T here is still no answer to William Harvey's rhetorical question. He included the right ventricle (RV), its "pulse," the large pulmonary arteries (PAs), and the lungs in the same sentence, emphasizing the concept of a "unit." Although Harvey realized the importance of the RV and its interactions with the pulmonary circulation, 4 centuries later, the RV is largely understudied. At the same time, there has been significant progress in our understanding of the pathology of pulmonary vascular disease and, over the past few years, an explosion of clinical therapeutic trials for PA hypertension (PAH). 1 This unbalanced approach has generated a number of problems and controversies. For example, it is now becoming apparent that even if experimental therapies improve or reverse PAH pathology, this does not necessarily lead to clinical improvement and prolonged survival unless accompanied by a parallel improvement in RV function. The degree of pulmonary hypertension (ie, PA pressure [PAP]) does not strongly correlate with symptoms or survival, whereas RV mass and size and right atrial pressure reflect functional status and are strong predictors of survival. 2 The 6-minute walk test, used as the primary end point in most PAH clinical trials, correlates better with RV function (ie, cardiac output) than with the degree of pulmonary pressure elevation. However, this test is being heavily criticized because of multiple inherent problems and the fact that it does not provide information on specific components of RV-pulmonary vascular function. 3 Although therapies aiming at reversing pulmonary vascular remodeling might also have a positive effect on the RV (eg, sildenafil, which has been shown to increase RV inotropy 4 and decrease RV hypertrophy, 5 in addition to its effects on the pulmonary circulation), others might have untoward effects on the RV. For example, imatinib, an antiproliferative/proapoptotic agent that shows preliminary promise in reversing pulmonary vascular remodeling, 6 is potentially associated with primary negative (ie, proapoptotic) effects on the myocardium. 7 As our knowledge of RV physiology and biology increases, it is becoming apparent that a comprehensive approach to the RV, the pulmonary circulation, and their interactions will be beneficial in both clinical management of PAH patients and clinical research. The evolution of RV pathology from the normal to a compensated (hypertrophied) and then decompensated state parallels the evolution of pulmonary vascular pathology from a vasodilated highcapacitance state to vasoconstricted arteries and early loss of endothelial cells/capillaries to an end-stage proliferative and obliterative vascular remodeling (Figure 1). Therefore, it is important to study the RV and the PAs comprehensively and simultaneously as a unit. Here, we discuss standard clinical tests (eg, right heart catheterization and echocardiography) and evolving technologies (eg, magnetic resonance [MR] imaging [MRI] and positron emission tomography [PET]) that have the ability to study the ...