Hypertriglyceridemia and cardiovascular outcomes

Hypertriglyceridemia and

cardiovascular outcomes

F. Hadaegh

Prevention of Metabolic Disorders Research Center, Research Institute for Endocrine Sciences,

Shahid  Beheshti University of Medical Sciences.

November 2018 - Tehran

CASE SCENARIO

A 58-year-old obese male patient with type 2  diabetes mellitus (T2DM) presents with a history of acute coronary syndrome and previous CABG 2 years earlier. His HbA1C value has been stable at 7.2% with metformin and liraglutide 1.8 mg daily.

He is currently normotensive with Lozartan/HCT 50 mg/12.5 mg with a urine/albumin creatinine ratio at 80 mg/mg and an estimated glomerular filtration rate of 48 ml/min.

The patient’s current lipid profile with rosuvastatin 40 mg and ezetimibe 10mgdaily is as follows: (LDL-C), 66 mg/dl; (TGs), 320 mg/dl; (HDL-C), 38 mg/dl; and non–  HDL-C, 130 mg/dl.

The patient and his primary care physician are concerned about his residual risk of recurrent ASCVD events and his overall prognosis. What is your recommendation for the patient?

Agenda

5. Overview of pathophysiology
5. Role of triglycerides as a CHD risk factor (observational  & Genetic studies)
5. Residual risk after statins
5. Effect of triglyceride reduction on cardiovascular outcomes (clinical trials); REDUCE –IT (BREAKING  NEWS !)
5. Guidelines
5. Conclusions

Figure 1  Metabolism of triglycerides. Chylomicrons are formed in the small intestine from dietary fat, and contain triglycerides and apolipoprotein B‑48. Chylomicrons enter the circulation, where they are hydrolysed by lipoprotein lipase (LPL), which is activated by apolipoprotein C‑II (apoC‑II). Free fatty acids, which are produced by hydrolysis of triglycerides, are either used in muscle cells as a source of energy or resynthesized into triglycerides and stored in adipose cells. Chylomicron remnant particles, also rich in triglycerides, are removed from the circulation in the liver. Triglycerides are also synthesized in liver cells and, together with apolipoprotein B‑100, form very low-density lipoprotein (VLDL) particles, which are secreted in blood. VLDL particles are also hydrolysed by LPL, and are transformed into intermediate-density lipoprotein (IDL) particles. IDL particles are either catabolized in the liver or transformed into low-density lipoprotein (LDL) particles by LPL.