Ventricular remodeling
Overview[edit | edit source]
Ventricular remodeling refers to the changes in size, shape, structure, and function of the heart's ventricles following cardiac injury, such as a myocardial infarction. This process can lead to heart failure if the remodeling is maladaptive. Ventricular remodeling involves complex interactions between cardiomyocytes, the extracellular matrix, and various signaling pathways.
Pathophysiology[edit | edit source]
Ventricular remodeling is initiated by the death of cardiomyocytes due to ischemic injury. The loss of viable myocardium triggers a cascade of events, including inflammation, fibrosis, and hypertrophy of the remaining myocytes. These changes are mediated by neurohormonal activation, including the renin-angiotensin-aldosterone system and the sympathetic nervous system.
Cellular Changes[edit | edit source]
The primary cellular change in ventricular remodeling is the hypertrophy of myocardiocytes. This hypertrophy is an adaptive response to increased wall stress and is characterized by an increase in cell size and protein synthesis. However, prolonged hypertrophy can lead to cell death and further deterioration of cardiac function.
Extracellular Matrix[edit | edit source]
The extracellular matrix (ECM) undergoes significant remodeling during this process. There is an initial degradation of the ECM, followed by excessive deposition of collagen and other matrix proteins, leading to fibrosis. This fibrosis increases the stiffness of the ventricular wall and impairs diastolic function.
Clinical Implications[edit | edit source]
Ventricular remodeling is a critical determinant of the clinical outcome following a myocardial infarction. Patients with significant remodeling are at higher risk of developing heart failure and have a worse prognosis. Therapeutic strategies aimed at preventing or reversing remodeling include the use of ACE inhibitors, beta-blockers, and aldosterone antagonists.
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