A REVIEW ON PULMONARY HYPERTENSION

Pulmonary arterial hypertension (PAH) is a chronic disorder of the pulmonary vasculature, characterised by a progressive increase in pulmonary vascular resistance leading to right heart failure and death. Pulmonary hypertension also characterised by lung endothelial cell dysfunction and vascular remodelling. Five groups of disorders that cause PH was identified During the Fifth World Symposium held in 2013 in Nice, France. Estimates of incidence range from one to two new cases per million per year in the general population and are thought to be similar in children. The prevalence of IPAH in children was estimated to be 2.2 cases per million, and the overall prevalence of PAH was 3.7 cases per million. The precise mechanism(s) of PAH development in adults and children is not thoroughly understood. Nevertheless, endothelial cell dysfunction is thought to play a key role in addition to smooth muscle cell migration, dysfunction and abnormal apoptosis. Smooth muscle cells de-differentiate, achieving a more synthetic than contractile phenotype, grow into the sub-endothelial space, and produce fibrous material responsible for intimal fibrosis. The symptoms of PAH include breathlessness, fatigue, weakness, angina, syncope, and abdominal distension. PAH can also be detected by using Electrocardiogram, Chest radiograph, Echocardiography, Cardiac magnetic resonance imaging etc. Pulmonary vasodilators in general and prostacyclin analogues in particular have improved the outcome of patients with pulmonary arterial hypertension (PAH). Therapy of PAH includes: oxygen, calcium channel-blockers, diuretics, anticoagulants, prostanoids, endothelin receptor antagonists and phosphodiesterase-5 inhibitors. But the treatment of this pulmonary disease is still about to develop. There is a huge scope for researcher to look into different molecular mechanisms responsible for the development of this disease.