNIC), Madrid, Spain; Network Center for Cardiovascular Biomedical Research (CIBERCV), Madrid, Spain; La Moraleja University Hospital, Madrid, Spain.

Beatriz López-Melgar (B)

National Center of Cardiovascular Investigations (CNIC), Madrid, Spain; La Princesa University Hospital, Madrid, Spain; Icahn School of Medicine at Mount Sinai, New York, New York, USA.

Jose J Fuster (JJ)

National Center of Cardiovascular Investigations (CNIC), Madrid, Spain; Network Center for Cardiovascular Biomedical Research (CIBERCV), Madrid, Spain.

Vicente Andres (V)

National Center of Cardiovascular Investigations (CNIC), Madrid, Spain; Network Center for Cardiovascular Biomedical Research (CIBERCV), Madrid, Spain.

Cristina Pérez-Herreras (C)

Banco de Santander, Madrid, Spain.

Hector Bueno (H)

National Center of Cardiovascular Investigations (CNIC), Madrid, Spain; Network Center for Cardiovascular Biomedical Research (CIBERCV), Madrid, Spain; Department of Cardiology, October 12 University Hospital, i+12 Research Institute, Madrid, Spain.

Antonio Fernández-Ortiz (A)

National Center of Cardiovascular Investigations (CNIC), Madrid, Spain; Network Center for Cardiovascular Biomedical Research (CIBERCV), Madrid, Spain; San Carlos Clinical Hospital, Complutense University, Health Research Institute (IdISSC), Madrid, Spain.

Javier Sanchez-Gonzalez (J)

Philips Healthcare, Madrid, Spain.

Ana García-Alvarez (A)

National Center of Cardiovascular Investigations (CNIC), Madrid, Spain; Cardiology Service, Clínic Cardiovascular Institute, Hospital Clínic of Barcelona, Barcelona, Spain; August Pi i Sunyer Institute of Biomedical Research (IDIBAPS), Barcelona, Spain; Network Center for Cardiovascular Biomedical Research (CIBERCV), Madrid, Spain; Department of Medicine, University of Barcelona, Barcelona, Spain.

Borja Ibáñez (B)

National Center of Cardiovascular Investigations (CNIC), Madrid, Spain; Network Center for Cardiovascular Biomedical Research (CIBERCV), Madrid, Spain; Department of Cardiology, Jiménez Díaz Foundation University Hospital Health Research Institute (IIS), Madrid, Spain. Electronic address: bibanez@cnic.es.

Valentin Fuster (V)

National Center of Cardiovascular Investigations (CNIC), Madrid, Spain; The Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, New York, USA. Electronic address: vfuster@cnic.es.

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