Spanish 
Chinese 
Russian 
German 
French 
Japanese 
Portuguese 
Hindi Commentary, Icrj Vol: 10 Issue: 12
The Importance of Prostanoids in Chronic Thromboembolic Pulmonary Hypertension Treatment
Hunninghake Koren
Abstract
Single or recurrent pulmonary thromboemboli developing from venous thrombosis sites are thought to cause chronic thromboembolic pulmonary hypertension (CTEPH). The disease's pathophysiology has yet to be fully understood. Acute pulmonary embolism following deep venous thrombosis could be the catalyst for local variables to mediate the abnormal organisation of pulmonary thromboemboli that is diagnostic of CTEPH. About two-thirds of CTEPH patients have a documented history of acute pulmonary embolism and/or deep venous thrombosis, including those who have a convincing history of acute pulmonary embolism despite not being diagnosed with thromboembolic disease at the time.
Despite a single report documenting a cumulative incidence of 3.8 percent of CTEPH within two years of a first-time acute pulmonary embolism, the vast majority of those who suffer an acute pulmonary embolism do not go on to develop CTEPH, according to the unpublished observations of many other groups. CTEPH was initially distinguished from PAH by its major vessel involvement in the vascular remodelling process, making it accessible to surgical intervention with removal of the obstructing lesions. In contrast to PAH, which manifests in pulmonary vessels of 300m diameter, CTEPH was initially distinguished from PAH by its major vessel involvement in the vascular remodelling process,3 rendering it accessible to surgical intervention with removal of the obstructing lesions.
Keywords: Pulmonary Hypertension
Single or recurrent pulmonary thromboemboli developing from venous thrombosis sites are thought to cause chronic thromboembolic pulmonary hypertension (CTEPH)[1]. The disease's pathophysiology has yet to be fully understood. Acute pulmonary embolism following deep venous thrombosis could be the catalyst for local variables to mediate the abnormal organisation of pulmonary thromboemboli that is diagnostic of CTEPH. About two-thirds of CTEPH patients have a documented history of acute pulmonary embolism and/or deep venous thrombosis, including those who have a convincing history of acute pulmonary embolism despite not being diagnosed with thromboembolic disease at the time[2].
Despite a single report documenting a cumulative incidence of 3.8 percent of CTEPH within two years of a first-time acute pulmonary embolism, the vast majority of those who suffer an acute pulmonary embolism do not go on to develop CTEPH, according to the unpublished observations of many other groups[3,4]. CTEPH was initially distinguished from PAH by its major vessel involvement in the vascular remodelling process, making it accessible to surgical intervention with removal of the obstructing lesions. In contrast to PAH, which manifests in pulmonary vessels of 300m diameter, CTEPH was initially distinguished from PAH by its major vessel involvement in the vascular remodelling process,3 rendering it accessible to surgical intervention with removal of the obstructing lesions[5].
