Abstract
Chronic heart failure (CHF) is one of the most common and complex diseases of the cardiovascular system, characterized by the heart's inability to pump enough blood to meet the body's needs. This pathology, as a global health issue, negatively affects the quality of life and life expectancy of many patients. This article provides an in-depth analysis of the main pathophysiological mechanisms involved in the development of CHF, including hemodynamic changes, activation of neurohormonal systems (renin-angiotensin-aldosterone system and sympathetic nervous system), inflammation and oxidative stress, mitochondrial dysfunction, calcium handling disorders, and myocardial remodeling processes. These mechanisms impair the contractile function of the heart muscle and enhance cardiomyocyte necrosis, fibrosis, and apoptosis. Persistent activation of neurohormonal systems leads to morphological and functional changes in the heart muscle, contributing to the progression of heart failure. Additionally, inflammatory mediators (e.g., TNF-α, IL-1, IL-6) have been shown to cause ongoing myocardial tissue damage and remodeling.
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