Key result
Myocardial fibrosis detected by late gadolinium enhancement was associated with a higher risk of cardiac death, CHF, or aborted sudden cardiac death (HR 5.10; 95% CI 2.78-9.36; P<0.001).
Why the study?
Does the presence of myocardial fibrosis detected by LGE on CMR predict adverse outcomes in patients with non-ischemic cardiomyopathy without congestive heart failure?
Cohort (n=228)
Yes
Does the presence of myocardial fibrosis detected by LGE on CMR predict adverse outcomes in patients with non-ischemic cardiomyopathy without congestive heart failure?
Myocardial fibrosis detected by LGE on CMR provides strong, independent prognostic value for adverse cardiac events in patients with non-ischemic cardiomyopathy prior to the onset of clinical heart failure.
Answers are grounded in this paper and cite their sources.
May aid risk stratification in non-ischemic cardiomyopathy; leaves open whether LGE-CMR should guide management.
BACKGROUND: We conducted a prospective longitudinal study to investigate the yet unknown clinical significance of myocardial fibrosis in patients with non-ischemic cardiomyopathy without history of congestive heart failure (CHF). METHODS AND RESULTS: At 3 tertiary referral centers, 228 patients with non-ischemic cardiomyopathy without history of CHF were studied with cardiovascular magnetic resonance for late gadolinium enhancement (LGE) detection and quantification and prospectively followed up for a median of 23 months. The end point was a composite of cardiac death, onset of CHF, and aborted sudden cardiac death. LGE was detected in 61 (27%) patients. Thirty-one of 61 (51%) patients with LGE reached combined end point when compared with 18 of 167 (11%) patients without LGE (hazard ratio, 5.10 [2.78-9.36]; P<0.001). Patients with LGE had greater risk of developing CHF than patients without LGE (hazard ratio, 5.23 [2.61-10.50]; P<0.001) and higher rate of aborted sudden cardiac death (hazard ratio, 8.31 [1.66-41.55]; P=0.010). Multivariate analysis showed that LGE was associated with high likelihood of composite end point independent of other prognostic determinants, including age; duration of cardiomyopathy; and left ventricular volumes, mass, and ejection fraction (hazard ratio, 4.02 [2.08-7.76]; P<0.001). Improvement χ(2) analysis disclosed that LGE addition to models, including clinical data alone or in combination with parameters of left ventricular remodeling and function, yielded an improvement in outcome prediction (P<0.001). Addition of LGE to age and left ventricular ejection fraction improved risk stratification for composite end point (net reclassification improvement, 29.6%) and onset of CHF (net reclassification improvement, 25.4%; both P<0.001). CONCLUSIONS: In patients with non-ischemic cardiomyopathy without history of CHF, myocardial fibrosis is a strong and independent predictor of outcome, providing incremental prognostic information and improvement in risk stratification beyond clinical data and degree of left ventricular dysfunction.
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Masci et al. (2014) conducted a cohort in Non-ischemic cardiomyopathy without congestive heart failure (n=228). Myocardial fibrosis (late gadolinium enhancement) vs. No myocardial fibrosis was evaluated on Composite of cardiac death, onset of CHF, and aborted sudden cardiac death (HR 5.10, 95% CI 2.78-9.36, p=<0.001). Myocardial fibrosis detected by late gadolinium enhancement was associated with a higher risk of cardiac death, CHF, or aborted sudden cardiac death (HR 5.10; 95% CI 2.78-9.36; P<0.001).
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