Bioscience Methods 2024, Vol.15, No.3, 124-138 http://bioscipublisher.com/index.php/bm 125 recent advancements and future directions, this study seeks to underscore the importance of integrating AI into HHD diagnostic workflows to improve patient care and outcomes. 2 Pathophysiology of Hypertensive Heart Disease 2.1 Mechanisms of HHD development Hypertensive heart disease (HHD) is primarily driven by chronic elevation of arterial pressure, which imposes a mechanical overload on the heart. This persistent pressure overload leads to a series of adaptive and maladaptive responses within the myocardium. One of the earliest and most significant changes is left ventricular hypertrophy (LVH), where the heart muscle thickens in an attempt to counteract the increased workload and maintain cardiac output (Díez and Frohlich, 2010). This hypertrophic response is initially compensatory, aimed at normalizing wall stress and preserving left ventricular (LV) function. However, over time, the hypertrophy becomes maladaptive, contributing to pathological remodeling characterized by cardiomyocyte apoptosis, fibrosis, and alterations in the microcirculation (Díez and Frohlich, 2010). The development of LVH is influenced by both mechanical and neurohumoral factors. Mechanical stress from elevated blood pressure stimulates cardiomyocyte growth, while neurohumoral stimuli, such as the renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system activation, further exacerbate hypertrophic signaling pathways (Díez and Frohlich, 2010). Additionally, non-cardiomyocyte components of the myocardium, including fibroblasts, contribute to the development of interstitial fibrosis, which stiffens the myocardium and impairs diastolic function (Schumann et al., 2019). 2.2 Clinical manifestations and progression The clinical manifestations of HHD are diverse and can range from asymptomatic LVH to overt heart failure (HF). Early in the disease course, patients may remain asymptomatic or present with mild symptoms such as exertional dyspnea or fatigue. As the disease progresses, the structural and functional changes in the heart lead to more pronounced symptoms and complications. One of the hallmark features of HHD is diastolic dysfunction, which results from the stiffening of the LV due to hypertrophy and fibrosis. This impairs the heart's ability to relax and fill properly during diastole, leading to increased filling pressures and symptoms of heart failure with preserved ejection fraction (HFpEF) (Tadic et al., 2022). Over time, the continued pressure overload and myocardial remodeling can also lead to systolic dysfunction, where the heart's ability to contract and eject blood is compromised, resulting in heart failure with reduced ejection fraction (HFrEF) (Díez and Butler, 2022). In addition to heart failure, patients with HHD are at increased risk for other cardiovascular events, including atrial fibrillation, ischemic heart disease, and sudden cardiac death. The presence of LVH and fibrosis creates a substrate for arrhythmias, while the increased myocardial oxygen demand and reduced coronary reserve predispose patients to ischemic events (Figure 1) (Schumann et al., 2019; Díez and Butler, 2022). 2.3 Importance of early detection in managing HHD Early detection of HHD is crucial for preventing disease progression and improving patient outcomes. Identifying patients at risk for HHD allows for timely intervention with antihypertensive therapy and lifestyle modifications, which can mitigate the adverse effects of chronic hypertension on the heart (Tadic et al., 2022). Advanced imaging techniques and circulating biomarkers have emerged as valuable tools for the early detection and monitoring of HHD. Echocardiography remains the first-line imaging modality for assessing cardiac structure and function in hypertensive patients. Novel techniques such as speckle tracking echocardiography and myocardial strain analysis provide insights into subclinical LV dysfunction that may not be apparent with conventional echocardiography (Tadic et al., 2022). Cardiac magnetic resonance (CMR) imaging, particularly with T1 mapping, allows for the noninvasive assessment of diffuse myocardial fibrosis, which is a key feature of HHD and a predictor of adverse outcomes (Schumann et al., 2019; Saeed et al., 2022).
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