Abstract
Introduction: Advanced heart failure (HF) is characterized by metabolic abnormalities. We have recently shown myocardial lipid species to be significantly decreased in non-diabetic HF. The finding of deficient carnitine species has directed us to examine a key gene SLC22A5 the high-affinity carnitine transporter. Known mutations of this gene lead to primary carnitine deficiency and cardiomyopathy. Methods: Left ventricular samples procured at the time of orthotopic heart transplantation (OHT) from non-diabetic idiopathic dilated cardiomyopathy (DCM) n=16, and brain-dead organ donors without a history of diabetes or HF (NF) n=18 formed the study sample. All hearts received in situ cold cardioplegia. Lipids including carnitines were quantitated with liquid chromatography and high-resolution mass spectrometry (LC-HRMS) following the Folch extraction method. mRNA expression data of target genes including SLC22A5 from a separate study of n=117 DCM patients and n=67 NF patients p≤0.05 were analyzed. Results: Representative trends for all carnitine species assayed were shown to be significantly reduced in DCM. The figure below represents the mRNA expression between DCM and NF patients. There was a statistically significant reduction of SLC22A5 expression in the DCM population (Figure: ***p≤ 0.0001, dots 95 th percentiles). Conclusions: A statistically significant deficiency of carnitine species and a reduction in the expression of the carnitine transporter SLC22A5 was demonstrated in non-diabetic HF. Future studies will attempt to resolve the mechanisms behind these observations.
Published Version
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