It has been suggested that mitochondrial dysfunction might play a role in the development of diabetic cardiomyopathy. From animal studies, it has been suggested that an altered PPAR and PGC1 expression is involved in the reduced cardiac mitochondrial function, however human data on cardiac mitochondrial function and PPAR regulation is scarce. The latter is due to the fact that there is no validated measurement for assessing cardiac mitochondrial function non-invasively in vivo. It has been suggested that measuring PCr/ATP ratio with 31P-MRS in the heart reflects cardiac mitochondrial function. However, so far no direct validation of this method has been performed. The aim of this study will be to validate in vivo 31P-MRS with ex vivo measurements of mitochondrial function. To this end, the hypothesis is that in vivo 31P-MRS is a valid method for measuring cardiac mitochondrial function when compared with ex vivo mitochondrial respirometry.
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Cardiac energy status in vivo
Timeframe: 1 week before surgery the patient will undergo the MRS scan. That same week the investigators will analyse the ATP/PCr ratio. Data will be presented through study completion, an average of 2 years.
Cellular respiration ex vivo
Timeframe: At surgery the investigators obtain tissue samples. Within an hour the investigatorswill use the oxygraph to measure the cellular respiration. Data will be presented through study completion, an average of 2 years.