Author + information
- Received June 25, 2018
- Revision received August 13, 2018
- Accepted August 15, 2018
- Published online August 5, 2019.
- Tomas Vita, MD, MPHa,∗,
- Christoph Gräni, MD, PhDb,∗,
- Siddique A. Abbasi, MD, MSca,
- Tomas G. Neilan, MDc,
- Ethan Rowin, MDa,
- Kyoichi Kaneko, MD, PhDb,
- Otavio Coelho-Filho, MD, MPH, PhDb,
- Eri Watanabe, MD, PhDa,
- Francois-Pierre Mongeon, MD, SMd,
- Hoshang Farhad, MDb,
- Carlos Henrique Rassi, MDb,
- Yuna L. Choi, BAb,
- Kathleen Cheng, BAb,
- Michael M. Givertz, MDb,
- Ron Blankstein, MDa,b,
- Michael Steigner, MDa,
- Ayaz Aghayev, MDa,
- Michael Jerosch-Herold, PhDa and
- Raymond Y. Kwong, MD, MPHa,b,∗ ()
- aNoninvasive Cardiovascular Imaging Program, Department of Radiology, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts
- bCardiovascular Division, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts
- cCardiac MR PET CT Program and Division of Cardiology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts
- dDepartment of Medicine, Montreal Heart Institute, Université de Montréal, Montréal, Quebec, Canada
- ↵∗Address for correspondence:
Dr. Raymond Y. Kwong, Brigham and Women's Hospital, Cardiovascular Division, Department of Medicine, Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115.
Objectives In patients with nonischemic dilated cardiomyopathy (NIDCM), native T1, partition coefficient (λGd), and extracellular volume fraction (ECV) mapping may offer prognostic values beyond late gadolinium enhancement (LGE), by scaling the range of myocardial changes.
Background In patients with NIDCM, LGE is seen in 30% of patients and it indicates adverse prognosis.
Methods The study mapped 6 anatomical locations using all 4 cardiac magnetic resonance (CMR) tissue-characterizing methods and associated with outcome. The authors performed T1 mapping of the myocardium and the blood pool, before and serially after contrast injection, using a Look-Locker cine gradient-echo technique to obtain T1 and the corresponding reciprocal R1 values. λGd values were derived from the slopes of the least-squares regression lines for myocardial versus blood R1, then adjusted to serum hematocrit to yield ECV.
Results Consecutive 240 NIDCM patients (49 ± 16 years of age; 38% women) underwent CMR for cardiac function, LGE, native T1, λGd, and ECV. After a median of 3.8 years, 36 (15%) experienced major adverse cardiac events (MACE), including 22 heart failure hospitalizations and 14 deaths. Nonischemic LGE was detected in 34%, whereas ECV was elevated (≥1 location) in 58%. Comparing the 4 methods, mean ECV and λGd both demonstrated strong association with MACE (both p < 0.001). In contrast to native T1 and LGE, ECV values from all 6 locations were associated with MACE and death, with the anteroseptum being the most significant (p < 0.0001). The number of abnormal ECV locations correlated linearly with annual MACE rates (p = 0.0003). Mean ECV was the only predictor to enter a prognostic model that contained age, sex, New York Heart Association functional class, and left ventricular ejection fraction. For every 10% increase, mean ECV portended to a 2.8-fold adjusted increase risk to MACE (p < 0.001).
Conclusions In this study of patients with NIDCM, mapping the myocardial extent of abnormality using ECV offers prognostication toward heart failure outcomes incremental to LGE or native T1 mapping.
↵∗ Drs. Vita and Gräni contributed equally to this paper and are joint first authors.
Dr. Vita was supported by National Institutes of Health training grant T32-HL094301-05. Dr. Kwong was supported by National Institutes of Health award 1UH2 TR000901; and has received research grant support from GlaxoSmithKline, Myokardia, and the Society for Cardiovascular Magnetic Resonance. Dr. Coelho-Filho is supported by a National Council for Scientific and Technological Development Productivity in Research award grant (303366/2015-0); and is supported by a Young Investigators Grant from the São Paulo Research Foundation (2015/15402-2). Dr. Mongeon has received research funding from Bracco and the Montreal Heart Institute has a research agreement with Siemens. Dr. Jerosch-Herold was supported by National Institutes of Health award R01 HL090634. Dr. Abbasi is a currently an employee of Amgen. Dr. Gräni has received funding support from the Novartis Foundation for Medical-Biological Research, Bangerter-Rhyner Foundation, Swiss Sports Medicine Society, and Kreislauf Kardiologie Foundation. Dudley Pennell, MD, served as Guest Editor for this paper.
- Received June 25, 2018.
- Revision received August 13, 2018.
- Accepted August 15, 2018.
- 2019 American College of Cardiology Foundation
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