Angiotensin receptor neprilysin inhibitor LCZ696 attenuates cardiac remodeling and dysfunction after myocardial infarction by reducing cardiac fibrosis and hypertrophy

Thomas G von Lueder, Bing Hui Wang, Andrew Richard Kompa, Li Huang, Randy Webb, Pierre Jordaan, Dan Atar, Henry Krum

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259 Citations (Scopus)

Abstract

Background-Angiotensin-receptor neprilysin inhibitors (ARNi), beyond blocking angiotensin II (AngII)-signalling, augment natriuretic peptides by inhibiting their breakdown by neprilysin (NEP). The myocardial effects of ARNi have been little studied until recently. We hypothesized that LCZ696 attenuates left ventricular (LV) remodeling after experimental myocardial infarction (MI), and that this may be contributed to by inhibition of hypertrophy and fibrosis in cardiac cells. Methods and Results?One week after MI, adult male Sprague-Dawley rats were randomized to treatment for four weeks with LCZ696 (68 mg/kg body weight PO; MI-ARNi, n=11) or vehicle (MI-Vhc, n=6). Five weeks after MI, MI-ARNi versus MI-Vhc demonstrated lower LV end-diastolic diameter (LVEDD, by echocardiography; 9.7?0.2 vs 10.5?0.3 mm), higher LV ejection fraction (LVEF, 60?2 vs 47?5 ), diastolic wall strain (0.23?0.02 vs 0.13?0.02), and circular strain (CS, -9.8?0.5 vs -7.3?0.5 ; all P
Original languageEnglish
Pages (from-to)71 - 78
Number of pages8
JournalCirculation: Heart Failure
Volume8
Issue number1
DOIs
Publication statusPublished - 2015

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