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Abstract Pulmonary hypertension (PH) is defined as a systolic pulmonary artery pressure (sPAP) greater than 30 mm Hg or a mPAP more than 25 mmHg at rest or more than 30 mmHg on exercise. WHO proposed a new classification of PH, and this was updated in 2003. This update classified PH into five groups. group I, Pulmonary arterial hypertension. group II, pulmonary venous hypertension. group III, PH associated with disorders of the respiratory system and/or hypoxemia. group IV, PH due to chronic thrombotic and/or embolic disease. group V, PH owing to disorders directly affecting the pulmonary vasculature. The lesions in PH are characterized by cellular proliferation that involves the intima, media, and adventitia of the small pulmonary arteries and arterioles. Symptoms of PH are often subtle and nonspecific. However, the most frequent symptom is progressive dyspnea. When the disease is present, several tests can be done to confirm the diagnosis and determine the type of PH that is present. The treatment of PH until a few years ago was only symptomatic. It was shown that patients could be maintained on continuous iv epoprostenol. In patients with an acute response to vasodilators, a high dose of calcium channel blockers is an important line of treatment. It was later realised that oral anticoagulant alone improved survival. The other main approach to PH has been the blockade of endothelin - receptors. Endothelial production of nitric oxide (NO) is diminished with PH, prompting attempts to reverse this defect either by giving continuous inhaled NO, or by increasing the substrate for NO, L- arginine. Phosphodiesterase type 5 inhibitor could be a relatively selective pulmonary vasodilator. Finally, gene therapy directed at gene replacement of the mutated 2q33 chromosome, or overexpression of vasodilator genes. As regard surgical treatment, lung transplantation, and atrial septostomy/septectomy have been utilised in patients with PH. |