Prevention of left ventricular remodelling after acute myocardial infarction: an update
Roberta Rossini1, Michele Senni, Giuseppe Musumeci
1Dipartimento Cardiovascolare, Ospedali Riuniti di Bergamo, Bergamo, Italy. roberta_rossini@yahoo.it
Insights
Left ventricular remodeling after heart attack is a progressive issue. Current drugs like ACE inhibitors help, but new targets like stem cell therapy show promise for reversing this damage.
Area of Science:
- Cardiology
- Pharmacology
- Regenerative Medicine
Background:
- Left ventricular remodeling begins after acute myocardial infarction, leading to heart failure.
- This process involves chamber dilation, increased wall stress, and impaired heart function.
- Neurohormonal activation and sympathetic stimulation contribute to post-infarction left ventricular dysfunction.
Purpose of the Study:
- To review recent patents and experimental studies on drugs preventing left ventricular remodeling.
- To explore novel therapeutic targets for reversing left ventricular remodeling.
Main Methods:
- Review of scientific literature, including patents and experimental studies.
- Analysis of pharmacological interventions targeting left ventricular remodeling.
- Evaluation of emerging regenerative and molecular targets.
Main Results:
- Angiotensin-Converting Enzyme Inhibitors, Angiotensin Receptor Blockers, and Beta-Blockers are effective in modulating remodeling and reducing adverse events.
- High-risk patients were often excluded from trials, leaving clinical questions unanswered.
- Experimental data suggests stem cell transfer, oxidant stress pathways, inflammatory pathways, and matrix-metalloproteinase activation as new targets.
Conclusions:
- Established drug classes effectively manage left ventricular remodeling post-myocardial infarction.
- Further research is needed to address clinical uncertainties and explore novel therapeutic strategies.
- Emerging targets like stem cells and specific molecular pathways offer potential for reversing cardiac damage.
Abstract:
Left ventricular remodelling is a progressive process, which starts immediately after acute myocardial infarction and evolves in the chronic phase of heart failure. It is characterized by left ventricular chamber dilatation and increased wall stress, which results in alteration of the contractile properties of the non-infarct zone and impairment of the systolic and diastolic performances of the left ventricle. Neurohormonal activation and increased sympathetic stimulation are among the factors that have been linked to the development and progression of left ventricular dysfunction after acute myocardial infarction. The present review will address recent insights from new patents and experimental studies of drugs, which ought to prevent left ventricular remodelling. Angiotensin-Converting Enzyme Inhibitors, Angiotensin Receptor Blockers and Beta-Blockers have been proven effective in modulating the process of remodelling and in reducing the occurrence of adverse events. However, in most of the trials high risk patients have been excluded, and uncertainty still exists regarding a number of clinically relevant questions. Data from experimental studies have identified new targets for interventions to prevent reverse left ventricular remodelling, i.e. stem cell transfer, activation of cardiac and leukocyte-dependent oxidant stress pathways, inflammatory pathway activation, matrix-metalloproteinase activation.
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