Association Between Left Ventricular Noncompaction and Vigorous Physical Activity.


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:
13 10 2020
Historique:
received: 09 06 2020
revised: 21 07 2020
accepted: 12 08 2020
entrez: 9 10 2020
pubmed: 10 10 2020
medline: 3 2 2021
Statut: ppublish

Résumé

Left ventricular (LV) hypertrabeculation fulfilling noncompaction cardiomyopathy criteria has been detected in athletes. However, the association between LV noncompaction (LVNC) phenotype and vigorous physical activity (VPA) in the general population is disputed. The aim of this study was to assess the relationship between LVNC phenotype on cardiac magnetic resonance (CMR) imaging and accelerometer-measured physical activity (PA) in a cohort of middle-aged nonathlete participants in the PESA (Progression of Early Subclinical Atherosclerosis) study. In PESA participants (n = 4,184 subjects free of cardiovascular disease), PA was measured by waist-secured accelerometers. CMR was performed in 705 subjects (mean age 48 ± 4 years, 16% women). VPA was recorded as total minutes per week. The study population was divided into 6 groups: no VPA and 5 sex-specific quintiles of VPA rate (Q1 to Q5). The Petersen criterion for LVNC was evaluated in all subjects undergoing CMR. For participants meeting this criterion (noncompacted-to-compacted ratio ≥2.3), 3 more restrictive LVNC criteria were also evaluated (Jacquier, Grothoff, and Stacey). LVNC phenotype prevalence according to the Petersen criterion was significantly higher among participants in the highest VPA quintile (Q5 = 30.5%) than in participants with no VPA (14.2%). The Jacquier and Grothoff criteria were also more frequently fulfilled in participants in the highest VPA quintile (Jacquier Q5 = 27.4% vs. no VPA = 12.8% and Grothoff Q5 = 15.8% vs. no VPA = 7.1%). The prevalence of the systolic Stacey LVNC criterion was low (3.6%) and did not differ significantly between no VPA and Q5. In a community-based study, VPA was associated with a higher prevalence of CMR-detected LVNC phenotype according to diverse established criteria. The association between VPA and LVNC phenotype was independent of LV volumes. According to these data, vigorous recreational PA should be considered as a possible but not uncommon determinant of LV hypertrabeculation in asymptomatic subjects.

Sections du résumé

BACKGROUND
Left ventricular (LV) hypertrabeculation fulfilling noncompaction cardiomyopathy criteria has been detected in athletes. However, the association between LV noncompaction (LVNC) phenotype and vigorous physical activity (VPA) in the general population is disputed.
OBJECTIVES
The aim of this study was to assess the relationship between LVNC phenotype on cardiac magnetic resonance (CMR) imaging and accelerometer-measured physical activity (PA) in a cohort of middle-aged nonathlete participants in the PESA (Progression of Early Subclinical Atherosclerosis) study.
METHODS
In PESA participants (n = 4,184 subjects free of cardiovascular disease), PA was measured by waist-secured accelerometers. CMR was performed in 705 subjects (mean age 48 ± 4 years, 16% women). VPA was recorded as total minutes per week. The study population was divided into 6 groups: no VPA and 5 sex-specific quintiles of VPA rate (Q1 to Q5). The Petersen criterion for LVNC was evaluated in all subjects undergoing CMR. For participants meeting this criterion (noncompacted-to-compacted ratio ≥2.3), 3 more restrictive LVNC criteria were also evaluated (Jacquier, Grothoff, and Stacey).
RESULTS
LVNC phenotype prevalence according to the Petersen criterion was significantly higher among participants in the highest VPA quintile (Q5 = 30.5%) than in participants with no VPA (14.2%). The Jacquier and Grothoff criteria were also more frequently fulfilled in participants in the highest VPA quintile (Jacquier Q5 = 27.4% vs. no VPA = 12.8% and Grothoff Q5 = 15.8% vs. no VPA = 7.1%). The prevalence of the systolic Stacey LVNC criterion was low (3.6%) and did not differ significantly between no VPA and Q5.
CONCLUSIONS
In a community-based study, VPA was associated with a higher prevalence of CMR-detected LVNC phenotype according to diverse established criteria. The association between VPA and LVNC phenotype was independent of LV volumes. According to these data, vigorous recreational PA should be considered as a possible but not uncommon determinant of LV hypertrabeculation in asymptomatic subjects.

Identifiants

pubmed: 33032733
pii: S0735-1097(20)36328-2
doi: 10.1016/j.jacc.2020.08.030
pii:
doi:

Types de publication

Journal Article Multicenter Study Observational Study Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1723-1733

Commentaires et corrections

Type : CommentIn
Type : CommentIn
Type : CommentIn

Informations de copyright

Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.

Auteurs

Jose A de la Chica (JA)

Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain; Hospital Quironsalud, Malaga, Spain.

Sandra Gómez-Talavera (S)

Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain; IIS-Hospital Universitario Fundación Jiménez Díaz, Madrid, Spain; CIBER Enfermedades Cardiovasculares, Madrid, Spain.

Jose M García-Ruiz (JM)

Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain; CIBER Enfermedades Cardiovasculares, Madrid, Spain; Hospital de Cabueñes, Gijón, Spain.

Ines García-Lunar (I)

Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain; CIBER Enfermedades Cardiovasculares, Madrid, Spain; Hospital Universitario Quirón, Madrid, Spain.

Belén Oliva (B)

Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.

Juan M Fernández-Alvira (JM)

Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain; CIBER Enfermedades Cardiovasculares, Madrid, Spain; Hospitales HM, Madrid, Spain.

Beatriz López-Melgar (B)

Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain; CIBER Enfermedades Cardiovasculares, Madrid, Spain; Hospitales HM, Madrid, Spain.

Javier Sánchez-González (J)

Philips Healthcare, Madrid, Spain.

José L de la Pompa (JL)

Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain; CIBER Enfermedades Cardiovasculares, Madrid, Spain; Intercellular Signalling in Cardiovascular Development & Disease Laboratory, Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.

Jose M Mendiguren (JM)

Banco de Santander, Madrid, Spain.

Vicente Martínez de Vega (V)

Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain; Hospital Universitario Quirón, Madrid, Spain.

Antonio Fernández-Ortiz (A)

Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain; CIBER Enfermedades Cardiovasculares, Madrid, Spain; Hospital Clínico San Carlos, Madrid, Spain.

Javier Sanz (J)

Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain; Icahn School of Medicine at Mount Sinai, New York, New York.

Leticia Fernández-Friera (L)

Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain; CIBER Enfermedades Cardiovasculares, Madrid, Spain; Hospitales HM, Madrid, Spain. Electronic address: leticia.fernandez@cnic.es.

Borja Ibáñez (B)

Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain; IIS-Hospital Universitario Fundación Jiménez Díaz, Madrid, Spain; CIBER Enfermedades Cardiovasculares, Madrid, Spain. Electronic address: bibanez@cnic.es.

Valentín Fuster (V)

Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain; Icahn School of Medicine at Mount Sinai, New York, New York.

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Classifications MeSH