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Importantly, this macrophage-mediated inflammatory activation exhibits clear RV specificity, as no comparable pathological changes were observed in the left ventricle or in models of isolated pressure overload ( Together, these pathological processes interact to form a vicious cycle, ultimately driving the progression of the RV from compensatory hypertrophy to irreversible decompensated dilation, loss of contractile function, and extensive fibrosismaking right heart failure the key determinant of prognosis in patients with PAH (66)