Cardiovascular Research Institute

You are here

Pressure overload leads to coronary plaque formation, progression, and myocardial events in ApoE-/- mice.

TitlePressure overload leads to coronary plaque formation, progression, and myocardial events in ApoE-/- mice.
Publication TypeJournal Article
Year of Publication2019
AuthorsMarino, A, Zhang, Y, Rubinelli, L, Riemma, MAntonietta, Ip, JE, Di Lorenzo, A
JournalJCI Insight
Volume4
Issue9
Date Published2019 May 02
ISSN2379-3708
Abstract

Hypercholesterolemia and hypertension are two major risk factors for coronary artery diseases, which remain the major cause of mortality in the industrialized world. Current animal models of atherosclerosis do not recapitulate coronary plaque disruption, thrombosis, and myocardial infarction occurring in humans. Recently, we demonstrated that exposure of the heart to high pressure, by transverse aortic constriction (TAC), induced coronary lesions in ApoE-/- mice on chow diet. The aim of this study was to characterize the magnitude and location of coronary lesions in ApoE-/- mice after TAC and to assess the susceptibility of coronary plaque to disruption, leading to myocardial events. Here, we describe a reliable pathological condition in mice characterized by the development of coronary lesions and its progression, leading to myocardial infarction; this model better recapitulates human disease. Following TAC surgery, about 90% of ApoE-/- mice developed coronary lesions, especially in the left anterior descending artery, with 59% of the mice manifesting a different magnitude of LAD stenosis. Myocardial events, identified in 74% of the mice, were mainly due to coronary plaque thrombosis and occlusion. That TAC-induced development and progression of coronary lesions in ApoE-/- mice, leading to myocardial events, represents a potentially novel and important tool to investigate the development of coronary lesions and its sequelae in a setting that better resemble human conditions.

DOI10.1172/jci.insight.128220
Alternate JournalJCI Insight
PubMed ID31045580