Type two diabetes mellitus (T2DM) remains a leading contributor to cardiovascular (CV) mortality worldwide. Although obese and metabolic syndrome are discussed key factors contributing a higher risk of T2DM, the exact molecular mechanisms underlying to the progression of dysmetabolic states are still not completely clear. There is large body of evidence regarding endothelial dysfunction as a key player in increasing CV risk and that vascular damage in the dysmetabolic patients might mediate through an imbalance between various populations of micro particle (MP). The short commentary is discussed a role of impaired ratio between apoptotic MPs and activated MPs derived from endothelial cells that was recognized as “impaired phenotype” of endothelial cell-derived MPs. It has considered the causality epigenetic reprogramming, metabolic disorders, inflammation, and oxidative stress in forming of “impaired phenotype” of MPs. The incorporation of measurement of the endothelial cell-derived MP number into a conventional CV risk factor model aimed improving of risk stratification of the dysmetabolic patients with high probability of CV disease is discussed.