Author + information
- Received July 25, 2013
- Revision received August 27, 2013
- Accepted September 5, 2013
- Published online December 1, 2013.
- Yuichi J. Shimada, MD∗,
- Jonathan J. Passeri, MD†,
- Aaron L. Baggish, MD†,
- Caitlin O'Callaghan, NP†,
- Patricia A. Lowry, MS, RN, APRN-BC†,
- Gia Yannekis, BA†,
- Suhny Abbara, MD‡,
- Brian B. Ghoshhajra, MD‡,
- Richard D. Rothman, MD†,
- Carolyn Y. Ho, MD∗,
- James L. Januzzi, MD†,
- Christine E. Seidman, MD∗,§,‖ and
- Michael A. Fifer, MD†∗ ()
- ∗Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts
- †Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts
- ‡Cardiac MR PET CT Program, Department of Radiology and Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts
- §Howard Hughes Medical Institute, Boston, Massachusetts
- ‖Department of Genetics, Harvard Medical School, Boston, Massachusetts
- ↵∗Reprint requests and correspondence:
Dr. Michael A. Fifer, Massachusetts General Hospital, Cardiology Division, 55 Fruit Street, Gray/Bigelow 800, Mailstop 843, Boston, Massachusetts 02114.
Objectives The aim of this study was to evaluate the effects of losartan on left ventricular (LV) hypertrophy and fibrosis in patients with nonobstructive hypertrophic cardiomyopathy (HCM).
Background Despite evidence that myocardial hypertrophy and fibrosis are mediated by angiotensin II and are important determinants of morbidity and mortality in patients with HCM, no prior studies have evaluated the effects of angiotensin receptor blockers on LV hypertrophy and fibrosis with cardiac magnetic resonance imaging.
Methods In double-blind fashion, 20 patients (3 women, 17 men; age: 51 ± 13 years) with HCM were randomly assigned to receive placebo (n = 9) or losartan 50 mg twice a day (n = 11) for 1 year. Cardiac magnetic resonance imaging was performed at baseline and 1 year to measure LV mass and extent of fibrosis as assessed by late gadolinium enhancement.
Results There was a trend toward a significant difference in the percent change in LV mass (median [interquartile range]: +5% [−4% to +21%] with placebo vs. −5% [−11% to −0.9%] with losartan; p = 0.06). There was a significant difference in the percent change in extent of late gadolinium enhancement, with the placebo group experiencing a larger increase (+31% ± 26% with placebo vs. −23% ± 45% with losartan; p = 0.03).
Conclusions This pilot study suggests attenuation of progression of myocardial hypertrophy and fibrosis with losartan in patients with nonobstructive HCM. Confirmation of these results in a larger trial is required to confirm a place for angiotensin receptor blockers in the management of patients with HCM. (Effect of Losartan in Patients With Nonobstructive Hypertrophic Cardiomyopathy; NCT01150461)
- angiotensin II receptor blocker
- cardiac magnetic resonance imaging
- hypertrophic cardiomyopathy
- late gadolinium enhancement
- left ventricular fibrosis
Dr. Ho has received financial support from the National Institutes of Health. Dr. Januzzi has received grants from Roche, Critical Diagnostics, BG Medicine, Siemens, Singulex, Novartis, Amgen, Zensun, and Thermo Fisher Scientific. Dr. Seidman is a founder and owns shares of Myokardia Inc., a startup company that is developing therapeutics that target the sarcomere; and has received financial support from the National Institutes of Health and the Howard Hughes Medical Institute. Dr. Fifer has received financial support from Merck & Co., Inc. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received July 25, 2013.
- Revision received August 27, 2013.
- Accepted September 5, 2013.
- American College of Cardiology Foundation