Log in to MyACC
Myocardial Fibrosis and Clinical Outcomes in Nonischemic Cardiomyopathy
Quick Takes
- In this small cohort of patients with nonischemic dilated cardiomyopathy, progressive myocardial fibrosis, identified by LGE on CMR, was independently associated with all-cause mortality and MACE.
- Progressive myocardial fibrosis may occur in the absence of major changes in LVEF.
Study Questions:
Among patients with nonischemic dilated cardiomyopathy (DCM), how does myocardial fibrosis change over time, and how does fibrosis correlate with left ventricular ejection fraction (LVEF) and clinical outcomes?
Methods:
Subjects were retrospectively identified from a longitudinal outcome registry of patients with DCM who were referred for clinical cardiovascular magnetic resonance (CMR) from 2003-2011. Only patients who had undergone baseline and follow-up CMRs were included. All patients had increased LV end-diastolic volume index and reduced LVEF as compared to reference values. Notable exclusion criteria were ischemic heart disease, hypertrophic or arrhythmogenic right ventricular cardiomyopathy, and acute inflammatory or infiltrative heart disease. All CMR delayed enhancement images were reviewed by two blinded expert readers, and fibrosis was quantified as a percentage of LV mass.
Results:
The study included 85 patients (median age 56 years, 45% women, 38% non-Caucasian patients). Median time between CMRs was 1.5 years. Guideline-directed medical therapy for heart failure at the time of the second CMR included beta-blockers in 81%, angiotensin-converting enzyme inhibitors/angiotensin receptor blockers in 73%, and spironolactone in 18%.
In the entire cohort, LVEF was 39 ± 9% on initial CMR and 42 ± 11% on follow-up CMR (p < 0.01). Late gadolinium enhancement (LGE) evidence of fibrosis was present in 34 patients (40%) on initial CMR and 41 patients (48%) on follow-up CMR (p < 0.01). Most patients (70, 82%) had no fibrosis or stable fibrosis. No patients exhibited resolution of fibrosis on follow-up CMR. In the group of 15 patients (18%) with progressive fibrosis, mean LV volumes increased and LVEF decreased (40 ± 7% vs. 34 ± 10%, p < 0.01). However, in nine patients with progression of fibrosis, only minimal change in LVEF (<5%) occurred. Progressive fibrosis was associated with decrease in right ventricular EF on follow-up CMR (53 ± 8% vs. 43 ± 12%; p < 0.01). In multivariable models, fibrosis progression was an independent predictor of all-cause mortality (hazard ratio [HR], 3.4; 95% confidence interval [CI], 1.5-7.9; p < 0.01) and major adverse cardiovascular events (MACE) (HR, 3.5; 95% CI, 1.5-8.1; p < 0.01).
Conclusions:
In nonischemic DCM, progressive myocardial fibrosis identified by CMR is independently associated with all-cause mortality and MACE. Progressive fibrosis may occur without a major change in LVEF.
Perspective:
In virtually every clinical context, the presence of myocardial LGE is a negative prognostic indicator. Though progression of fibrosis on CMR may identify patients at higher risk of mortality and adverse events, further research is needed to determine whether routine serial CMR in DCM patients can be useful in directing clinical management. Myocardial T1 mapping, a newer technique that can detect diffuse fibrosis, was not included in the CMR protocol. Other limitations of this study include small sample size and potential for selection bias, as all patients were referred for clinical CMR and therefore may have been more clinically complex than the overall DCM population.
Clinical Topics: Heart Failure and Cardiomyopathies, Noninvasive Imaging, Acute Heart Failure, Magnetic Resonance Imaging
Keywords: Adrenergic beta-Antagonists, Angiotensin-Converting Enzyme Inhibitors, Cardiomyopathy, Dilated, Diagnostic Imaging, Fibrosis, Gadolinium, Heart Failure, Magnetic Resonance Imaging, Myocardial Ischemia, Spironolactone, Stroke Volume, Ventricular Function, Left
< Back to Listings
