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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
Left ventricular remodelling after acute myocardial infarction--solved and unsolved issues
1Service de Cardiologie, Hospital Saint Jacques, Besancon, France.
Insights
Left ventricular remodelling post-myocardial infarction can lead to heart failure. Interventions targeting the renin-angiotensin system show promise in limiting this remodelling and reducing mortality, though optimal strategies require further study.
Area of Science:
- Cardiology
- Cardiovascular Research
- Pharmacology
Background:
- Left ventricular remodelling following acute myocardial infarction (MI) can lead to progressive left ventricular dysfunction and congestive heart failure.
- The renin-angiotensin system (RAS) plays a critical role in mediating these adverse remodelling processes.
- While RAS inhibition has shown benefits, optimal therapeutic strategies and patient selection remain areas of active investigation.
Purpose of the Study:
- To review the mechanisms of left ventricular remodelling after acute MI.
- To discuss the role of the renin-angiotensin system in this process.
- To evaluate the current evidence and controversies surrounding pharmacological interventions, particularly ACE inhibitors, in managing post-MI remodelling and heart failure.
Main Methods:
- Review of existing literature on left ventricular remodelling after acute myocardial infarction.
- Analysis of the impact of systemic and tissue renin-angiotensin systems.
- Evaluation of clinical trial data on pharmacological interventions, focusing on ACE inhibitors.
Main Results:
- Key predictors of late left ventricular function impairment include akinetic surface >20%, left ventricular ejection fraction <40%, anterior MI location, low stroke volume, and persistent infarct artery occlusion.
- ACE inhibitors have demonstrated benefits in reducing mortality and limiting remodelling, particularly in patients with low ejection fraction.
- Controversies persist regarding the optimal timing of ACE inhibitor initiation, combination therapy with thrombolytics, and the role of angioplasty.
Conclusions:
- Left ventricular remodelling is a critical determinant of long-term outcomes after acute MI.
- Understanding predictors of LV dysfunction aids in identifying high-risk patients.
- Further research is needed to optimize RAS-targeted therapies and address current clinical controversies to improve post-MI patient management.
Abstract:
Left ventricular remodelling after acute myocardial infarction, through long-term left ventricular chamber dilatation and increased wall stress can result in alteration of the contractile properties of the non-infarct zone, impairment of the systolic and diastolic performances of the left ventricle, and eventually congestive heart failure. Left ventricular remodelling is influenced by several factors, among which the role of systemic and tissue renin angiotensin systems is determinant. Pharmacological interventions on the renin angiotensin systems were shown to limit left ventricular remodelling and reduce mortality from acute myocardial infarction in rats and humans, although the results of some trials remain controversial. To date, the beneficial effects of ACE inhibitors have only been demonstrated in patients with a low residual ejection fraction. Recent observations of changes in left ventricular chamber dilatation and left ventricular wall hypertrophy occurring over the course of time after acute myocardial infarction allow better definition of the subset of patients who are at risk of progressive left ventricular dysfunction and congestive heart failure. An akinetic surface >20%, a left ventricular ejection fraction <0 x 40, an anterior location of the infarction, a stroke volume <31 ml.m(-2) during the acute phase, and persistent occlusion of the infarct-related artery are the most powerful predictors of late left ventricular function impairment. Some issues remain controversial, such as the optimal time for introducing ACE inhibitors after the onset of symptoms, the potential additive effects of ACE inhibitors given in conjunction with thrombolytic therapy, and the role of systemic angioplasty of the infarct-related artery.
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