Prognostic Relevance of Gene-Environment Interactions in Patients With聽Dilated Cardiomyopathy: Applying the MOGE(S) Classification

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• 作者：Mark R. Hazebroek ; MD^&lowast ; ; ^{mark.hazebroek@mumc.nl" class="auth_mail" title="E-mail the corresponding author} ; Suzanne Moors ; BSc^&lowast ; ; Robert Dennert ; MD ; PhD^&lowast ; ; Arthur van den Wijngaard ; MD ; PhD^&dagger ; ; Ingrid Krapels ; MD ; PhD^&dagger ; ; Marije Hoos ; MD ; PhD^&lowast ; ; Job Verdonschot ; MSc^&lowast ; ; Jort J. Merken ; MD^&lowast ; ; Bart de Vries ; MD ; PhD^&Dagger ; ; Petra F. Wolffs ; MD ; PhD^§ ; ; Harry J.G.M. Crijns ; MD ; PhD^&lowast ; ; Hans-Peter Brunner-La Rocca ; MD ; PhD^&lowast ; ; Stephane Heymans ; MD ; PhD^&lowast ; ; ^鈥?/sup>
• 关键词：autoimmune ; etiology ; toxic ; virus
• 刊名：Journal of the American College of Cardiology
• 出版年：2015
• 出版时间：22 September 2015
• 年：2015
• 卷：66
• 期：12
• 页码：1313-1323
• 全文大小：1011 K

文摘

The multifactorial pathogenesis leading to dilated cardiomyopathy (DCM) makes stratification difficult. The recent MOGE(S) (morphofunctional, organ involvement, genetic or familial, etiology, stage) classification addresses this issue.

Objectives

The purpose of this study was to investigate the applicability and prognostic relevance of the MOGE(S) classification in patients with DCM.

Methods

This study used patients from the Maastricht Cardiomyopathy Registry in the Netherlands and excluded patients with ischemic, valvular, hypertensive, and congenital heart disease. All other patients underwent a complete diagnostic work-up, including genetic evaluation and endomyocardial biopsy.

Results

A total of 213 consecutive patients with DCM were included: organ involvement was demonstrated in 35 (16%) and genetic or familial DCM in 70 (33%) patients, including 16 (8%) patients with a pathogenic mutation. At least 1 cause was found in 155 (73%) patients, of whom 48 (23%) had more than 1 possible cause. Left ventricular reverse remodeling was more common in patients with nongenetic or nonfamilial DCM than in patients with genetic or familial DCM (40% vs. 25%; p = 0.04). After a median follow-up of 47 months, organ involvement and higher New York Heart Association functional class were associated with adverse outcome (p < 0.001 and p = 0.02, respectively). Genetic or familial DCM per se was of no prognostic significance, but when it was accompanied by additional etiologic-environmental factors such as significant viral load, immune-mediated factors, rhythm disturbances, or toxic triggers, a worse outcome was revealed (p = 0.03). A higher presence of MOGE(S) attributes (≥2 vs. ≤1 attributes) showed an adverse outcome (p = 0.007).

Conclusions

The MOGE(S) classification in DCM is applicable, and each attribute or the gene-environment interaction is associated with outcome. Importantly, the presence of multiple attributes was a strong predictor of adverse outcome. Finally, adaptation of the MOGE(S) involving multiple possible etiologies is recommended.