Cardiomyocyte changes in the metabolic syndrome and implications for endogeneous protective strategies

Abstract

The deadly quartet of the metabolic syndrome includes obesity, impaired glucose tolerance, an atherogenic lipid profile and hypertension. The synergistic effects of these comorbidities lead to a combination of functional and structural cardiomyocyte changes and finally result in a global adverse remodeling process. Overall cardiovascular outcome is significantly impaired. Furthermore, these changes increase the need for surgical or endovascular interventions and impair their outcomes. This is potentially due to current cardioprotective techniques being insufficiently tailored to the specific needs of these patients. The following review discusses the observed cardiomyocyte changes and systemic factors contributing to these changes. It describes the ensuing problems in cardioprotection and discusses strategies that can be taken to divert or circumvent these detrimental changes.

Keywords::

• cardiomyocyte changes
• cardioprotection
• ischemic heart disease
• metabolic syndrome

Financial & competing interests disclosure

W Oosterlinck received a PhD fellowship of the Research Foundation – Flanders (FWO) and the study was partly funded by research project G.0966.11. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Key issues

• Prevalence of the metabolic syndrome rises rapidly.

• Components of metabolic syndrome increase cardiovascular risk synergistically.

• The metabolic syndrome leads to specific cardiomyocyte changes.

• The natural course of the metabolic syndrome is detrimental.

• The metabolic syndrome necessitates a tailored approach with correction of the individual risk factors and prevention of the hypertrophic and inflammatory stimuli.

• New pharmacological insights might enable us to reactivate endogenous cardioprotective pathways in this high-risk population.

Notes