International Journal of Healthcare Sciences ISSN 2348-5728 (Online) Vol. 10, Issue 1, pp: (161-167), Month: April 2022 - September 2022, Available at: www.researchpublish.com
Genetic Risks of Cardiovascular Diseases Wachirawit Angkatavanich Triam Udom Suksa School, Pathum Wan, Bangkok, Thailand 10330 DOI: https://doi.org/10.5281/zenodo.6890951
Published Date: 23-July-2022
Abstract: Coronary Heart Disease (CHD) is the number one cause of death in the current world. Since numerous reasons heighten the risk of CHD, this review will focus only on genetic risk factors. Known for its ability to analyze and enhance chromosome mapping by garnering tons of human tests by its agnostic approach, conducting GenomeWide Association Studies (GWAS) to examine genetic patterns in patients has perceived many undiscovered hidden genes. For instance, Sortilin is a gene vitally linked to cardiovascular diseases (CVD) risks and plasma LDL cholesterol levels. Moreover, GWAS could predict CVD risk furthermore and is beneficial for personalized medical treatment. Applying the understanding of genetics could create biomarkers that detect early stages of disease development and provide a precise diagnosis. Precise risk assessments and individualized treatment benefit projections are necessary. Accurate risk ratings, more potent drugs, and specialized evaluation of treatment are three tools to improve traditional risk estimation of CVD. Keywords: Coronary Heart Disease; Genome-Wide Association Studies (GWAS); SORT1
I. INTRODUCTION The threat of Coronary Heart Disease (CHD) could be partially indicated by using Genetic Risk Scores (GRS) found in Coronary Artery Diseases (CAD) [1]. Note whether the GRS of CAD dominates the Coronary Artery Calcification (CAC) of CHD or whether the disparity between male and female CHD risks from utilizing the GRS of CAD is ambiguous [2]. Cardiovascular diseases such as coronary heart disease, cerebrovascular disease, peripheral arterial disease, rheumatic and congenital heart diseases, and venous thromboembolism lead to the number of global casualties [3]. Although most European nations have seen a reduction in deaths from CVD [4]. The decreasing mortality rate in Central and Eastern Europe (CEE) from CVD and stroke happens significantly slower. Genotyping and sequencing are key roles in disease diagnosis, therapeutic management, and prognosis markers for hypertrophic cardiomyopathy or familial hypercholesterolemia [5]. Genetic testing should be carried out in well-phenotyped individuals and coupled with a complete family appraisal to assist in interpreting and applying the results [5]. Cardiovascular studies pertained to molecular genetics technologies and expanded the understanding of chromosome mapping and the many unexplored genomes associated with primary etiology [5, 6]. Over the past two decades, our knowledge about genetics, how DNA variants co-operate, and how CVDs are inheritable could explain the dramatic growth of treatment [7]. This review aims to explore the relationship between genetic factors and risk of developing CVD.
II. CVD PATIENTS: GENOME-WIDE ASSOCIATION STUDY (GWAS) Sortilin is the second example of a "new" gene discovered by GWAS (OMIM acc. No. 602458). The CELSR2/PSRC1/SORT1 gene cluster GWAS results were among the most crucial signal related to CVD risk and plasma LDL cholesterol levels [8-10]. In addition, the processes by which SORT1 affects plasma cholesterol levels in this instance were unclear (and remain so to date) [8, 11]. SORT1 encodes a multiligand sorting receptor primarily expressed in the liver and involved in intracellular trafficking [12]. Essential proteins involved in lipid metabolism, apolipoproteins E, B, and A5, with which they interact (reviewed by SORT1 affect VLDL transport through the hepatic Golgi apparatus and interact with PCSK9 to affect LDLR degradation [13, 14]. Lastly, it might function as a low-capacity alternate LDL receptor. Although the effects of SORT1 on plasma cholesterol levels and MI risk have been conclusively demonstrated and frequently validated, the data from animal models is inconsistent and often contradictory [15]. The roles of SORT1 appear to be highly complicated and contentious, and the precise molecular process is yet unknown [15]. Thus, the fundamental response has not been provided regarding the relationship between increased or decreased hepatic expression and an increased risk of
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