Related Experiment Video
Updated: Aug 7, 2026

Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR
Published on: April 8, 2013
The prevention of congestive heart failure: left ventricular dilation and its management
1Cardiology Division, University of Texas Southwestern Medical Center, Dallas 75235.
Insights
Left ventricular remodeling after myocardial infarction can lead to heart failure. Early interventions with nitroglycerin or captopril may help prevent this adverse cardiac remodeling.
Area of Science:
- Cardiology
- Cardiovascular Research
- Pathophysiology
Background:
- Left ventricular dilation and remodeling affect 35-40% of anterior transmural myocardial infarcts.
- These changes are key precursors to late congestive heart failure.
- The process begins within 24 hours post-infarction and can progress over years.
Purpose of the Study:
- To investigate the mechanisms of left ventricular remodeling post-myocardial infarction.
- To explore potential therapeutic interventions to ameliorate adverse cardiac remodeling.
Main Methods:
- Observational study of myocardial infarction patients.
- Analysis of left ventricular wall changes, including thinning and hypertrophy.
- Review of existing data on pharmacological interventions.
Main Results:
- Left ventricular remodeling involves both infarcted and uninfarcted myocardium.
- Cell slippage contributes to left ventricular wall thinning.
- Compensatory hypertrophy in uninfarcted segments may become pathological, impairing pump function.
Conclusions:
- Left ventricular remodeling is a significant complication of myocardial infarction, predisposing to heart failure.
- Nitroglycerin and captopril show promise in mitigating this process.
- Further research is needed to determine the role of a patent infarct-related artery.
Abstract:
Left ventricular dilation and remodelling occur in 35-40% of anterior transmural myocardial infarcts and these events are important antecedents to the development of late congestive heart failure. This process commences within the first 24 hours following myocardial infarction and may be steadily progressive over months to years. Both the infarcted and the uninfarcted regions of myocardium are equally involved in the process. Thinning of the left ventricular wall occurs mainly as a result of cell slippage. In addition, compensatory hypertrophy occurs in the uninfarcted segment of the myocardium. While this hypertrophy may initially be physiological, it ultimately appears to become a pathological process and thereby contributes to pump dysfunction. At the present time there are encouraging data to suggest that nitroglycerin, administered in the setting of the acute infarction, or the angiotensin converting enzyme inhibitor captopril, may ameliorate this process. Whether a patent infarct related artery further limits dilation is uncertain and is currently under investigation.
Related Concept Videos
Aortic Regurgitation III: Medical Management
Heart Failure IV: Classification and Diagnostic Evaluation
Heart Failure V: Medical Management
Heart Failure VI: Adjunct Therapies
Cardiomyopathy II: Dilated Cardiomyopathy
Cardiomyopathy V: Interprofessional Care

