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Published on: July 14, 2021
Remodelling and adverse remodelling in CAD
1Department of Internal Medicine I/Comprehensive Heart Failure Center, University Hospital Würzburg, Oberdürrbacherstr. 6, 97080, Würzburg, Germany.
Insights
Cardiac remodelling is the heart
Area of Science:
- Cardiovascular Research
- Cardiac Pathophysiology
Background:
- Cardiac remodelling is a key response to heart injury or overload.
- Maladaptive cardiac remodelling can lead to heart failure and sudden cardiac death.
- Ischemic injury in coronary artery disease alters heart structure and function.
Purpose of the Study:
- To summarize the current understanding of cardiac remodelling in response to ischemic injury.
- To highlight therapeutic strategies for reversing adverse cardiac remodelling.
- To identify future targets for preventing and reversing ischemic remodelling.
Main Methods:
- Review of existing literature on cardiac remodelling.
- Analysis of cellular, extracellular, molecular, and genetic alterations in ischemic heart disease.
- Evaluation of therapeutic interventions for adverse remodelling.
Main Results:
- Adverse cardiac remodelling leads to heart failure and sudden cardiac death.
- Ischemic injury causes significant changes in heart architecture and contractility.
- Therapeutic concepts have been developed, showing potential for reversing remodelling.
Conclusions:
- Understanding the mechanisms of ischemic remodelling is crucial for developing new therapies.
- Further research into cellular and molecular pathways can reveal novel therapeutic targets.
- Reversal of adverse remodelling is achievable and a key goal in treating heart disease.
Abstract:
Remodelling is the adaptive or maladaptive response to cardiac overload or injury resulting in changes of size and function of the heart. The final pathway of maladaptive or adverse cardiac remodelling is the evolution of heart failure or sudden cardiac death. In coronary artery disease, ischemic injury leads to changes in the cellular and extra-cellular architecture of the infarcted and non-infarcted region resulting in cavity enlargement and loss of contractility of the entire heart. During the last three decades, potential therapeutic concepts have been established and reversal of adverse remodelling could be demonstrated in up-to end-stage disease. A further understanding of the underlying cellular, extracellular, molecular and genetic alterations in ischemic remodelling should reveal other promising targets for prevention and reversal of remodelling.
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