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J Am Coll Cardiol, 2006; 48:1977-1985, doi:10.1016/j.jacc.2006.07.049
(Published online 31 October 2006). © 2006 by the American College of Cardiology Foundation |
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,2
,2


,*,1
* Cardiovascular Magnetic Resonance Unit, Royal Brompton Hospital, London, United Kingdom
National Heart and Lung Institute, Imperial College, London, United Kingdom
Medical Statistics Unit, Royal Brompton Hospital, London, United Kingdom
Pathology Department, Royal Brompton Hospital, London, United Kingdom.
Manuscript received February 21, 2006; revised manuscript received May 25, 2006, accepted July 12, 2006.
* Reprint requests and correspondence: Dr. Dudley Pennell, Cardiovascular Magnetic Resonance Unit, Royal Brompton Hospital, Sydney Street, London SW3 6NP, United Kingdom. (Email: d.pennell{at}imperial.ac.uk).
OBJECTIVES: We studied the prognostic implications of midwall fibrosis in dilated cardiomyopathy (DCM) in a prospective longitudinal study.
BACKGROUND: Risk stratification of patients with nonischemic DCM in the era of device implantation is problematic. Approximately 30% of patients with DCM have midwall fibrosis as detected by late gadolinium-enhancement (LGE) cardiovascular magnetic resonance (CMR), which may increase susceptibility to arrhythmia and progression of heart failure.
METHODS: Consecutive DCM patients (n = 101) with the presence or absence of midwall fibrosis were followed up prospectively for 658 ± 355 days for events.
RESULTS: Midwall fibrosis was present in 35% of patients and was associated with a higher rate of the predefined primary combined end point of all-cause death and hospitalization for a cardiovascular event (hazard ratio 3.4, p = 0.01). Multivariate analysis showed midwall fibrosis as the sole significant predictor of death or hospitalization. However, there was no significant difference in all-cause mortality between the 2 groups. Midwall fibrosis also predicted secondary outcome measures of sudden cardiac death (SCD) or ventricular tachycardia (VT) (hazard ratio 5.2, p = 0.03). Midwall fibrosis remained predictive of SCD/VT after correction for baseline differences in left ventricular ejection fraction between the 2 groups.
CONCLUSIONS: In DCM, midwall fibrosis determined by CMR is a predictor of the combined end point of all-cause mortality and cardiovascular hospitalization, which is independent of ventricular remodeling. In addition, midwall fibrosis by CMR predicts SCD/VT. This suggests a potential role for CMR in the risk stratification of patients with DCM, which may have value in determining the need for device therapy.
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