Publication

Progression of Myocardial Fibrosis in Nonischemic DCM and Association With Mortality and Heart Failure Outcomes

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Last modified
  • 08/20/2025
Type of Material
Authors
    Aditya Mandawat, Duke University Medical CenterPairoj Chattranukulchai, Duke UniversityAnant Mandawat, Emory UniversityAlexander J Blood, Brigham and Womens Hospital, BostonSindhoor Ambati, Duke University Medical CenterBrenda Hayes, Duke University Medical CenterWolfgang Rehwald, Duke University Medical CenterHan W Kim, Duke University Medical CenterJohn F Heitner, New York Methodist HospitalDipan J Shah, Methodist DeBakey Heart&Vascular CenterIgor Klem, Duke University Medical Center
Language
  • English
Date
  • 2021-07-05
Publisher
  • ELSEVIER SCIENCE INC
Publication Version
Copyright Statement
  • © 2021, American College of Cardiology Foundation. Published by Elsevier
License
Final Published Version (URL)
Title of Journal or Parent Work
Volume
  • 14
Issue
  • 7
Start Page
  • 1338
End Page
  • 1350
Grant/Funding Information
  • This research was supported by Medtronic Inc., Mounds View, Minnesota (I. Klem) and by NIH training grant 5T32HL069749-14, Bethesda, Maryland (A. Mandawat). The other authors do not have conflicts of interest associated with this article.
Abstract
  • Objectives: The purpose of this study was to assess whether the presence and extent of fibrosis changes over time in patients with nonischemic, dilated cardiomyopathy (DCM) receiving optimal medical therapy and the implications of any such changes on left ventricular ejection fraction (LVEF) and clinical outcomes. Background: Myocardial fibrosis on cardiovascular magnetic resonance (CMR) imaging has emerged as important risk marker in patients with DCM. Methods: In total, 85 patients (age 56 ± 15 years, 45% women) with DCM underwent serial CMR (median interval 1.5 years) for assessment of LVEF and fibrosis. The primary outcome was all-cause mortality; the secondary outcome was a composite of heart failure hospitalization, aborted sudden cardiac death, left ventricular (LV) assist device implantation, or heart transplant. Results: On CMR-1, fibrosis (median 0.0 [interquartile range: 0% to 2.6%]) of LV mass was noted in 34 (40%) patients. On CMR-2, regression of fibrosis was not seen in any patient. Fibrosis findings were stable in 70 (82%) patients. Fibrosis progression (increase >1.8% of LV mass or new fibrosis) was seen in 15 patients (18%); 46% of these patients had no fibrosis on CMR-1. Although fibrosis progression was on aggregate associated with adverse LV remodeling and decreasing LVEF (40 ± 7% to 34 ± 10%; p < 0.01), in 60% of these cases the change in LVEF was minimal (<5%). Fibrosis progression was associated with increased hazards for all-cause mortality (hazard ratio: 3.4 [95% confidence interval: 1.5 to 7.9]; p < 0.01) and heart failure–related complications (hazard ratio: 3.5 [95% confidence interval: 1.5 to 8.1]; p < 0.01) after adjustment for clinical covariates including LVEF. Conclusions: Once myocardial replacement fibrosis in DCM is present on CMR, it does not regress in size or resolve over time. Progressive fibrosis is often associated with minimal change in LVEF and identifies a high-risk cohort.
Author Notes
  • Igor Klem, MD, Duke University Medical Center, DUMC-3934, Durham, NC 27710. Tel. (919)668-3539, Fax (919)668-3554, Email: igorklem@duke.edu
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