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Pathology And Treatment Of Pulmonary Arterial Hypertension

2205 words - 9 pages

The pulmonary vasculature contains arteries and arterioles, which branch in the lungs to create a dense capillary bed to provide blood flow. The pulmonary capillary bed is a high-volume, low-pressure, low-resistance system that delivers blood to and from the lungs via the arterial and venous circulation systems. The right ventricle of the heart is responsible for pumping blood to the pulmonary artery and to the lungs so it can be oxygenated while the left ventricle pumps oxygenated blood to the tissues. Typically, hypertension refers to high blood pressure in the systemic circulation, however, an increase in blood pressure may also occur in pulmonary circulation. The pulmonary artery supplying blood to the lungs can become narrowed, resulting in less blood flow and high pressure in the pulmonary system causing right heart dysfunction and eventually right heart failure (Huether & McCane, 2012). Pulmonary arterial hypertension (PAH) is hemodynamically defined as a resting pulmonary arterial pressure greater than 25 mm Hg (Rubin & Badesch, 2005). PAH is a progressive disease resulting from a combination of pulmonary vasoconstriction, vascular wall remodeling, in situ thrombosis and inflammation (Bajkumar, 2012). PAH is a rare disorder but affects men and women of all ages, from very young children to seniors, and people of all racial and ethnic backgrounds.
Although scientists and clinicians do not fully understand what causes pulmonary arterial hypertension, studies have identified diseases, substances and risk factors associated with developing PAH. Like cancer and atherosclerosis, PAH does not have a single cause: a “multi-hit model” is more likely. Idiopathic pulmonary arterial hypertension is diagnosed when a cause cannot be directly explained. IPAH is characterized by endothelial dysfunction, increased production of thromboxane and endothelin and a decreased production of prostacyclin, leading to increased vasoconstriction of pulmonary arteries (Huether & McCane, 2012). The walls of the vessels themselves undergo remodeling from the release of vascular growth factors. This results in a thickening of the vessel walls, narrowing of the lumen resulting in high pressure in the pulmonary arteries. It is not clear whether somatic mutations or epigenetic modifications lead to uncontrolled endothelial growth but it was proposed that there may be pulmonary arterial endothelial cells with variable contributions of bone marrow precursors (Tuder et al., 2009). IPAH is most common in women in there thirties and men in there forties. Twice as many cases are reported in women as in men (Savaj et al., 2012).
PAH is inherited in less than 10% of cases. Familial PAH is linked to the gene BMPR2, an autosomal dominant gene (McLaughlin et al., 2009). PAH demonstrates incomplete penetrence as only twenty percent of individuals with the bad gene develop the disease. BMPR2 modulates vascular cell growth by activating the intracellular pathways of SMAD and LIM...

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