Sudden cardiac death after early-onset myocardial infarction. A multicentre longitudinal cohort study with 20 years' follow-up.
Journal
European heart journal. Acute cardiovascular care
ISSN: 2048-8734
Titre abrégé: Eur Heart J Acute Cardiovasc Care
Pays: England
ID NLM: 101591369
Informations de publication
Date de publication:
06 Aug 2024
06 Aug 2024
Historique:
received:
04
03
2024
revised:
15
04
2024
accepted:
01
05
2024
medline:
7
8
2024
pubmed:
7
8
2024
entrez:
6
8
2024
Statut:
aheadofprint
Résumé
Sudden cardiac death (SCD) is a serious consequence of a myocardial infarction (MI), but identifying patients at risk of developing SCD remains a major clinical challenge especially in the case of juvenile MI. The aim of this study was to identify predictors of SCD after early-onset MI using long-term follow-up data relating to a large nationwide patient cohort. The Italian Genetic Study on Early-onset MI enrolled 2,000 patients experiencing a first MI before the age of 45 years, who were followed up for a median of 19.9 years. Fine-Gray proportional hazard models were used to assess the associations between their clinical, demographic and index event data and the occurrence of SCD. SCD occurred in 195 patients, who were more frequently males, hypertensive and/or diabetic; had a history of previous thromboembolic events with a greater atherosclerotic burden; and had a lower left ventricular ejection fraction (LVEF) after the index event. Multivariable analysis showed that the independent predictors of SCD were diabetes, hypertension, previous thromboembolic events, higher Syntax score, and a lower LVEF. There was no clear evidence of the clustering of SCD events during follow-up. SCD was the first post-MI clinical event in 101 patients; the remaining 94 experienced SCD after a non-fatal MI or hospitalisation for coronary revascularisation. SCD frequently occurs during the 20 years after early-onset MI. The nature of the identified predictors and the absence of clustering suggests that the pathophysiological basis of SCD may be related to progressive coronary atherosclerosis.
Sections du résumé
BACKGROUND
BACKGROUND
Sudden cardiac death (SCD) is a serious consequence of a myocardial infarction (MI), but identifying patients at risk of developing SCD remains a major clinical challenge especially in the case of juvenile MI. The aim of this study was to identify predictors of SCD after early-onset MI using long-term follow-up data relating to a large nationwide patient cohort.
METHODS
METHODS
The Italian Genetic Study on Early-onset MI enrolled 2,000 patients experiencing a first MI before the age of 45 years, who were followed up for a median of 19.9 years. Fine-Gray proportional hazard models were used to assess the associations between their clinical, demographic and index event data and the occurrence of SCD.
RESULTS
RESULTS
SCD occurred in 195 patients, who were more frequently males, hypertensive and/or diabetic; had a history of previous thromboembolic events with a greater atherosclerotic burden; and had a lower left ventricular ejection fraction (LVEF) after the index event. Multivariable analysis showed that the independent predictors of SCD were diabetes, hypertension, previous thromboembolic events, higher Syntax score, and a lower LVEF. There was no clear evidence of the clustering of SCD events during follow-up. SCD was the first post-MI clinical event in 101 patients; the remaining 94 experienced SCD after a non-fatal MI or hospitalisation for coronary revascularisation.
CONCLUSIONS
CONCLUSIONS
SCD frequently occurs during the 20 years after early-onset MI. The nature of the identified predictors and the absence of clustering suggests that the pathophysiological basis of SCD may be related to progressive coronary atherosclerosis.
Identifiants
pubmed: 39107249
pii: 7728411
doi: 10.1093/ehjacc/zuae089
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.