Understanding cardiac remodeling
death, necrosis
ACUTE MI, MYOCARDIAL INFARCTION, NECROSIS, HYPERTENSION, VOLUME OVERLOAD
It is essential to understand the process of cardiac remodeling before interpreting the results of this study. Physiological cardiac remodeling and pathological cardiac remodeling are the two kinds of cardiac remodeling. Physiological cardiac remodeling occurs as a result of healthy exercise and endurance training, while pathological cardiac remodeling occurs due to chronic stresses such as hypertension, volume overload, neuroendocrine activation, and MI [The extracellular matrix (ECM) is also altered in combination with cardiomyocyte death due to necrosis or apoptosis, which happens concurrently with these cellular and molecular modifications within the cardiomyocyte. The heart responds differently to stress and injury on a macroscopic level. After a myocardial infarction, the area of damage expands immediately, followed by regional dilatation and thinning. Similar variations in cardiomyocyte and microtubule cell structure are generally accompanied by cardiac remodeling as a whole. After a myocardial infarction, the length and width of cardiomyocytes may increase, while the thickness of the local ventricular wall may decrease. The apparent difference can be ascribed to alterations in wall structure, slippage between cardiomyocytes and the ECM, and a decline in cardiomyocyte quantity. After an acute MI, a complicated remodeling mechanism is initiated.