International Journal of Clinical Case Reports 2024, Vol.14, No.3, 144-156 http://medscipublisher.com/index.php/ijccr 145 a comprehensive overview of the outcomes of pharmacological and non-pharmacological interventions in clinical cases and discusses future directions for HHD management. This research will serve as a valuable resource for clinicians and researchers seeking to improve the care and prognosis of patients with hypertensive heart disease. 2 Pathophysiology of Hypertensive Heart Disease 2.1 Mechanisms of disease development 2.1.1 Role of Hypertension in Cardiovascular System Damage Hypertension induces cardiovascular damage through both direct and indirect mechanisms (Figure 1). Chronic high blood pressure exerts sustained mechanical stress on the arterial walls, leading to endothelial dysfunction and vascular remodeling. This remodeling process involves the thickening of the arterial wall due to increased collagen deposition and smooth muscle cell proliferation, resulting in reduced arterial compliance and increased vascular resistance (Touyz et al., 2018). Over time, these changes increase the workload on the left ventricle, causing hypertrophy and compromising myocardial function. Figure 1 Mechanisms involved in the development of the lesions responsible for hypertensive heart disease (Adopted from Díez and Frohlich, 2010) The increased afterload from sustained hypertension causes the heart to pump against a higher resistance, leading to left ventricular hypertrophy (LVH). LVH is an adaptive response to maintain cardiac output, but it eventually becomes maladaptive, resulting in reduced myocardial perfusion and ischemia due to inadequate blood supply to the thickened myocardium. This condition can progress to heart failure if not managed effectively (Nwabuo and Vasan, 2020). 2.1.2 Neurohormonal factors and myocardial remodeling The renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system (SNS) are critical in the pathogenesis of hypertensive heart disease. Activation of the RAAS leads to vasoconstriction, sodium retention, and increased blood pressure, which contribute to cardiac hypertrophy and fibrosis. Angiotensin II, a key mediator in the RAAS, promotes hypertrophy of cardiomyocytes, fibrosis, and remodeling of the extracellular matrix. It also stimulates the release of aldosterone, which further exacerbates sodium retention and fibrosis (Slivnick and Lampert, 2019). The SNS is also upregulated in hypertensive patients, leading to increased norepinephrine release. This neurohormonal activation causes direct myocardial damage by promoting hypertrophy, fibrosis, and apoptosis of
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