作者
S Bricoli,Giulia Magnani,Maddalena Ardissino,Giuseppe Maglietta,Patrizia Celli,Maurizio Ferrario,Umberto Canosi,Carlo Cernetti,Francesco Negri,Piera Angelica Merlini,Marco Tubaro,Carlo Berzuini,Chiara Manzalini,Luigi Moschini,E Ponte,Roberto Pozzi,Silvia Buratti,Andrea Botti,Federico Barocelli,Andrea Biagi,Rosario Bonura,L Bearzot,Tiziano Moccetti,Antonio Crocamo,Maria Francesca Notarangelo,Elisabetta Moscarella,Paolo Calabrò,Giampaolo Niccoli,Diego Ardissino
摘要
Abstract Aims 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 is to identify predictors of SCD after early-onset MI using long-term follow-up data relating to a large nationwide patient cohort. Methods and results The Italian Genetic Study on Early-onset MI enrolled 2000 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. Sudden cardiac death occurred in 195 patients, who were more frequently males, were hypertensive and/or diabetic, had a history of previous thrombo-embolic events with a greater atherosclerotic burden, and had a lower left ventricular ejection fraction (LVEF) after the index event. A multivariable analysis showed that the independent predictors of SCD were diabetes, hypertension, previous thrombo-embolic events, a higher SYNTAX score, and a lower LVEF. There was no clear evidence of the clustering of SCD events during the follow-up. Sudden cardiac death was the first post-MI clinical event in 101 patients; the remaining 94 experienced SCD after a non-fatal MI or hospitalization for coronary revascularization. Conclusion Sudden cardiac death frequently occurs during the 20 years after early-onset MI. The nature of the identified predictors and the absence of clustering suggest that the pathophysiological basis of SCD may be related to progressive coronary atherosclerosis.