Key result
Acute RV pressure overload after CPB inhibits fatty acid oxidation without lactate compensation, causing energy deficiency.
Why the study?
Acute right ventricular pressure overload often leads to low cardiac output syndrome after congenital heart surgery, and whether the right ventricle has limited ability to modify substrate utilization under these conditions was unknown.
RCT (n=16)
Randomized
In a porcine model of acute right ventricular pressure overload after cardiopulmonary bypass, there is a significant inhibition of long-chain fatty acid oxidation without compensatory lactate oxidation, leading to energy deficiency.
Acute right ventricular pressure overload (RVPO) occurs following congenital heart surgery and often results in low cardiac output syndrome. We tested the hypothesis that the RV exhibits limited ability to modify substrate utilization in response to increasing energy requirements during acute RVPO after cardiopulmonary bypass (CPB). We assessed the RV fractional contributions (Fc) of substrates to the citric acid cycle in juvenile pigs exposed to acute RVPO by pulmonary artery banding (PAB) and CPB. Sixteen Yorkshire male pigs (median 38 days old, 12.2 kg of body weight) were randomized to SHAM (Ctrl, n = 5), 2‐h CPB (CPB, n = 5) or CPB with PAB (PAB‐CPB, n = 6). Carbon‐13 (13C)‐labeled lactate, medium‐chain, and mixed long‐chain fatty acids (MCFA and LCFAs) were infused as metabolic tracers for energy substrates. After weaning from CPB, RV systolic pressure (RVSP) doubled baseline in PAB‐CPB while piglets in CPB group maintained normal RVSP. Fc‐LCFAs decreased significantly in order PAB‐CPB > CPB > Ctrl groups by 13C‐NMR. Fc‐lactate and Fc‐MCFA were similar among the three groups. Intragroup analysis for PAB‐CPB showed that the limited Fc‐LCFAs appeared prominently in piglets exposed to high RVSP‐to‐left ventricular systolic pressure ratio and high RV rate‐pressure product, an indicator of myocardial oxygen demand. Acute RVPO after CPB strongly inhibits LCFA oxidation without compensation by lactate oxidation, resulting in energy deficiency as determined by lower (phosphocreatine)/(adenosine triphosphate) in PAB‐CPB. Adequate energy supply but also metabolic interventions may be required to circumvent these RV energy metabolic abnormalities during RVPO after CPB.
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Kajimoto et al. (2022) conducted an RCT in Acute right ventricular pressure overload after cardiopulmonary bypass (n=16). Cardiopulmonary bypass with pulmonary artery banding (PAB-CPB) vs. SHAM or 2-h CPB was evaluated on Right ventricular fractional contributions of substrates to the citric acid cycle. Acute right ventricular pressure overload after cardiopulmonary bypass strongly inhibited long-chain fatty acid oxidation without compensation by lactate oxidation, causing energy deficiency.
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