Why the study?
Does the compensated human failing heart have reduced myocardial fatty acid uptake compared to healthy controls or patients with type 2 diabetes?
Does the compensated human failing heart have reduced myocardial fatty acid uptake compared to healthy controls or patients with type 2 diabetes?
Direct quantification using arterio-venous blood sampling demonstrates that the compensated human failing heart does not have reduced myocardial fatty acid uptake compared to healthy controls.
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Preserved myocardial substrate uptake in compensated HF; hypothesis-generating and should not yet change practice.
Metabolic substrate utilization of the human failing heart is an area of controversy. The purpose of this study is to directly quantify myocardial substrate utilization in moderately severe heart failure, type 2 diabetes and healthy controls using simultaneous coronary sinus and arterial blood sampling. Patients with heart failure (n = 9, mean NYHA 2.7+/-0.5), with type 2 diabetes (n = 5) and with normal heart function (n = 10) were studied after an overnight fast in connection with electrophysiological investigations/treatments.A systemic infusion of [(2)H(2)]palmitate allowed for the calculation of absolute palmitate extraction across the heart. Blood samples were analysed for non-esterified fatty acids, triacylglycerol, glycerol, glucose, pyruvate, lactate, 3-hydroxybutyrate, and blood gases after simultaneous sampling of arterial and coronary sinus blood. Arterio-coronary sinus metabolite concentration differences and fractional extractions for all substrates were similar between the groups. The absolute NEFA uptakes assessed by [(2)H(2)]palmitate extraction were also similar between the groups. Using direct measurements of metabolic substrate uptake by arterio-venous difference technique, the compensated human failing heart does not appear to have reduced myocardial fatty acid uptake.
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Funada et al. (2009) studied this question.
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