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Diabetes mellitus (DM) remains one of the leading factors of morbidity and mortality worldwide augmenting social and medical care burden.1 Currently, advances in pathophysiological understanding of the innate mechanisms of DM-related complications in part affecting heart and vessels are impressed, while they are not fully clear. Recent basic and clinical studies have shown that DM directly induces changes in various organ systems in close conjunction with glucotoxicity, lipid toxicity, oxidative stress and low-grade inflammation, which lead to microvascular and macrovascular complications mediating cardiovascular (CV) risk.2 Moreover, accelerating atherosclerosis, endothelial dysfunction and cardiomyopathy play a causative role in the development and progression of DM-related CV outcomes and death.3 In this context, use of cardiac biomarkers for risk stratification in patients with DM appears to be promising, especially in individuals without known CV disease.
The abundant biomarkers representing several pathophysiological pathways of DM development have been investigated to improve the prediction of CV events and DM-related deaths (table 1). Although all these biomarkers have strongly accompanied to staging of evolution of target organ damage in DM, it is completely unknown whether cardiac biomarkers associated with CV risk in general population may predict future incident of CV disease in DM. Yet, several biomarkers reflected endothelial cell activation and dysfunction, cell growth and differentiation, vascular remodelling and angiogenesis have not exhibited an ability to improve CV-event prediction based on traditional CV risk factors, that is, smoking, obesity, hypertension, dyslipidaemia, etc. Nevertheless, natural evolution of metabolic disease from pre-diabetes including impaired fasting glucose and/or impaired glucose tolerance to type-1 or type-2 DM has not obligatorily associated with sufficient changes in …
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