Why the study?
Poor access to human left ventricular myocardium has been a significant limitation in the study of heart failure.
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Population
51 LV samples from 44 cryopreserved human ICM and DCM hearts plus donor controls
Comparison
Human ICM and DCM hearts vs age-, gender-, and BMI-matched normal donor controls
Design
Proteomic and metabolomic biobank study
Offers direct human myocardial insights into ICM/DCM; hypothesis-generating and requires validation before clinical translation.
Poor access to human left ventricular myocardium is a significant limitation in the study of heart failure (HF). Here, we utilise a carefully procured large human heart biobank of cryopreserved left ventricular myocardium to obtain direct molecular insights into ischaemic cardiomyopathy (ICM) and dilated cardiomyopathy (DCM), the most common causes of HF worldwide. We perform unbiased, deep proteomic and metabolomic analyses of 51 left ventricular (LV) samples from 44 cryopreserved human ICM and DCM hearts, compared to age-, gender-, and BMI-matched, histopathologically normal, donor controls. We report a dramatic reduction in serum amyloid A1 protein in ICM hearts, perturbed thyroid hormone signalling pathways and significant reductions in oxidoreductase co-factor riboflavin-5-monophosphate and glycolytic intermediate fructose-6-phosphate in both; unveil gender-specific changes in HF, including nitric oxide-related arginine metabolism, mitochondrial substrates, and X chromosome-linked protein and metabolite changes; and provide an interactive online application as a publicly-available resource.
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Li et al. (2020) studied this question.
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