e539 Correspondence To the Editor:

Patients who have pulmonary arterial hypertension (PAH) are fac-ing a battle on two fields: Whereas progressive vascular remodeling increases pulmonary vascular resistance, maladaptive myocardial remodeling eventually culminates in right-sided heart failure and death. PAH was initially understood as a condition of excessive pul-monary vasoconstriction, but today elements of exuberant cellular proliferation, unguided angiogenesis, and apoptosis-resistance are seen as central to the development of the disease.1 Although the tran-sition from right-sided heart adaptation to failure has only recently become a focus of research, it has already become clear that the failing right ventricle is characterized by the morphological triad of apoptotic loss of cardiomyocytes, fibrosis, and loss of capillaries.2 As such, there is an obvious therapeutic dilemma in PAH that can be stated as follows: What is good for the lung (inhibition of angio-genesis and induction of apoptosis) may be bad for the heart. Thi