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Permanent Ligation of the Left Anterior Descending Coronary Artery in Mice: A Model of Post-myocardial Infarction Remodelling and Heart Failure
Published on: December 2, 2014
Infarct size and post-infarct inflammation determine the risk of cardiac rupture in mice
Xiao-Ming Gao1, Ziqiu Ming, Yidan Su
1Experimental Cardiology Laboratory, Baker IDI Heart Diabetes Institute, and Alfred Heart Centre, the Alfred Hospital, Monash University, 75 Commercial Road, Prahran, Melbourne, Victoria 3004, Australia.
Background/Objectives:
Infarct size (IS) is a determinant of pathophysiological events after myocardial infarction (MI), but its relation to the risk of cardiac rupture remains undefined.
Methods:
MI was induced in 129sv and C57Bl/6 mice. Left ventricular (LV) remodelling was examined by echocardiography prior to the onset of rupture. Changes in muscle tensile strength and expression of inflammatory factors were determined. Autopsy was performed and IS measured.
Results:
Rupture incidence was higher in 129sv than C57Bl/6 mice (62% vs. 33%, P<0.001). Rupture occurred in mice with IS over a threshold, which was smaller in 129sv than C57Bl/6 mice (20% vs. 30%). 129sv mice with IS>30% had a higher incidence of rupture than those with IS 20-30%. Echocardiography revealed IS-dependent LV remodelling and dysfunction and 129sv mice had a better-preserved function compared with C57Bl/6 counterparts. 129sv but not C57Bl/6 mice that subsequently developed rupture showed more severe regional dysfunction and remodelling compared with IS-matched non-ruptured hearts. Tensile strength of the infarcted myocardium was reduced significantly, which was IS-related. 129sv mice had higher expression levels of inflammatory mediators in the infarcted myocardium or circulating inflammatory cells, underlying the higher risk of rupture in this strain than C57Bl/6.
Conclusions:
A critical IS level is necessary for post-MI rupture and IS correlates with the reduction in muscle tensile strength. Strain differences exist in global function and regional or systemic inflammation that explain the different risk of rupture or heart failure between strains. Limiting IS or minimizing inflammation would lower the risk of ventricular rupture.
Insights
A critical infarct size is needed for cardiac rupture after myocardial infarction (MI). Mouse strain differences in inflammation and function influence rupture risk, suggesting limiting infarct size and inflammation may prevent rupture.
Area of Science:
- Cardiovascular Research
- Myocardial Infarction Pathophysiology
- Cardiac Mechanics
Background:
- Infarct size (IS) is a key factor in post-myocardial infarction (MI) events.
- The relationship between infarct size and cardiac rupture risk is not fully understood.
Purpose of the Study:
- To investigate the correlation between infarct size and cardiac rupture risk.
- To explore strain-dependent differences in cardiac remodeling, inflammation, and rupture susceptibility after MI.
Main Methods:
- Myocardial infarction (MI) was induced in 129sv and C57Bl/6 mice.
- Left ventricular (LV) remodeling was assessed via echocardiography.
- Myocardial tensile strength and inflammatory factor expression were measured; autopsy determined infarct size.
Main Results:
- Rupture incidence was significantly higher in 129sv mice (62%) compared to C57Bl/6 mice (33%).
- Cardiac rupture occurred when infarct size exceeded a strain-specific threshold, which was lower in 129sv mice.
- Reduced myocardial tensile strength correlated with infarct size; 129sv mice exhibited greater inflammation and higher rupture risk.
Conclusions:
- A critical infarct size threshold is essential for post-MI cardiac rupture.
- Infarct size directly impacts myocardial tensile strength and LV remodeling.
- Strain-specific differences in inflammation and cardiac function contribute to varying rupture risks, highlighting potential therapeutic targets.
