title: The effect of ramipril on left ventricular mass, myocardial fibrosis, diastolic function, and plasma neurohormones in Maine Coon cats with familial hypertrophic cardiomyopathy without heart failure.
abstract: BACKGROUND
  Hypertrophic cardiomyopathy (HCM) is the most common heart disease of cats, resulting in left ventricular (LV) hypertrophy, myocardial fibrosis, and diastolic dysfunction.
  
  
  OBJECTIVE
  Ramipril will reduce LV mass, improve diastolic function, and reduce myocardial fibrosis in cats with HCM without congestive heart failure (CHF).
  
  
  METHODS
  This prospective, blinded, placebo-controlled study included 26 Maine Coon and Maine Coon cross-bred cats with familial HCM but without CHF.
  
  
  METHODS
  Cats were matched for LV mass index (LVMI) and were randomized to receive ramipril (0.5 mg/kg) or placebo q24h for 1 year, with investigators blinded. Plasma brain natriuretic peptide (BNP) concentration, plasma aldosterone concentration, Doppler tissue imaging (DTI), and systolic blood pressure were measured at baseline and every 3 months for 1 year. Cardiac magnetic resonance imaging (cMRI) was performed to quantify LV mass and myocardial fibrosis by delayed enhancement (DE) cMRI at baseline and 6 and 12 months. Plasma angiotensin-converting enzyme (ACE) activity was measured on 16 cats 1 hour after PO administration.
  
  
  RESULTS
  Plasma ACE activity was adequately suppressed (97%) in cats treated with ramipril. LV mass, LVMI, DTI, DE, blood pressure, plasma BNP, and plasma aldosterone were not different in cats treated with ramipril compared with placebo (P = .85, P = .94, P = .91, P = .89, P = .28, P = .18, and P = .25, respectively).
  
  
  CONCLUSIONS
  Treatment of Maine Coon cats with HCM without CHF with ramipril did not change LV mass, improve diastolic function, alter DE, or alter plasma BNP or aldosterone concentrations in a relevant manner.
authors.affiliation: Department of Veterinary Medicine and Epidemiology, University of California, Davis 95616, USA. kamacdonald@ucdavis.edu
authors.forename: Kristin A
authors.initials: KA
authors.lastname: MacDonald
authors.forename: Mark D
authors.initials: MD
authors.lastname: Kittleson
authors.forename: Richard F
authors.initials: RF
authors.lastname: Larson
authors.forename: Philip
authors.initials: P
authors.lastname: Kass
authors.forename: Tyler
authors.initials: T
authors.lastname: Klose
authors.forename: Erik R
authors.initials: ER
authors.lastname: Wisner
mesh_terms: D000450:Aldosterone / Q000097:blood; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D024741:Cardiomyopathy, Hypertrophic, Familial / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology / Q000662:veterinary*; D002371:Cat Diseases / Q000097:blood / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D002415:Cats; D015150:Echocardiography, Doppler / Q000662:veterinary; D005355:Fibrosis / Q000188:drug therapy / Q000473:pathology / Q000662:veterinary; D006339:Heart Rate / Q000187:drug effects; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy / Q000662:veterinary; D008279:Magnetic Resonance Imaging / Q000662:veterinary; D009206:Myocardium / Q000473:pathology; D020097:Natriuretic Peptide, Brain / Q000097:blood; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism; D011446:Prospective Studies; D017257:Ramipril / Q000627:therapeutic use*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D020097:Natriuretic Peptide, Brain; D000450:Aldosterone; D007703:Peptidyl-Dipeptidase A; D017257:Ramipril