Abstract

While a molecular assessment of the perturbations and injury arising from diseases is essential in their diagnosis and treatment, understanding changes due to preventative strategies is also imperative. Currently, complex diseases such as cardiovascular disease (CVD), the leading cause of death worldwide, suffer from a limited understanding of how the molecular mechanisms taking place following preventive measures (e.g., exercise) differ from changes occurring due to the injuries caused from the disease (e.g., myocardial infarction (MI)). Therefore, this manuscript assesses lipidomic changes before and one hour after exercise treadmill testing (ETT) and before and one hour after a planned myocardial infarction (PMI) in two separate patient cohorts. Strikingly, unique lipidomic perturbations were observed for these events, as could be expected from their vastly different stresses on the body. The lipidomic results were then combined with previously published metabolomic characterizations of the same patients. This integration provides complementary insights into the exercise and PMI events, thereby giving a more holistic understanding of the molecular changes associated with each.

Highlights

  • Physical activity and diet have been considered the primary preventative strategies for numerous diseases, including cardiovascular disease (CVD)

  • IMS–collision induced dissociation (CID)–Mass spectrometry (MS) analyses yielded a total of 352 unique lipid identifications for the exercise treadmill testing (ETT) cohort and 299 for the planned myocardial infarction (PMI) cohort across the same five lipid categories: glycerolipids, sphingolipids, phospholipids, fatty acids and sterols [57]

  • The metabolomic and lipidomic findings observed for the exercise and PMI cohorts showcased their unique pathophysiology

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Summary

Introduction

Physical activity and diet have been considered the primary preventative strategies for numerous diseases, including cardiovascular disease (CVD). Despite the prevalence of CVD and resulting MI events worldwide, the complex pathophysiology underlying CVD origins has yet to be fully defined [2]. Even with advancements such as diagnosis with CK-MB and cTn assays and methods for CVD prediction from traditional risk factors alone or in tandem with molecular predictors, CVD-related events continue to be the leading cause of death worldwide [1,3,4,5]. Improving our understanding of these disease mechanisms could serve to reduce the current morbidity rate of CVD by providing more effective prevention, intervention and treatment strategies.

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