Right ventricular (RV) failure is the leading cause of death in pulmonary arterial hypertension. (PAH) Right ventricular ejection fraction is one of the most important predictors of prognosis in heart failure patients regardless of cause. It is estimated that 30-50% of patients with heart failure and preserved ejection fraction (HFpEF) have right ventricular dysfunction and up to 70% of these patients will have significant pulmonary hypertension (PH), both of which are related to much worse prognosis. Right ventricular failure is becoming an increasingly prevalent and significant cause of morbidity in patients with left heart disease. Despite the significance of RV function to survival, there are no therapies available that directly or selectively improve RV function. The overall theme of this research project is to evaluate the mechanisms that contribute to the cause of right heart failure. This small study is designed to look at the role of heart and lung metabolism and pulmonary hypertension as they relate to the development of right heart failure in cardiovascular disease.(PH-LHD)
The hemodynamic definition of PH-LHD involves a mean pulmonary artery pressure (mPAP) \>25mm Hg at rest and pulmonary capillary wedge pressure (PCWP) of ≥15.The coexistence of mitral insufficiency is also a characteristic of PH-LHD. HFpEF is a condition caused by impaired relaxation of a stiffened myocardium as a consequence of an increased load to the left ventricle due to elevated systemic pressures. Pulmonary hemodynamics can be used to classify PH LHD as either passive or reactive, irrespective of LV function. It has been suggested that diastolic pressure gradient (DPG) may offer added prognostic value as a more accurate indicator of pulmonary vascular remodeling.
Study Type
INTERVENTIONAL
Allocation
NA
Purpose
BASIC_SCIENCE
Masking
NONE
Enrollment
2
Following an overnight fast, subjects will be positioned in the Discovery 660 PET/VCT scanner. Following a scout scan to confirm patient positioning, low dose xray CT scan is performed for photon attenuation. A 20 minute dynamic PET scan is started simultaneously with 3 MBq/kg of N-13 ammonia to measure myocardial perfusion. Following N-13 decay,a 60 minute dynamic PET scan with 3 MBq/kg F-18- FDG to measure myocardial glucose uptake. Blood sampling for glucose and insulin will occur at pre specified time points throughout the scan.
University of OttawaHeart Institute
Ottawa, Ontario, Canada
Cardiac and pulmonary metabolism role in development of right heart failure in pulmonary hypertension in left heart disease.
Relationship between lung fludeoxyglucose (FDG)uptake and hemodynamic type pulmonary hypertension using PET scanning
Time frame: Baseline
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