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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 O2 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 O2 consumption (MVO2). 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 MVO2 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 MVO2 in IPAH.In 18 IPAH patients (New York Heart Association class II and III), RV MVO2 was determined using positron emission tomography and 15O tracers. PAP and HR were measured during right heart catheterization. RV MVO2 was found to be related to systolic PAP (R2 = 0.54, P < 0.001), and inversely to stroke volume (R2 = 0.32, P = 0.015) and HR (R2 = 0.32, P = 0.014). Relationships of MVO2 to the rate pressure product (RPP), i.e. systolic pressure × HR, and wall stress were R2 = 0.55, P < 0.001, and R2 = 0.30, P = 0.020, respectively. Multiple regression of MVO2 on HR and systolic PAP gave R2 = 0.59, P = 0.001.Systolic PAP and HR are the major determinants of RV MVO2 in IPAH. A further increase of HR and PAP with IPAH progression suggests a compromised RV myocardial oxygen availability.