Role of diet to combat Heart Failure and Stroke comorbidities: based on metabolomic approach

Description

Heart Failure (HF) and stoke affects significant proportion of older population, with a subsequently increased number of people living with its comorbidities. Sarcopenia, is the loss of muscle mass and muscle function, which is a frequent co-morbidity among patients with HF and stroke, which significantly exceeds the prevalence observed in individuals of the same age with no HF. In these patients with sarcopenia exercise capacity, weight-adjusted peak VO2, functional mobility, disease severity, oxygen consumption, left ventricular function, and re-hospitalization rates are significantly worsening compared to those without sarcopenia.

Given the potential effect of dietary intervention on these phenotypes, it seems to be a potential for effective, novel therapies for heart failure to arise from dietary intervention with simultaneous molecular understanding by high-throughput metabolomics profiling in relation to the diet-muscle-heart axis. Compared with individual foods/nutrients, dietary patterns reflect a person’s habitual diet, and incorporate the synergistic and accumulative effects of various dietary components, thereby minimizing confounding by individual dietary factors. Prior trial studies have identified various metabolites associated with intakes of dietary patterns, and CVD risk and type 2 diabetes.

Aim:

To develop a multivariate/multidimensional modelling of a panel of complementary biomarkers (imaging, circulating metabolites (metabolic profile), and functional tests) for (i) the early detection of otherwise subclinical HF conditions; (ii) the diagnostic assessment of clinically manifest HF-sarcopenia; (iii) the risk stratification of subjects with a suspected or confirmed diagnosis; (iv) the tracking of the conditions over time; (v) the selection of an appropriate therapeutic intervention; and (vi) the monitoring of the response to our designed dietary intervention.

Method:

To utilize the existing findings (e.g., inflammation metabolites) in the literature to design and employ a semi-targeted metabolomics approach to confirm "HF-Sarcopenic phenotype" and “Stroke-sarcopenic phenotype” at the plasma metabolite level.