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The concept of cardioreparation: Part 1. Pathophysiology of remodelling
C G Brilla1, R L Murphy, J F Smits
1Division of Cardiology, Philipps University of Marburg, Germany.
Insights
Left ventricular hypertrophy, a common condition in heart disease patients, can be reversed through cardioreparation. This process involves reducing myocyte hypertrophy and myocardial fibrosis, potentially improving cardiac function and patient outcomes.
Area of Science:
- Cardiology
- Pathophysiology
Background:
- Left ventricular hypertrophy (LVH) is prevalent in patients with hypertension, congestive heart failure, and post-myocardial infarction.
- LVH is linked to increased risks of adverse cardiovascular events like angina, myocardial infarction, and heart failure.
Purpose of the Study:
- To explain the link between LVH and adverse cardiovascular events by examining cardiac structural changes (remodeling).
- To explore the potential of reversing cardiac remodeling (cardioreparation) to improve patient prognosis.
Main Methods:
- Review of laboratory investigations from animal models of cardiovascular diseases.
- Identification of key features of cardiac remodeling: myocyte hypertrophy, myocardial fibrosis, and coronary vascular pathology.
Main Results:
- Cardiac remodeling disrupts heart structure, impairs pumping function, and compromises blood supply.
- Reversal of remodeling (cardioreparation) shows potential to restore cardiac structure and function.
Conclusions:
- Cardioreparation involves the regression of myocyte hypertrophy and myocardial fibrosis.
- Myocyte hypertrophy results from ventricular pressure/volume overload; fibrosis involves renin-angiotensin-aldosterone systems.
- Angiotensin-converting enzyme inhibitors may induce cardioreparation by reducing blood pressure and inhibiting these systems.
Purpose:
Left ventricular hypertrophy is common in patients with hypertension or congestive heart failure and in survivors of myocardial infarction. It is associated with increased risks of adverse cardiovascular events, including angina, myocardial infarction and congestive heart failure. We aimed to explain these observations in terms of changes in the structure of the heart, collectively described as remodelling.
Data Extraction:
Laboratory investigations of animal models of cardiovascular diseases were reviewed. The most prominent features of remodelling are myocyte hypertrophy, excessive accumulation of collagen in the heart (myocardial fibrosis) and pathological changes in the coronary blood vessels. Remodelling disrupts the structure of the heart and impairs its pumping function and blood supply. The reversal of remodelling, termed cardioreparation, could restore cardiac structure and function towards normal and improve the prognosis of patients with cardiovascular diseases.
Conclusions:
Cardioreparation implies the regression of myocyte hypertrophy and myocardial fibrosis. Myocyte hypertrophy is primarily a response to chronic pressure or volume overload of the ventricles, whereas myocardial fibrosis depends on activation of circulating and tissue renin-angiotensin-aldosterone systems. Angiotensin converting enzyme inhibitors reduce blood pressure and inhibit these systems. They might therefore induce cardioreparation.