Pathology of Pulmonary Hypertension

Estradiol improves right ventricular function in rats with severe angioproliferative pulmonary hypertension: effects of endogenous and exogenous sex hormones

“…Our data suggest significant RV-protective ER-mediated effects of E2 in a model of severe PH. sex differences; right ventricular failure; exercise capacity; apoptosis; estrogen receptor PULMONARY ARTERIAL HYPERTENSION (PAH; WHO group 1 pulmonary hypertension) is a sexually dimorphic disease of multifactorial etiology that, if left untreated, results in severe pulmonary vascular remodeling and profound hemodynamic alterations, eventually leading to right ventricular (RV) failure and death (44,51,52). Despite the development of several new drugs over the last 20 years, morbidity and mortality of PAH remain high, and the 3-year survival of incidence patients in the modern treatment era is only 54.9% (19).…”

“…tifactorial etiology that, if left untreated, results in severe pulmonary vascular remodeling and profound hemodynamic alterations, eventually leading to right ventricular (RV) failure and death (44,51,52). Despite the development of several new drugs over the last 20 years, morbidity and mortality of PAH remain high, and the 3-year survival of incidence patients in the modern treatment era is only 54.9% (19).…”

Pulmonary hypertensive vascular changes in lungs of patients with sudden unexpected death. Emphasis on congenital heart disease, Eisenmenger syndrome, postoperative deaths and death during pregnancy and postpartum

“…Plexiform lesions may be obscured by pulmonary oedema and congestion and will be missed if there is only a cursory review of the material. Vascular changes can be notoriously heterogeneous and variable throughout the lung in PH 9. One needs to look carefully especially in the smaller arterioles and preacinar arterioles for the classic evidence of medial hypertrophy, intimal thickening, blocked vessels and outgrowth of plexiform vein-like lesions around the blocked vessels with or without fibrinoid necrosis in the blocked vessel walls.…”

Mitochondria dysfunction: A novel therapeutic target in pathological lung remodeling or bystander?

“…vasoconstrictor mediators (endothelin-1, serotonin) favoring vasoconstriction and ensuing increased intimal and medial thickening within the pulmonary (Tuder, Stacher, Robinson, Kumar, &Graham, 2013 andStacher, et al, 2012). Recent detailed histological analysis of lungs from PAH patients revealed that significant heterogeneity exists in both the extent and complexity of vascular remodeling within PAH patients; however, key processes such as increased proliferation of vascular smooth muscle cells, phenotypic alternations in endothelial cells giving rise to apoptosis resistance, influx of inflammatory and progenitor cells and ultimately formation of occlusive, complex, multicellular vascular lesions are thought to be responsible for sustained increase of pulmonary arterial pressure (Rabinovitch, Keane, Norwood, Castaneda, & Reid, 1984).…”