The Association between Cardiovascular Risk and Elevated Triglycerides

Djanggan Sargowo, Olivia Handayani

Abstract


BACKGROUND: The association between elevated triglycerides and cardiovascular risk has been extensively studied. The elevated level of triglycerides occurs through abnormalities in hepatic very low-density lipoprotein (VLDL) production and intestinal chylomicron synthesis, dysfunctional lipoprotein lipase (LPL)-mediated lipolysis or impaired remnant clearance.

CONTENT: Hypertriglyceridemia (HTG) commonly leads to a reduction in high-density lipoprotein (HDL) and increase in atherogenic small dense low-density lipoprotein (LDL) cholesterol, called the atherogenic dyslipidemia (AD). Triglycerides may also stimulate atherogenesis by mechanisms, such excessive release of free fatty acids, and production of pro-inflammatory cytokines, fibrinogen, coagulation factors and impairment of fibrinolysis. Genetic studies strongly support hypertriglyceridemia (HTG) and high concentration of triglyceride-rich lipoprotein (TRL) as causal risk factors for cardiovascular disease. Therefore, lipid management is crucial in reducing cardiovascular risk. Combination of lipid lowering drug therapy may be needed to achieve both LDL and non-HDL cholesterols treatment goal for cardiovascular disease prevention in patients with elevated triglyceride levels, particularly those with triglyceride ≥500 mg/dL.

SUMMARY: LDL and non-HDL cholesterol can be a promising target therapy in HTG. Additional clinical outcomes data are needed to provide a more evidence-based rationale for clinical lipid management of hypertriglyceridemic patients.

KEYWORDS: hypertriglyceridemia, non-HDL cholesterol, dyslipidemia, CV risk


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References


Chan DC, Barrett PHR, Watts GF. The metabolic and pharmacologic bases for treating atherogenic dyslipidemia. Best Pract Res Clin Endocrinol Metab. 2014; 28: 369-85, CrossRef.

Aguiar C, Alegria E, Bonadonna RC, Catapano AL, Consentino F, Elisaf M, et al. A review of the evidence on reducing macrovascular risk in patients with atherogenic dyslipidemia: A report from an expert consensus meeting on the role of fenofibrate-statin combination therapy. Atheroclerosis. 2015; 19 (Suppl): 1-12, CrossRef.

Sparks JD, Sparks CE, Adeli K. Selective hepatic insulin resistance, VLDL overproduction, and hypertriglyceridemia. Arterioscler Throm Vasc Biol. 2012; 32: 2104-12, CrossRef.

Yuan G, Al-Shali KZ, Hegele RA. Hypertriglyceridemia: Its etiology, effects and treatment. Can Med Assoc J. 2007; 176: 1113-20, CrossRef.

Balakumar P, Babbar L, Kalra S, Mahadevan N, Sritharan S, Krishan P. Is hypertriglyceridemia a key detrimental factor or associative triggering factor for cardiovascular abnormalities? Syst Rev Pharm. 2012; 3: 1-3, CrossRef.

Boullart ACI, de Graaf J, Stalenhoef AF. Serum triglycerides and risk of cardiovascular disease. Biochimica Biophysica Acta. 2012; 1821: 867-75, CrossRef.

Maki KC, Bays HE, Dicklin MR. Treatment options for the management of hypertriglyceridemia: Strategies based on the best-available evidence. J Clin Lipidol. 2012; 6: 413-26, CrossRef.

Hassing HC, Surendran RP, Mooij HL, Stroed ES, Nieuwdorp M, Dallinga-Thie GM. Pathophysiology of hypertriglyceridemia. Biochimica Biophysica Acta. 2012; 1821: 826-32, CrossRef.

Nordestgaard BG, Varbo A. Triglycerides and cardiovascular disease. Lancet. 2014; 384: 626-35, CrossRef.

Borén J, Matikainen N, Adiels M, Taskinen MR. Postprandial hypertriglyceridemia as a coronary risk factor. Clinica Chimica Acta. 2014; 431: 131-42, CrossRef.

Watts GF, Karpe F. Why, when and how should hypertriglyceridemia be treated in the high-risk cardiovascular patient? Expert Rev Cardiovasc Ther. 2011; 9: 987-97, CrossRef.

Tenenbaum A, Klempfner R, Fisman EZ. Hypertriglyceridemia: A too long unfairly neglected major cardiovascular risk factor. Cardiovasc Diabetol. 2014; 13: 159-68, CrossRef.

Berglund L, Brunzell JD, Goldberg AC, Goldberg IJ, Stalenhoef A. Treatment options for hypertriglyceridemia: From risk reduction to pancreatitis. Best Pract Res Clin Endocrinol Metab. 2014; 28: 423-37, CrossRef.




DOI: http://dx.doi.org/10.18585/inabj.v9i1.266

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