Preclinical models of myocardial infarction: from mechanism to translation.

Tamara P Martin,Ali Ali Mohamed Elbassioni,Stuart A Nicklin,Dylan O'Toole,Ali Abdullah I Zaeri,Christopher M Loughrey,Gillian A Gray,Eilidh A Macdonald

doi:10.1111/bph.15595

Tamara P Martin, Ali Ali Mohamed Elbassioni + Show 6 more

Open Access

https://doi.org/10.1111/bph.15595

Copy DOI

Abstract

Approximately 7 million people are affected by acute myocardial infarction (MI) each year, and despite significant therapeutic and diagnostic advancements, MI remains a leading cause of mortality worldwide. Preclinical animal models have significantly advanced our understanding of MI and have enabled the development of therapeutic strategies to combat this debilitating disease. Notably, some drugs currently used to treat MI and heart failure (HF) in patients had initially been studied in preclinical animal models. Despite this, preclinical models are limited in their ability to fully reproduce the complexity of MI in humans. The preclinical model must be carefully selected to maximise the translational potential of experimental findings. This review describes current experimental models of MI and considers how they have been used to understand drug mechanisms of action and support translational medicine development. LINKED ARTICLES: This article is part of a themed issue on Preclinical Models for Cardiovascular disease research (BJP 75th Anniversary). To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v179.5/issuetoc.

Highlights

Cardiovascular diseases (CVDs) remain the leading cause of death worldwide accounting for 31% of all deaths, approximating to 17.9 million people each year (Virani et al, 2020)
Preclinical models are important experimental tools that have significantly enhanced our understanding of the pathogenesis of myocardial infarction (MI) and the benefit of therapeutic interventions used to treat MI
No single preclinical model can perfectly reproduce the complexity of MI in humans

Summary

| INTRODUCTION

Cardiovascular diseases (CVDs) remain the leading cause of death worldwide accounting for 31% of all deaths, approximating to 17.9 million people each year (Virani et al, 2020). Mice are more resistant to developing HF than humans and tend to maintain sufficient cardiac function following large infarcts, allowing assessment of severe injury for several weeks after MI (Sam et al, 2000) This is advantageous when investigating long-term post-MI remodelling and testing the efficacy of novel therapies (Bayat et al, 2002; Sam et al, 2000). Similar minimally invasive approaches have been undertaken in rabbits (Fujita et al, 2004)

| Ablation methods

Findings

| CONCLUDING REMARKS