Bioscience Methods 2024, Vol.15, No.3, 124-138 http://bioscipublisher.com/index.php/bm 126 Figure 1 The 3 pathophysiological phases of myocardial interstitial fibrosis in hypertensive heart disease (Adopted from Díez and Butler, 2022) Image caption: In response to alterations triggered by chronic pressure overload and non-hemodynamic mechanisms, activated fibroblasts and myofibroblasts originated from resident cardiac fibroblasts secrete collagen precursors and enzymes that facilitate the synthesis and deposition of highly cross-linked collagen fibers (mostly, type I) resistant to degradation by metalloproteinases. As a consequence an excess of collagen fibers is deposited diffusely across the myocardial interstitium, thereby facilitating alterations in left ventricular diastolic and systolic function that, in turn, may lead to heart failure with either preserved ejection fraction (HFpEF) or reduced ejection fraction (HFrEF), respectively. DAMP indicates damage-associated molecular patterns (Adopted from Díez and Butler, 2022) Circulating biomarkers, such as N-terminal pro-B-type natriuretic peptide (NT-proBNP) and soluble ST2 (sST2), have also shown promise in the early detection and prognostication of HHD. These biomarkers reflect myocardial stress and fibrosis, respectively, and can aid in identifying patients at higher risk for disease progression and heart failure (Ojji et al., 2020). In conclusion, understanding the pathophysiology of HHD, recognizing its clinical manifestations, and emphasizing the importance of early detection are essential components in the management of this condition. Utilizing advanced imaging techniques and biomarkers can enhance the early identification and monitoring of HHD, ultimately leading to better patient outcomes through timely and targeted therapeutic interventions.
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