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Aaron B. Waxman, MD, PhD; Laurie Lawler, RN; Glenn Cornett, MD, PhD

Arch Intern Med. 2008;168(19):2164-2166.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Pulmonary arterial hypertension (PAH) (World Health Organization [WHO] group I pulmonary hypertension) is characterized by elevated pulmonary arterial pressure leading to progressive dyspnea, right-sided heart failure, and ultimately death. The goal in treating PAH is to reduce pulmonary vascular resistance and pulmonary artery pressure as well as improve the functional status of the patient. The pathogenic hallmark of PAH is increased pulmonary vascular resistance, a result of vasoconstriction, vascular remodeling (abnormal proliferation of smooth muscle and sometimes other vascular tissue), and in situ thrombosis. An important root cause of this pathologic condition is endothelial dysfunction, ie, the uncoupling of endothelial nitric oxide synthetase (eNOS), which drives the decrease in the production of the endogenous vasodilator nitric oxide along with increases in the production of the reactive oxygen species peroxynitrite and superoxide.

Unfortunately, for many patients the current treatments . . . [Full Text of this Article]

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