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Recent genetic studies in patients with familial and sporadic primary pulmonary hypertension (PPH) have provided new opportunities to address the pathophysiologic mechanisms of this disease (1, 2). This past year, mutations in the bone morphogenetic protein receptor 2 (BMPR2) gene have been identified in even a higher proportion of individuals than was first appreciated (3). In addition, mutations associated with impaired signaling through other members of the TGF-β receptor family have also been uncovered (4). How aberrant processing of these signals is related to the cellular mechanisms previously described in patients with pulmonary hypertension remains to be completely elucidated. In addition, we need to understand how other kinds of stimuli, such as inflammatory disorders associated with collagen vascular disease, mechanical forces related to congenital heart defects, and serotonin analogs like the appetite suppressant dexfenfluoramine, initiate cellular abnormalities that lead to severe progressive pulmonary hypertension.

Linking a serotonin transporter polymorphism to vascular smoothmuscle proliferation in patients with primary pulmonary hypertension