Open AccessThe 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
Author(s) -
MacDonald Kristin A.,
Kittleson Mark D.,
Larson Richard F.,
Kass Philip,
Klose Tyler,
Wisner Erik R.
Publication year - 2006
Publication title -
journal of veterinary internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.356
H-Index - 103
eISSN - 1939-1676
pISSN - 0891-6640
DOI - 10.1111/j.1939-1676.2006.tb00707.x
Subject(s) - medicine , ramipril , cardiology , hypertrophic cardiomyopathy , heart failure , aldosterone , left ventricular hypertrophy , diastole , brain natriuretic peptide , blood pressure , cats , myocardial fibrosis
Background:Hypertrophic Cardiomyopathy (HCM) is the most common heart disease of cats, resulting in left ventricular (LV) hypertrophy, myocardial fibrosis, and diastolic dysfunction. Hypothesis:Ramipril will reduce LV mass, improve diastolic function, and reduce myocardial fibrosis in cats with HCM without congestive heart failure (CHF). Animals: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). Conclusion: 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.