Pragmatic Analysis of Dyslipidemia Involvement in Coronary Artery Disease: A Narrative Review

Abstract

Background: Dyslipidemia is the main factor involved in the occurrence and progression of coronary artery disease. Objective: The research strategy is aimed at analyzing new data on the pathophysiology of dyslipidemia involvement in coronary artery disease, the modalities of atherogenic risk estimation and therapeutic advances. Method: Scientific articles published in PubMed from January 2017 to February 2018 were searched using the terms "dyslipidemia" and "ischemic heart disease". Results: PCSK9 contributes to the increase in serum levels of low-density lipoprotein-cholesterol and lipoprotein (a). The inflammation is involved in the progression of hyperlipidemia and atherosclerosis. Hypercholesterolemia changes the global cardiac gene expression profile and is thus involved in the increase of oxidative stress, mitochondrial dysfunction, and apoptosis initiated by inflammation. Coronary artery calcifications may estimate the risk of coronary events. The cardioankle vascular index evaluates the arterial stiffness and correlates with subclinical coronary atherosclerosis. The carotid plaque score is superior to carotid intima-media thickness for risk stratification in patients with familial hypercholesterolemia and both can independently predict coronary artery disease. The lipoprotein (a) and familial hypercholesterolemia have a synergistic role in predicting the risk of early onset and severity of coronary atherosclerosis. A decrease in atherosclerotic coronary plaque progression can be achieved in patients with plasma LDL-cholesterol levels below 70 mg/dL. A highly durable RNA interference therapeutic inhibitor of PCSK9 synthesis could be a future solution. Conclusion: The prophylaxis and treatment of coronary artery disease in a dyslipidemic patient should be based on a careful assessment of cardio-vascular risk factors and individual metabolic particularities, so it may be personalized.

Effect of polyphenol, flavonoid, and saponin fractions from Thymus atlanticus on acute and chronic hyperlipidemia in mice

“…Cardiovascular diseases are the leading cause of morbidity and mortality worldwide [1]. These diseases are related to several risk factors especially dyslipidemia, which is a metabolic disorder that is manifested by elevated levels of plasma total cholesterol (TC), triglycerides (TG), and low-density lipoprotein cholesterol (LDL-C), along with a reduced level of high-density lipoprotein cholesterol (HDL-C) [2]. Dyslipidaemia is closely linked with occurrence and progression of several pathologies including atherosclerosis and its complications such as coronary artery disease [2].…”

“…These diseases are related to several risk factors especially dyslipidemia, which is a metabolic disorder that is manifested by elevated levels of plasma total cholesterol (TC), triglycerides (TG), and low-density lipoprotein cholesterol (LDL-C), along with a reduced level of high-density lipoprotein cholesterol (HDL-C) [2]. Dyslipidaemia is closely linked with occurrence and progression of several pathologies including atherosclerosis and its complications such as coronary artery disease [2]. Several clinical trials confirmed that the reduction of plasma levels of TC, TG, and LDL-C induce a significant reduction of the morbidity and mortality rate related to these diseases [3].…”

Insulin mimetic effect of D‐allulose on apolipoprotein A‐I gene

“…Coronary artery disease (CAD) is the number one cause of mortality in industrialized countries (Dalen et al, 2014;Sidney et al, 2019). A risk factor associated with CAD is low high-density lipoprotein (HDL) cholesterol and apolipoprotein A-I (apo A-I) concentrations in plasma (Malakar et al, 2019;Mihăilă, 2020;Oikonomou et al, 2020;Stone & Grundy, 2019). Though increasing HDL/apo A-I levels may slow and reverse atherosclerosis (Lebherz et al, 2007;Shaw et al, 2008), approaches to increase apo A-I via various pharmaceutical agents have not been successful in preventing major adverse cardiovascular events (Feghaly & Mooradian, 2020).…”

Polymorphism in Apolipoprotein C3 (APOC3) and Fatty Acid-Binding Proteins (FABP2) Genes in Nondiabetic Dyslipidemic Patients: A Tertiary Care Hospital-Based Pilot Study

“…5 Single nucleotide polymorphism in a few genes is associated with high triglyceride (TG) and CHOL levels significantly contributing to dyslipidemia. 6 A gene associated with TG and CHOL level is the gene encoding for fatty acid-binding proteins (FABP2) located at the chromosome 4q2-q31, another gene apolipoprotein C3 gene (APOC3) located on the chromosome 11q23, allele *3238 C is also involved in the regulation of plasma TG levels. 7,8 The circulating lipid biomarkers, mainly polymorphism APOC3 (rs5128) and FABP2 (rs1799883), had been independently studied in diabetic patients, but the associations between these biomarkers and occurrence of dyslipidemia in nondiabetic patients had rarely been studied.…”

“…Single nucleotide polymorphism in a few genes is associated with high triglyceride (TG) and CHOL levels significantly contributing to dyslipidemia. 6 A gene associated with TG and CHOL level is the gene encoding for fatty acid-binding proteins ( FABP2 ) located at the chromosome 4q2–q31, another gene apolipoprotein C3 gene ( APOC3 ) located on the chromosome 11q23, allele *3238 C is also involved in the regulation of plasma TG levels. 7 8 …”