Evaluating Sacubitril/Valsartan's Efficacy in Reducing Myocardial Hypertrophy and Fibrosis in Feline Models.

Sacubitril/valsartan significantly reduced LV hypertrophy and fibrosis in a feline pressure-overload model.

This exploratory pilot study investigated the efficacy of sacubitril/valsartan (Sac/Val), an angiotensin receptor-neprilysin inhibitor (ARNi), in reducing myocardial hypertrophy and fibrosis in a feline pressure-overload model relevant to hypertrophic cardiomyopathy (HCM). Twelve healthy cats were equally randomized into three groups: sham surgery (SHAM), abdominal aortic constriction (AAC), and AAC with Sac/Val treatment (AAC+Sac/Val). Cardiac remodeling was assessed via transthoracic echocardiography, CT imaging, serial measurement of NT-proBNP and cardiac troponin I (cTnI), histological evaluation of myocardial fibrosis, and qRT-PCR targeting key fibrosis-associated transcripts (BNP, ACTA, TGF-β, COL-I). By Day 90, Sac/Val-treated cats demonstrated significantly lower NT-proBNP (0.241 vs. 0.921 ng/mL) and cTnI (0.958 vs. 3.313 ng/mL) compared to untreated AAC cats. Maximal LV wall thickness was also significantly reduced on both echocardiography (3.45 vs. 5.88 mm) and CT (3.54 vs. 5.68 mm). Histology confirmed reduced interstitial collagen deposition, and fibrosis-associated gene expression was significantly downregulated in the Sac/Val group. While the study is limited by its small sample size, short follow-up duration, and use of a surgically induced rather than naturally occurring HCM model, results suggest that Sac/Val has meaningful antihypertrophic and antifibrotic effects in cats. These findings support further investigation of Sac/Val as a potential therapeutic agent for feline HCM.

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