Aims: Increased afterload in idiopathic pulmonary arterial hypertension (IPAH) causes right ventricular (RV) hypertrophy and failure. Since RV remodelling occurs with alterations in RV oxygen metabolism, increasing our understanding in the factors determining RV O(2) consumption in IPAH is necessary. In the left ventricle, it is known that heart rate and systolic blood pressure are the main determinants of myocardial O(2) consumption (MVO(2)). However, the normal right heart has lower oxygen extraction and perfusion than the left myocardium, and RV energy metabolism is changed in hypertrophy. Therefore, it is not obvious that the relationsships of pressure and heart rate to MVO(2) hold for the overloaded human right heart. We hypothesize that systolic pulmonary artery pressure (PAP) and heart rate (HR) are the major determinants of RV MVO(2) in IPAH.
Methods and results: In 18 IPAH patients (New York Heart Association class II and III), RV MVO(2) was determined using positron emission tomography and (15)O tracers. PAP and HR were measured during right heart catheterization. RV MVO(2) was found to be related to systolic PAP (R(2) = 0.54, P < 0.001), and inversely to stroke volume (R(2) = 0.32, P = 0.015) and HR (R(2) = 0.32, P = 0.014). Relationships of MVO(2) to the rate pressure product (RPP), i.e. systolic pressure × HR, and wall stress were R(2) = 0.55, P < 0.001, and R(2) = 0.30, P = 0.020, respectively. Multiple regression of MVO(2) on HR and systolic PAP gave R(2) = 0.59, P = 0.001.
Conclusion: Systolic PAP and HR are the major determinants of RV MVO(2) in IPAH. A further increase of HR and PAP with IPAH progression suggests a compromised RV myocardial oxygen availability.