Keywords: Heart Failure, Cardiovascular
Motivation: Right ventricular (RV) failure in pulmonary arterial hypertension (PAH) increases mortality risk, yet its metabolic characteristics is largely unknown, primarily due to limitations of imaging the RV.
Goal(s): This study examines the relative contribution of oxidative metabolism versus glycolysis in the failing RV before and after initiation of pulmonary vasodilator therapy for PAH.
Approach: Patients with newly diagnosed PAH are examined by HP [1-13C]pyruvate MRI at baseline and again 4-6 months after initiation of pulmonary vasodilator therapy.
Results: Patients exhibited hyperintense HP bicarbonate signals in RV free wall. After treatment, normalized myocardial [13C]bicarbonate production increased.
Impact: Importance of metabolic flexibility in RV heart failure is underexplored. A better understanding of how the RV myocardium remodels in RV failure from PAH and in response to therapy may allow for development of RV-targeted therapies to maintain RV function.
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