Coronary artery disease (CAD) is one of the most commonly diagnosed heart diseases. Diabetes, an elevation in blood pressure and high-fat diets are considered as some of the factors that contribute to the causation of CAD [
1]. Among these factors, an elevation in triglycerides (TG) levels have shown a correlation with CAD occurrence although the exact mechanism is still obscure [
2]. Hypertriglyceridemia can develop as a result of primary factors including mainly genetics, or secondary factors such as diabetes and hyperlipidemia [
2]. Genetic abnormalities have contributed in causing hypertriglyceridemia through influencing the metabolism of triglycerides [
3]. The overproductions of apo C-III through genetic modifications and Lipoprotein lipase (LPL) have shown an association with variations in triglycerides levels [
4].
Recently, the sequencing of human genomic DNA has led to the discovery of Apolipoprotein A5 (APOA5) gene which belongs to a regulatory gene family including APOA1, APOC3 and APOA4 [
5].This gene is located on chromosome 11q23 in about 30 kb downstream of APOA4, and contains four exons. Several studies have indicated that the newly identified apolipoprotein locus plays a major role in triglycerides hemostasis [
6]. It encodes for apoA-V protein which reduces triglycerides plasma levels [
6]. Therefore, genetic alterations in APOA5 could result in changes in TG levels. Point mutations in APOA5 yield incomplete assembly of apoA-V protein, and were observed mostly in patients with hypertriglyceridemia. Nevertheless, no specific mutations were known to cause severe illnesses, but certain studies have predicted the association of single nucleotide polymorphisms (SNPs) in APOA5 with medical conditions. The variants -1131 T > C and c.56C > G (S19 W) for APOA5s are examples of SNPs that have correlations with high triglycerides plasma levels [
7].Accordingly, A novel variant c.553G > T was lately identified through the sequencing of APOA5 coding region. This SNP causes a substitution of the amino acid cysteine with a glycine molecule [
4]. The effect of which has been researched and the conclusion is still to be reached. Upon the effort to study c.553G > T variant, a very recent research revealed that introducing a free cysteine in APOA-V protein allows the binding of it with other proteins through the formation of disulfide bonds which affects TG modulation [
8]. Furthermore, c.553G > T variant (rs2075291); was detected in a higher rate in patients with acute coronary syndrome when compared to the control group [
1]. Atorvastatin is a commonly known drug that is used to regulate lipid metabolism [
9]. Based on Biopharmaceutics Classification System, atorvastatin is considered as a class II drug [
10], and is a member of statins family also known as 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors [
11]. Therefore, atorvastatin is found to reduce cholesterol levels in CAD patients. In a study that was conducted to analyze the effects of atorvastatin on various lipoproteins, atorvastatin showed no effects on TG levels in Chylomicron, LDL, IDL and VLDL while it reduced cholesterol levels in these lipoproteins [
12]. Here, we examine the effects of the genetic variant c.553G > T (rs2075291); on TG levels in CAD patients receiving atorvastatin daily as a lipid lowering medicine.