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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 dilatation following myocardial infarction: clinical course and potential for therapy
1Harvard Medical School, Brigham and Women's Hospital, Boston, Mass 02115.
Insights
Cardiac enlargement after myocardial infarction (MI) is linked to reduced survival. Angiotensin-converting enzyme (ACE) inhibition with captopril may halt this progressive left ventricular enlargement, with ongoing trials assessing its impact on survival.
Area of Science:
- Cardiology
- Heart Failure Research
- Clinical Trials
Background:
- Cardiac enlargement is a known indicator of systolic dysfunction and reduced survival.
- Progressive left ventricular (LV) enlargement occurs after acute myocardial infarction (AMI).
- This enlargement involves infarct expansion, regional lengthening, and overall LV volume increase over time.
Purpose of the Study:
- To investigate the progressive nature of cardiac enlargement following acute myocardial infarction (AMI).
- To evaluate the potential of angiotensin-converting enzyme (ACE) inhibition to halt post-infarction LV enlargement.
- To inform the ongoing Survival and Ventricular Enlargement (SAVE) trial on captopril's efficacy.
Main Methods:
- Review of experimental and clinical studies on cardiac enlargement post-AMI.
- Analysis of the temporal progression of LV volume changes after infarction.
- Consideration of pharmacological interventions, specifically ACE inhibition with captopril.
Main Results:
- Cardiac enlargement post-AMI is a multi-stage process occurring over days, weeks, and up to a year.
- Experimental and clinical data suggest ACE inhibition can mitigate progressive LV enlargement.
- The SAVE trial is investigating if captopril improves survival after infarction.
Conclusions:
- Progressive left ventricular enlargement after AMI is a significant factor impacting survival.
- Angiotensin-converting enzyme inhibition, exemplified by captopril, shows promise in preventing detrimental cardiac remodeling.
- Further clinical validation through trials like SAVE is crucial to confirm survival benefits.
Abstract:
The enlarged heart has long been recognized as an important sign of systolic dysfunction of many different etiologies. Regardless of etiology, cardiac enlargement is associated with decreased survival. Cardiac enlargement after acute myocardial infarction (AMI) may be a progressive process. Early after AMI, the process of infarct expansion, or thinning and stretching of the infarct region leads to early volume enlargement detectable within 3 days of the infarct. During the next 2 weeks, volume enlargement takes place which includes lengthening of both the infarcted and the non-infarcted regions. Finally, additional left ventricular enlargement occurs during the next year after the infarction. Both experimental and clinical studies have demonstrated that such progressive LV enlargement may be halted by angiotensin converting enzyme inhibition with captopril. A large scale randomized trial is currently under way to determine whether captopril improves survival after infarction (Survival and Ventricular Enlargement, SAVE).
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