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[Ischemic cardiomyopathy: remodeling, hypertrophy, subendocardial risk. Can processes be controlled?]
D Himbert1, A Guiomard, M C Aumont
1Service de cardiologie, hôpital Bichat, Paris.
Insights
Ischaemic cardiomyopathy, caused by coronary artery disease, leads to heart failure through ventricular remodelling and hibernating myocardium. Revascularisation and ACE inhibitors can halt its progression and improve prognosis.
Area of Science:
- Cardiology
- Cardiovascular Diseases
- Heart Failure Research
Context:
- Ischaemic cardiomyopathy (ICM) is myocardial dysfunction stemming from coronary artery disease.
- ICM involves segmental infarction causing ventricular remodelling and viable but dysfunctional (hibernating) myocardium.
- This progression often leads to heart failure.
Purpose:
- To outline the pathophysiology of ischaemic cardiomyopathy.
- To discuss therapeutic strategies for arresting the progression of ICM.
- To highlight the role of revascularisation and medical management in improving outcomes.
Summary:
- ICM results from coronary disease, causing myocardial infarction, ventricular remodelling, and myocardial hibernation.
- Therapeutic interventions include myocardial revascularisation (emergency or elective) and limiting ventricular remodelling.
- Angiotensin-converting enzyme (ACE) inhibitors and nitroglycerin are key in managing ventricular remodelling and load.
Impact:
- Revascularisation can halt the adverse progression of ICM.
- Limiting ventricular remodelling through ACE inhibitors and nitroglycerin improves secondary prevention post-infarction.
- The Survival and Ventricular Enlargement (SAVE) study confirmed the benefits of ACE inhibitors in reducing ventricular remodelling and improving prognosis.
Abstract:
Ischaemic cardiomyopathy reflects the myocardial dysfunction caused by coronary disease. It results from the association of 1. segmental infarction(s) responsible for ventricular "remodelling", i.e. expansion of the necrotic area(s) and hypertrophy-dilatation of the rest of the ventricle, eventually concurring to heart failure; 2. areas which are viable but with a function that is reversibly compromised by severe acute or chronic ischaemia (myocardial sideration or hibernation) affecting mainly the subendocardium. The spontaneous course of cardiomyopathy towards the worst can be arrested by 1. revascularisation of the myocardium at risk by coronary reperfusion performed either as an emergency in case of infarct in the process of formation, or after detection of the viable myocardial areas by isotopic methods; 2. prevention or limitation of ventricular remodelling by coronary reperfusion and improvement of the ventricular load by administration of angiotensin-converting enzyme inhibitors and nitroglycerin. The Survival and Ventricular Enlargement study (SAVE) has been the first to demonstrate the relationship between limitation of ventricular remodelling and improvement of the secondary prognosis of infarction obtained by angiotensin-converting enzyme inhibitors.