Lipids and CVD

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LIPIDS AND CARDIOVASCULAR DISEASES

1 Contents Introduction ................................................................................................................................................. 2 Metabolism of Lipids .................................................................................................................................. 2 A. Exogenous Lipoprotein Pathway ..................................................................................................... 2 B. Endogenous Pathway (Feingold, 2021) ........................................................................................... 3 Role of Cholesterol in Atherosclerosis ........................................................................................................ 4 Familial Hypercholesterolemia .................................................................................................................... 4 References ................................................................................................................................................... 5

2 Introduction Cardiovascular diseases are contributing its major part for today’s morbidity and mortality worldwide. As per the reports illustrated by global health in 2017, there is increase in death by 21.1% from 2007 to 2017 due to cardiovascular diseases. The estimation was also reported stating that this would continue where it would grow up to 24million by 2030 (Pownall et al., 2019). However, many literature reviews reported that, atherosclerosis is the most common disease variant of cardiovascular diseases which shows clinical manifestation of ischemia and heart diseases and cardiac stroke. The atherogenisis, results due to accumulation of lipids within the vascular wall that can trigger the inflammatory reactions which stimulates the progression of atherosclerosis. This can also be triggered with few risk factors such as smoking, hypertension, diabetes, obesity, and varied lipid metabolism (Pownall et al., 2019). There is wide literature review which emerges lipids as the key players for atherosclerotic plaque formation. This paper demonstrates about lipid metabolism, its role in development of atherosclerosis and about an inherited disorder due to high cholesterol levels. Metabolism of Lipids Lipoproteins are lipid transport molecules which gets mobilized through plasma lipids. There are specific lipoproteins that can cause cardiovascular diseases and other metabolic syndromes. In lipoproteins, triglycerides and cholesterol esters form the central core of the molecules. This core complex is surrounded by different molecules such as phospholipids, free cholesterol, and apolipoproteins. Apolipoproteins classify the cholesterol into chylomicrons, high, low, and medium density lipoproteins. The mechanism divides into two pathways exogenous and endogenous pathways. A. Exogenous Lipoprotein Pathway The exogenous lipoprotein pathway starts from the intestine. The triglycerides through diet are hydrolyzed to free fatty acids and monoglycerol by intestinal lipases. This protein, which is a human sterol called C1-like 1, helps enterocytes take in free cholesterol (Feingold, 2021). AP2- clathrin complex interacts with high levels of extracellular cholesterol, allowing the cholesterol to enter the cell's membrane. A

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3 cholesterol ester protein helps in transfer of cholesterol esters to apoB lipoproteins including all variants of cholesterols. Before the lipases hydrolyze the triglycerides and release the fatty acids, this apoB permits lipid binding to the chylomicrons from circulation. A cofactor for the LPL, Apo C – II reduces the amount of chylomicrons following every interaction with ApoB. The Apo E enzyme acts as a ligand in signaling the hepatic chylomicron receptor. B. Endogenous Pathway (Feingold, 2021) VLDL, a kind of lipid that contains triglycerides and cholesterol esters, is the first stage of lipid metabolism in this route. Apo B-100, C-II, and E make up the VLDL surface chemicals. Triglyceride transfer protein (MTP), an endoplasmic protein, is essential for the lipidation of VLDL. In muscle and adipose tissue, the triglyceride components are processed via their interaction with LPL, which results in the synthesis of IDL. This IDL accumulates all of HDL's esters via CETP, and hepatic lipase combines IDL with cholesterol to form LDL. HDL may also take up cholesterol from cells through SR-B1 and deliver it straight to the liver via CETP-facilitated cholesterol transfer to VLDL or LDL.

4 Role of Cholesterol in Atherosclerosis Cholesterol is a key factor for causing atherosclerosis. It is the core component of atherosclerotic plaque that can give raise to the hypothesis of cholesterol for pathogenesis of atherosclerosis. The literature reviews reported, increased levels of LDL and apoB are directly associated with atherosclerosis events causing CVD. A study made for association of cholesterol and atherosclerosis revealed a 4S trial which showed that reduction in total cholesterol level, LDL cholesterol levels with elevated HDL resulted in formation of atherosclerotic plaque (Dong et al., 2021). High levels of cholesterol in the blood have been linked to an increased risk of cardiovascular disease (CVD) due to atherosclerotic plaques, according to research conducted by the authors of the paper in question. Endothelial dysfunction occurs as a consequence of the atherosclerotic plaque's high pressure on the arteries causing arterial damage, which in turn leads in apoB-containing lipoproteins entering the subendothelial region (Linton et al., 2019). ASCVE is caused by the rupture of these vessels, which favours thrombus development. LDL may become atherogentic particles by oxidative alteration, which can set up inflammatory reactions. Epidemiological studies have shown HDL's helpful characteristics in combating atherosclerosis, and malfunction of HDL has been linked to an increased risk of cardiovascular disease (CVD). Familial Hypercholesterolemia Premature coronary heart disease is a leading cause of death in people with Familial Hypercholesterolemia, an autosomal dominant inherited illness of lipid metabolism.

5 Atherosclerosis and other cardiovascular illnesses are accelerated when the body is exposed to LDL for an extended period of time. Mutations in the LDL receptor genes are the primary cause of the disease (LDLR). According to reports from throughout the world, the likelihood is as high as one in one hundred (Migliara et al., 2017). Simon Broome Criteria may be used to calculate cholesterol levels that incorporate clinical features, family history and molecular diagnostics. Adults who have total cholesterol levels more than 7.4mmol/L or LDL-C levels greater than 4.9mmol/L are considered to have FH, as are children who have total cholesterol levels greater than 6.7mmol/L or LDL-C levels larger than 4.0mmol/L in children under the age of 16 (Rasadi et al., 2014). References 1. Pownall, H. J., & Gotto, A. M., Jr (2019). Lipids and Cardiovascular Disease: Putting It All Together. Methodist DeBakey cardiovascular journal , 15 (1), 5–8. https://doi.org/10.14797/mdcj-15-1-5 2. Dong, J., Yang, S., Zhuang, Q., Sun, J., Wei, P., Zhao, X., Chen, Y., Chen, X., Li, M., Wei, L., Chen, C., Fan, Y., & Shen, C. (2021). The Associations of Lipid Profiles With Cardiovascular Diseases and Death in a 10-Year Prospective Cohort Study. Frontiers in cardiovascular medicine , 8 , 745539. https://doi.org/10.3389/fcvm.2021.745539 3. Feingold, K, R (2021) Introduction to Lipids and Lipoprotein, In: Feingold KR, Anawalt B, Boyce A, et al., editors. South Dartmouth (MA): MDText.com, Inc.; 2000-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK305896/ 4. Linton, M,R,F., Yancey, P,G., Davies, S,S (2019) The Role of Lipids and Lipoproteins in Atherosclerosis.In: Feingold KR, Anawalt B, Boyce A, et al., editors. Endotext. South Dartmouth (MA): MDText.com, Inc.; 2000-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK343489/ 5. Migliara, G., Baccolini, V., Rosso, A., D'Andrea, E., Massimi, A., Villari, P., & De Vito, C. (2017). Familial Hypercholesterolemia: A Systematic Review of Guidelines on Genetic Testing and Patient Management. Frontiers in public health , 5 , 252. https://doi.org/10.3389/fpubh.2017.00252 6. Al-Rasadi, K., Al-Waili, K., Al-Sabti, H. A., Al-Hinai, A., Al-Hashmi, K., Al-Zakwani, I., & Banerjee, Y. (2014). Criteria for Diagnosis of Familial Hypercholesterolemia: A

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6 Comprehensive Analysis of the Different Guidelines, Appraising their Suitability in the Omani Arab Population. Oman medical journal , 29 (2), 85–91. https://doi.org/10.5001/omj.2014.22

Lipids and CVD

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