Serum Lipids …. Again, and Always

Reports on the clinical importance of serum lipids appear early in the 1970s. Both hypercholesterolemia and hypertriglyceridemia (the main two components of serum lipids) were implicated in the risk of coronary artery disease1. Blood cholesterol fractions carry different functions in different body tissues. However, the low and very-low-density lipoprotein cholesterols (LDL-C & VLDL-C) enhance the process of atherosclerosis. In contrast, highdensity lipoprotein (HDL-C) is beneficial to stand against atherosclerosis of the coronary arteries2,3. Cholesterol phenotyping is of importance in the evaluation of the risk of atherosclerosis, especially when the value of cholesterol is on borderline4. The use of the atherogenic index LDLC/ HDLC ratio was found to be more informative than absolute cholesterol values5. Causes of the familial type of hypercholesterolemia have been referred to as amutation in the LDL receptor gene, apoprotein B, and the proprotein convertase subtilisin/Kexin type 9 gene, PCSK9. Such patients are at double risk for the development of cardiovascular disease and need early identification and treatment with the screening of all first-degree relatives. The use of inhibitors to the synthesis of apolipoprotein-100 has been recommended in the treatment of familial hypercholesterolemia along with other lipid-lowering drugs2,4. In the other atherogenic familial type mixed (combined) hyperlipidemia, which occurs at a frequency of 1-5 /5000, there is a decrease in high-density lipoprotein (HDL) cholesterol and an increase in non-HDL cholesterol (LDL and VLDL) showing hypercholesterolemia and hypertriglyceridemia. It is also termed Type IIIhyperlipidemia, dysbetalipoproteinemia, or broad beta disease. It is a genetic disorder characterized by accumulation, in the plasma, of remnant chylomicrons from intestinal lipoproteins and VLDL remnants derived from hepatic lipoproteins resulting in the development of premature atherosclerosis5,6. The cause could be referred to as the expression of different isoforms of Apoprotein E (Apo E) that do not bind to the receptor or Apo-E deficiency6,7. The molecular cause of this type is associated with the presence of ApoE2, which increases triglyceride and cholesterol levels by delaying clearance of hepatic and intestinal remnant lipoproteins 7. A recent review by Yao et al. 20208 mentioned the mechanisms of the direct action of hypercholesterolemia on the myocardium. One of those mechanisms was attributed to the change of membrane lipid bilayer, another to the regulation of intracellular calcium ions, or the isoform expression patterns of myosin heavy chain. Any or all of these will sensitize the myocardium to exogenous damage caused by hemodynamic overload, ischemia, diabetes, or probably other pathological stimuli9.