Coronary atherosclerosis is a potentially chronic circulatory condition that endangers human health. The biological cause underpinning cardiovascular disease is coronary atherosclerosis, and acute cardiovascular events can develop due to thrombosis, platelet aggregation, and unstable atherosclerotic plaque rupture. Coronary atherosclerosis is progressive, and three specific changes appear, with fat spots and stripes, atherosclerosis and thin-walled fiber atherosclerosis, and then complex changes in arteries. The progression and severity of cardiovascular disease are correlated with various levels of calcium accumulation in the coronary artery. The therapy and diagnosis of coronary atherosclerosis benefit from the initial assessment of the size and degree of calcification. This article will discuss the new progress in the early diagnosis of coronary atherosclerosis in terms of three aspects: imaging, gene and protein markers, and trace elements. This study intends to present the latest methods for diagnosing patients with early atherosclerosis through a literature review.

In clinical cohort studies, high expression of long-chain acyl-coenzyme A synthetases 1 (ACSL1 gene) in peripheral white blood cells of patients with acute myocardial infarction (AMI) has been utilized as molecular markers of myocardial infarction diagnosis. The plasma triglyceride level of AMI patients is significantly higher than that of healthy individuals. We hypothesized that the high expression of ACSL1 increases the level of triglyceride, which is one of the pathogenesis of AMI promoted by ACSL1. In this report, cell culture based methods were adopted to test the hypothesis and further investigate the effect and mechanism of ACSL1 on lipid metabolism. In this study, liver cells of healthy individuals were cultured, the overexpression and the knockdown vectors of ACSL1 were constructed and transfected into liver cells. The transfection was verified at the mRNA and protein level. Intracellular triglyceride content was quantitatively analyzed using ELISA. Changes of genes related to lipid metabolism were subsequently measured through PCR array. Overexpression of ACSL1 led to higher gene expression and protein levels compared to control and the triglyceride content was significantly increased in overexpressing cells. The expression level of fatty acid oxidation pathway PPARγ was significantly down-regulated compared with the control group, as were genes associated with fatty acid synthesis pathways: SREBP1, ACC, FAS, and SCD1. ACSL1 knockdown decreased the content of triglyceride whereas PPARγ was up-regulated and SREBP1, ACC, FAS, and SCD1 were down-regulated compared with the control group. In summary, high expression of ACSL1 reduced fatty acid β-oxidation through the PPARγ pathway, thereby increasing triglyceride levels.

Objective. To find molecular markers for the diagnosis of acute myocardial infarction (AMI), this research further verified the relationship between the expression level of FFAR2 gene and AMI by expanding the sample size based on the previous gene chip results. Methods. Peripheral venous leukocytes were collected from 113 patients with AMI and 94 patients with noncoronary artery disease as the experimental group and the control group, respectively. Real-time fluorescence quantitative polymerase chain reaction was used to detect the expression of the FFAR2 gene. Western blot analysis was applied to detect the relative expression of the FFAR2 gene at the level of protein. Furthermore, the relationship between gene expression and clinical data was also analyzed and compared. Results. The level of expression of FFAR2 gene in peripheral blood of patients with AMI was significantly lower than that of the control group (0.33 [0.04–1.08], 0.62 [0.07–1.86], respectively; p<0.05), which was 0.53 times that of the control group. Western blot results presented that the FFAR2 protein level in the peripheral blood of the AMI group was lower than that of the control group (0.114; p=0.004). Analyzing clinical data of the subjects indicated that the average age of the AMI group was significantly higher than the age of control group (p<0.01). Also, the fasting blood glucose level was higher (p<0.01), and the high-density lipoprotein cholesterol (HDL-C) level was lower (p=0.03). The FFAR2 mRNA level correlated positively with the HDL-C level (p<0.01). Logistic regression analysis suggested that the low expression of the FFAR2 gene in peripheral blood may be a risk factor for AMI independent of age, family history of diabetes, fasting blood glucose level, and HDL-C level (p=0.025). Compared with the high FFAR2 expression group, the risk of AMI in the low FFAR2 expression group was 6.308 times higher. Conclusion. The expression level of the FFAR2 gene in peripheral blood of patients with AMI was significantly lower than that in the control group. Low expression of the FFAR2 gene in peripheral blood is an independent risk factor for AMI. Hence, it may also be a potential biomarker to predict AMI.