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Abstract

Background: Elevated pulmonary pressures and increased resistance are hallmarks of a severe vascular disease called pulmonary arterial hypertension (PAH). It is essential to comprehend the molecular pathways behind PAH in order to create tailored treatments. The expression of the pulmonary vascular contractile protein is examined in this study in relation to the pathophysiology of PAH.
Objective: The purpose of this study is to investigate the complex interactions that exist between the pathophysiology of PAH and the production of pulmonary vascular contractile protein.
Methods: At Naseer Teaching and MMC Hospital in Peshawar, a cohort of 120 PAH patients was investigated during a nine-month period from April 2021 to December 2021. Pulmonary hemodynamic measures, such as mean pulmonary arterial pressure (mPAP), pulmonary vascular resistance (PVR), and cardiac output (CO), were monitored in addition to demographic and clinical features being evaluated. Western blot and immunohistochemistry were used to assess the expression of contractile proteins.
Results: The study population's average age of 53.6 years was in line with normal profiles of PAHs. Severe PAH was found by hemodynamic evaluations, with an average PVR of 8.6 Wood Units and a mean mPAP of 51.2 mmHg. Heart rate decreased somewhat, averaging 3.1 L/min. Notably, the pulmonary vasculature of PAH patients showed a notable overexpression of contractile proteins, specifically smooth muscle myosin and actin, with a 2.7-fold increase in smooth muscle myosin and a 2.3-fold rise in actin expression. These changes, especially greater mPAP and PVR values, showed a substantial correlation with the severity of the disease. Subgroup analysis revealed possible links between contractile protein changes and comorbid illnesses such as diabetes and connective tissue diseases.
Conclusion: The research emphasizes how important contractile protein expression is to the pathophysiology of PAH. These results offer a basis for focused treatment approaches as well as insights into the molecular nuances influencing the severity of the disease. In the end, this research may improve how this difficult condition is managed.
Keywords: Pulmonary Arterial Hypertension; Contractile Protein Expression; Hemodynamic Parameters; Smooth Muscle Myosin; Actin