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Updated: Aug 12, 2026

Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR
Published on: April 8, 2013
Ventricular remodeling and its prevention in the treatment of heart failure
R D Patten1, J E Udelson, M A Konstam
1Department of Medicine, New England Medical Center, Boston, MA 02111, USA.
Insights
Left ventricular remodeling after heart injury is a harmful process. Angiotensin-converting enzyme (ACE) inhibitors and beta-blockers can prevent this remodeling and improve patient survival.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Ventricular remodeling involves changes in left ventricular (LV) geometry, mass, and volume.
- LV remodeling after myocardial infarction or in heart failure predicts morbidity and mortality.
- LV remodeling is recognized as a maladaptive process.
Purpose of the Study:
- To review the role of pharmacologic agents in inhibiting left ventricular remodeling.
- To highlight the impact of angiotensin-converting enzyme (ACE) inhibitors and beta-blockers on LV remodeling and survival.
Main Methods:
- Review of existing data and studies on drug efficacy in preventing LV remodeling.
- Analysis of the role of the renin-angiotensin and sympathetic nervous systems in cardiac remodeling.
Main Results:
- Angiotensin-converting enzyme (ACE) inhibitors demonstrate significant benefits in improving survival and preventing progressive LV remodeling.
- Beta-adrenergic blockers also show a positive effect on both survival and remodeling.
- The renin-angiotensin system and sympathetic nervous system are implicated as causative factors in LV remodeling.
Conclusions:
- ACE inhibitors should be a standard treatment for patients with LV dysfunction to prevent remodeling.
- Beta-blockers may also be beneficial and should be considered in the pharmacologic regimen.
- Targeting the renin-angiotensin and sympathetic nervous systems is crucial for managing LV remodeling.
Abstract:
Ventricular remodeling refers to changes in left ventricular (LV) geometry, mass, and volume in response to myocardial injury or alterations in load. The extent of LV dilatation or remodeling after myocardial infarction (MI) or in patients with heart failure is a strong predictor of both morbidity and mortality. Based on these observations, it is clear that LV remodeling is a maladaptive process. Two classes of drugs appear to inhibit LV remodeling. A large amount of data support the use of angiotensin-converting enzyme (ACE) inhibitors to improve survival and to prevent progressive remodeling. In addition, recent studies suggest that beta-adrenergic blockers have a beneficial effect on both survival and remodeling. These data support a causative role of the renin-angiotensin system and perhaps the sympathetic nervous system in this process. Thus, ACE inhibitors and possibly beta-blockers should be part of the pharmacologic regimen for the treatment of patients with LV dysfunction to prevent progressive LV remodeling.
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