Key result
Terminal heart failure linked to ~28% lower myocardial mitochondrial oxidative capacity versus preserved graft function.
Why the study?
Cardiac output determination using the Fick method with measured oxygen consumption has potential sources of error related to air sampling and oxygen content analysis, motivating evaluation of a modified method using estimated oxygen consumption.
Population
Patients undergoing cardiac output measurement
Comparison
Modified Fick method using estimated oxygen consumption vs thermodilution technique
Design
Observational study
Authors
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Highlights potential bioenergetic impairment in terminal HF; hypothesis-generating and should not yet change practice.
Observational (n=69)
No
Absolute Event Rate: 127.4% vs 176.2%
p-value: p=<0.0001
Jeremy R. Dale (1987) conducted an observational in Terminal heart failure (n=69). Terminal heart failure vs. Stable heart transplant recipients with normal left ventricular function was evaluated on Mitochondrial state III respiration on octanoyl-carnitine, glutamate, and succinate (oxidative capacity) (p=<0.0001). Terminal heart failure was associated with a 38% reduction in maximal myocardial mitochondrial oxidative capacity compared to heart transplant recipients with normal left ventricular function (127.4 vs. 176.2 pmol/[s mg], p < 0.0001).
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