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Updated: Aug 11, 2026

Myocardial Infarction and Functional Outcome Assessment in Pigs
Published on: April 25, 2014
[Pathophysiology and therapeutic aspects of left ventricular "remodeling" in the post-infarct phase]
1II. Interne Abteilung mit Kardiologie und Internistischer Intensivmedizin, A. ö. Krankenhaus Wels, Grieskirchnerstrasse 42, A-4600 Wels. johann.auer@khwels.at
Insights
Left ventricular remodeling alters heart size and function after injury. Early interventions can mitigate damage and improve long-term outcomes in conditions like myocardial infarction.
Area of Science:
- Cardiology
- Physiology
- Pathology
Context:
- Left ventricular remodeling is a complex process influenced by mechanical, neurohormonal, and genetic factors.
- It can be adaptive during normal growth or pathological in conditions such as myocardial infarction, cardiomyopathy, hypertension, and valvular heart disease.
- Postinfarction remodeling occurs in early (within 72 hours) and late phases, involving infarct expansion, ventricular dilatation, shape distortion, and hypertrophy.
Purpose:
- To describe the mechanisms and phases of left ventricular remodeling.
- To highlight the adaptive responses and triggers involved in myocardial repair.
- To emphasize the role of infarct artery patency and pharmacological interventions in managing remodeling.
Summary:
- Left ventricular remodeling involves changes in size, shape, and function regulated by various factors.
- Early postinfarction remodeling includes infarct expansion, potentially leading to rupture or aneurysm.
- Late remodeling involves global ventricular changes, hypertrophy, and collagen degradation, influenced by infarct artery patency.
Impact:
- Understanding remodeling aids in developing strategies to prevent adverse cardiac events.
- Pharmacological interventions like ACE inhibitors and beta-blockers can minimize adverse remodeling and improve prognosis.
- Targeting infarct artery patency is crucial for managing postinfarction remodeling and cardiac repair.
Abstract:
Left ventricular remodeling is the process by which ventricular size, shape, and function are regulated by mechanical, neurohormonal, and genetic factors. Remodeling may be physiological and adaptive during normal growth or pathological due to myocardial infarction, cardiomyopathy, hypertension, or valvular heart disease. Postinfarction remodeling has been divided into an early phase within 72 hours and a late phase beyond 72 hours. The early phase involves expansion of the infarct zone, which may result in early ventricular rupture or aneurysm formation. Late remodeling involves the left ventricle globally and is associated with time-dependent dilatation, the distortion of ventricular shape, and mural hypertrophy. Hypertrophy and collagen degradation are adaptive responses during postinfarction remodeling. Myocardial repair is triggered by cytokines released from injured myocytes. Ventricular remodeling is influenced most by infarct artery patency. Once infarct evolution has occurred, pharmacological intervention, like ACE inhibition and beta-adrenoreceptor blocking agents, may minimize infarct expansion and ventricular dilatation and improve the long-term prognosis.
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