Scientific Sessions

The pathophysiology of heart diseases involves a complex interplay of structural, functional, and biochemical abnormalities that disrupt the normal performance of the heart. Most cardiovascular disorders—such as coronary artery disease, hypertension, heart failure, and cardiomyopathies—stem from underlying disturbances in blood flow, myocardial oxygen supply, or electrical conduction. For example, atherosclerosis leads to the narrowing of coronary arteries, reducing oxygen delivery to the myocardium and predisposing it to ischemia and infarction. Hypertension causes chronic pressure overload, resulting in ventricular hypertrophy and, eventually, impaired contractility. Similarly, valvular defects alter hemodynamics, increasing the strain on cardiac chambers and triggering compensatory remodeling processes that can become maladaptive over time.

At the cellular and molecular levels, heart diseases are characterized by oxidative stress, inflammation, apoptosis, and altered calcium handling within cardiac cells. These mechanisms collectively contribute to myocardial dysfunction, fibrosis, and remodeling of both structure and function. Neurohormonal activation—such as the overactivity of the renin-angiotensin-aldosterone system and sympathetic nervous system—further exacerbates the progression of heart failure. Advances in molecular research and imaging have provided deeper insights into these pathophysiological processes, aiding in early diagnosis and targeted therapy. Understanding the underlying mechanisms of heart diseases not only enhances clinical management but also paves the way for innovative treatments, including regenerative and gene-based therapies aimed at restoring normal cardiac function.