Revisiting cardiovascular risk reduction in type 2 diabetes and dyslipidemia

Abstract

Statin therapy has been a mainstay of cardiovascular disease (CVD) risk reduction for the past 20 years in type 2 diabetes management. Its application has been largely due to well-designed, randomized-control studies consistently showing 25–35% CVD risk reduction. However, the remaining 65–75% reduction potential for CVD risk has yet to be effectively addressed. With a push towards personalized medicine, the likelihood of a one-size-fits-all approach to CVD risk reduction in type 2 diabetes may not be as beneficial as anticipated. It is reasonable to suggest that we have aggregated separate CVD phenotypic groups under one treatment umbrella and consequently, dismissed further unaddressed CVD risk reduction potential.The hypothesis proposed in this review is that there are at least two phenotypic groups with distinct molecular mechanisms contributing to CVD risk requiring different treatment approaches that can be applied with present pharmacotherapy. The two phenotypes can be classified as the following: 1) high low-density lipoprotein (LDL) phenotype and 2) high triglyceride (TG) plus low high-density lipoprotein (HDL) phenotype. As both phenotypes are significantly represented in individuals with type 2 diabetes, a more precise understanding of molecular details can be merged with clinical CVD outcome studies to arrive at a new hypothesis for CVD treatment that can be substantiated with additional well-designed clinical trials. As we transition from 20th to 21st-century medicine, we should utilize new knowledge to adapt current CVD risk reduction measures for those with type 2 diabetes.