Aleesha Shaik1, Robert S Rosenson2. 1. Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA. 2. Cardiometabolics Unit, Zena and Michael A Wiener Cardiovascular Institute, Marie-Josee and Henry R Kravis Center for Cardiovascular Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA. robert.rosenson@mssm.edu.
Abstract
OBJECTIVE: Despite aggressive reduction of low-density lipoprotein cholesterol (LDL-C), there is a residual risk of cardiovascular disease (CVD). Hypertriglyceridemia is known to be associated with increased CVD risk, independently of LDL-C. Triglycerides are one component of the heterogenous class of triglyceride-rich lipoproteins (TGRLs). METHODS/ RESULTS: Growing evidence from biology, epidemiology, and genetics supports the contribution of TGRLs to the development of CVD via a number of mechanisms, including through proinflammatory, proapoptotic, and procoagulant pathways. CONCLUSION: New genetics-guided pharmacotherapies to reduce levels of triglycerides and TGRLs and thus reduce risk of CVD have been developed and will be discussed here.
OBJECTIVE: Despite aggressive reduction of low-density lipoprotein cholesterol (LDL-C), there is a residual risk of cardiovascular disease (CVD). Hypertriglyceridemia is known to be associated with increased CVD risk, independently of LDL-C. Triglycerides are one component of the heterogenous class of triglyceride-rich lipoproteins (TGRLs). METHODS/ RESULTS: Growing evidence from biology, epidemiology, and genetics supports the contribution of TGRLs to the development of CVD via a number of mechanisms, including through proinflammatory, proapoptotic, and procoagulant pathways. CONCLUSION: New genetics-guided pharmacotherapies to reduce levels of triglycerides and TGRLs and thus reduce risk of CVD have been developed and will be discussed here.
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