International Journal of Clinical Case Reports 2024, Vol.14, No.3, 144-156 http://medscipublisher.com/index.php/ijccr 146 cardiomyocytes. Additionally, chronic sympathetic stimulation results in adverse structural and functional changes in the myocardium, contributing to the progression of heart failure (Nandi et al., 2021). 2.1.3 Oxidative stress and inflammation Oxidative stress and inflammation are pivotal in the pathophysiology of hypertensive heart disease. Elevated blood pressure increases the production of reactive oxygen species (ROS) in the vasculature, leading to oxidative stress. ROS can damage endothelial cells, impairing nitric oxide (NO) availability and leading to endothelial dysfunction. This dysfunction results in vasoconstriction, increased vascular permeability, and further exacerbation of hypertension (Touyz et al., 2018). Inflammation plays a significant role in the progression of hypertensive heart disease. Hypertension induces a pro-inflammatory state characterized by the infiltration of immune cells, such as macrophages and T-lymphocytes, into the myocardium and vasculature. These immune cells release cytokines and chemokines that perpetuate inflammation, fibrosis, and adverse cardiac remodeling. This chronic inflammatory state contributes to the development and progression of LVH and heart failure. 2.1.4 Genetic and epigenetic factors Genetic predisposition and epigenetic modifications also play roles in the development of hypertensive heart disease. Variations in genes regulating blood pressure, sodium transport, and vascular tone can influence an individual's susceptibility to hypertension and its cardiovascular complications. Epigenetic modifications, such as DNA methylation and histone acetylation, can alter gene expression in response to environmental factors, contributing to the pathogenesis of hypertensive heart disease (Jia and Sowers, 2021). 2.2 Impact on cardiovascular system 2.2.1 Changes in cardiac structure and function Hypertensive heart disease (HHD) profoundly alters the structure and function of the heart. The most notable structural change is left ventricular hypertrophy (LVH), characterized by an increase in the size and thickness of the myocardial cells. This hypertrophy is a compensatory response to the elevated afterload imposed by chronic hypertension, aiming to normalize wall stress and maintain cardiac output. However, the hypertrophic myocardium becomes stiff and less compliant, impairing the diastolic filling of the heart (Cuspidi et al., 2019). Diastolic dysfunction is a common consequence of LVH in hypertensive patients. It is characterized by an impaired ability of the left ventricle to relax and fill properly during diastole, leading to increased left atrial pressure and pulmonary congestion. Over time, this can progress to heart failure with preserved ejection fraction (HFpEF), a condition where the heart maintains a normal ejection fraction but cannot accommodate normal blood volumes due to increased stiffness (Nwabuo and Vasan, 2020). Additionally, chronic hypertension leads to fibrosis, the accumulation of extracellular matrix proteins in the myocardium, which further decreases myocardial compliance. Fibrosis disrupts the normal architecture of the heart muscle, contributing to both diastolic and systolic dysfunction (Saheera and Krishnamurthy, 2020). This pathological remodeling also predisposes the heart to arrhythmias, as the fibrotic tissue can create electrical heterogeneity within the myocardium. 2.2.2 Left ventricular hypertrophy and its consequences Left ventricular hypertrophy (LVH) is not merely a compensatory mechanism; it has significant pathological consequences. LVH increases the risk of major cardiovascular events, including myocardial infarction, stroke, and heart failure. The thickened myocardium has an increased demand for oxygen, which, coupled with any existing coronary artery disease, can lead to ischemia and angina. The hypertrophic response also leads to changes in myocardial energetics. The hypertrophic myocardium is less efficient in its use of oxygen, and the increased myocardial mass exacerbates this inefficiency. This energy deficit contributes to further myocardial dysfunction and the progression to heart failure (Nwabuo and Vasan, 2020).
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