Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2026
Right ventricular metabolic adaptation to afterload and heterogeneous right ventricular-pulmonary arterial coupling in pre-capillary pulmonary hypertension: An 18F-fluorodeoxyglucose positron emission tomography /cardiac magnetic resonance study.
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Nakamura Tomohisa, Tahara Nobuhiro, Koga Yuki, Yamagata Yuki, Kugai Tadahiro, Eto Yoshiko, Maeda-Ogata Shoko, Honda Akihiro, Igata Sachiyo, Tahara Atsuko, Tanoue Shuichi, Fukumoto Yoshihiro
Аннотация
BACKGROUND: Right ventricular (RV) failure is the primary determinant of prognosis in pulmonary hypertension (PH) and is associated with metabolic remodeling. However, the relationship between RV metabolic activity, pulmonary vascular load, and right ventricular-pulmonary arterial (RV-PA) coupling remains incompletely understood. We hypothesized that increased pulmonary vascular afterload is associated with enhanced RV glucose metabolism and impaired RV-PA coupling, reflecting early maladaptive RV adaptation before overt structural remodeling develops. This study investigated the interplay among pulmonary vascular resistance (PVR), RV structure, RV-PA coupling, and RV myocardial glucose metabolism using integrated cardiac magnetic resonance (CMR) and 18F-fluorodeoxyglucose positron emission tomography (FDG-PET).
METHODS: Fifty patients with pre-capillary PH underwent CMR and FDG-PET. Ventricular volumes were quantified by CMR, and RV-PA coupling was estimated using the stroke volume-to-end-systolic volume ratio (SV/ESV). RV metabolic activity was quantified using standardized uptake value (SUV). Associations among PVR, RV structure, RV-PA coupling, and RV metabolic activity were analyzed.
RESULTS: PVR was positively correlated with SUV RV (r = 0.452, P < 0.001), indicating increased RV glucose uptake with higher afterload. PVR was inversely correlated with SV/ESV (r = -0.282, P = 0.048), indicating impaired RV-PA coupling. Right ventricular end-diastolic volume index showed a modest association with SUV RV (r = 0.273, P = 0.055) and was not significantly correlated with SV/ESV (r = -0.197, P = 0.170). These findings indicate that RV metabolic remodeling is more closely associated with pulmonary vascular afterload and RV-PA uncoupling than with overt RV dilatation.
CONCLUSIONS: RV glucose metabolism is significantly associated with pulmonary vascular load and impaired RV-PA coupling, potentially reflecting early maladaptive adaptation to increased afterload preceding overt structural remodeling. Integrated FDG-PET and CMR assessment provides complementary mechanistic insights into RV adaptation in PH.
METHODS: Fifty patients with pre-capillary PH underwent CMR and FDG-PET. Ventricular volumes were quantified by CMR, and RV-PA coupling was estimated using the stroke volume-to-end-systolic volume ratio (SV/ESV). RV metabolic activity was quantified using standardized uptake value (SUV). Associations among PVR, RV structure, RV-PA coupling, and RV metabolic activity were analyzed.
RESULTS: PVR was positively correlated with SUV RV (r = 0.452, P < 0.001), indicating increased RV glucose uptake with higher afterload. PVR was inversely correlated with SV/ESV (r = -0.282, P = 0.048), indicating impaired RV-PA coupling. Right ventricular end-diastolic volume index showed a modest association with SUV RV (r = 0.273, P = 0.055) and was not significantly correlated with SV/ESV (r = -0.197, P = 0.170). These findings indicate that RV metabolic remodeling is more closely associated with pulmonary vascular afterload and RV-PA uncoupling than with overt RV dilatation.
CONCLUSIONS: RV glucose metabolism is significantly associated with pulmonary vascular load and impaired RV-PA coupling, potentially reflecting early maladaptive adaptation to increased afterload preceding overt structural remodeling. Integrated FDG-PET and CMR assessment provides complementary mechanistic insights into RV adaptation in PH.