Nantarat Komanasin

Background/Aim: Atherosclerosis is a vascular inflammatory disease characterized by the activation and stress of various inflammatory cells, leading to the development of coronary artery disease and subsequently acute myocardial infarction (AMI). Among AMI cases, ST-segment elevation myocardial infarction (STEMI) is typically more severe than non-STEMI (NSTEMI). UL16-binding proteins (ULBPs), which are NKG2D ligands, can be expressed on the surface of stressed and activated cells, prompting these cells to generate microparticles (MPs). Consequently, MPs carrying ULBPs, particularly ULBP1 (ULBP1⁺ MPs), may be released into the bloodstream. This study aimed to investigate the association between ULBP1⁺ MPs and the presence of AMI and its severity. Materials and Methods: We recruited 58 AMI patients and 45 age-matched control subjects. Levels of ULBP1⁺ MPs and ULBP1⁺ MPs originating from T lymphocytes (ULBP1⁺ TMPs) were measured using flow cytometry. Results: Both ULBP1⁺ MP and ULBP1⁺ TMP levels were significantly elevated in AMI patients compared to controls. Elevated levels of these MPs were independent risk factors for AMI with odds ratios (OR) of 4.3 (95%CI=1.5-12.3) for ULBP1⁺ MPs and 5.8 (95%CI=2.0-17.0) for ULBP1⁺ TMPs. Additionally, ULBP1⁺ TMP levels were significantly higher in STEMI patients compared to NSTEMI patients, with an independent association observed between ULBP1⁺ TMPs and STEMI (OR=3.9; 95%CI=1.2-12.8). Conclusion: Elevated levels of ULBP1⁺ MPs and ULBP1⁺ TMPs are associated with AMI and its severity. These biomarkers could serve as indicators of vulnerable plaques that lead to AMI.

Background: Various cell types undergo activation and stress during atherosclerosis resulting in the development of acute myocardial infarction (AMI) in coronary artery disease (CAD). Major histocompatibility complex class I related chain A and B (MICA/B) can be expressed on the surface of activated and stressed cells and released into blood circulation in several forms including microparticles (MICA/B⁺ MPs) from various cell types. We aimed to investigate the association of these MICA/B⁺ MPs with the presence of AMI. Fifty-one AMI and 46 age-matched control subjects were recruited. Methods: Levels of MICA/B⁺ MPs derived from various parent cells including endothelial cells, platelets, monocytes, neutrophils, and T lymphocytes were determined by flow cytometry. Results: The levels and proportion of MICA/B⁺ MPs from all types of cell origin were significantly increased in AMI patients compared to those of the controls. A multivariate regression model showed an independent association between MICA/B⁺ MPs and AMI (OR = 11.6; 95% CI = 2.8, 47.3). Interestingly, based on the disease severity, we found that the levels of MICA/B⁺ MPs were significantly elevated in the ST-segment elevation myocardial infarction (STEMI) compared to the non-STEMI (NSTEMI) patients. Moreover, an independent association of MICA/B⁺ MPs with the occurrence of STEMI was also demonstrated (OR = 4.1; 95% CI = 1.5, 16.7). Conclusions: These results suggest that MICA/B⁺ MPs are associated with AMI and disease severity. They may act as mediators contributing to the pathological process of AMI. Alternatively, they are the results of various cell activations contributing to AMI.

Background: The imbalance of von Willebrand factor (vWF) and a disintegrin and metalloproteinase with a thrombospondin type 1 motif member 13 (ADAMTS13) has been associated with atherosclerosis progression. A high level of vWF which regulates thrombus formation is associated with diabetes mellitus (DM), and some ADAMTS13 and vWF polymorphisms have effects on their levels. Therefore, this study aimed to evaluate the associations of ADAMTS13 and vWF polymorphisms and their levels with DM and severity of coronary stenosis. Materials and Methods: Eighty-seven DM and 84 control individuals were recruited. vWF and ADAMTS13 activities as well as vWF antigen were measured by collagen-binding assay (CBA), residual-CBA, and in-house enzyme-linked immunosorbent assay, respectively. ADAMTS1 3 and vWF polymorphisms were determined by polymerase chain reaction-restriction fragment length polymorphism. Results: The E and G alleles and AA genotype of ADAMTS13 Q448E, rs2073932, and rs652600, respectively, were independently associated with DM (odds ratio [OR] [95% confidence interval (CI)] = 2.5 [1.1, 5.6], 2.3 [1.0, 5.2], and 4.7 [1.2, 18.6], respectively). Moreover, E allele and AA genotype of Q448E and rs652600 were also significantly associated with multi-vessel disease (OR [95% CI] = 2.2 [1.0, 4.8] and 3.2 [1.0, 10.0], respectively), while the E and G allele of Q448E and rs2073932 were associated with high Gensini score (OR [95% CI] = 2.3 [1.1, 4.9] and 2.3 [1.1, 5.1], respectively). Conclusion: Association of ADAMTS13 polymorphisms with DM, number of vessel stenosis, and Gensini score may indicate the possible contribution of ADAMTS13 polymorphisms to atherosclerosis progression and severity of coronary stenosis in DM.

Background: Increased arterial stiffness is a cardiovascular outcome of metabolic syndrome (MetS). The chromosome 9p21 locus has been identified as a major locus for risk of coronary artery disease (CAD). The single nucleotide polymorphism (SNP), rs1333049 on chromosome 9p21.3 has been strongly associated with CAD and myocardial infarction. Increased arterial stiffness could be the link between the 9p21 polymorphism and increased cardiovascular risk. Since the impact of a genetic polymorphism on arterial stiffness especially in Asian populations has not been well defined, we aimed to investigate the association of arterial stiffness with rs 1333049 variant on chromosome 9p21.3 in Thai subjects with and without MetS risk factors. Methods: A total of 208 Thai subjects, aged 35–75 years, 135 with and 73 without MetS, according to IDF and NCEP-ATPIII criteria, were included in this study. Aortic-femoral pulse wave velocity (afPWV), brachial-ankle pulse wave velocity (baPWV) and aortic ankle pulse wave velocity (aaPWV) were measured and used as markers of arterial stiffness. The chromosome 9p21.3 locus, represented by the rs 1333049 variant and blood biochemistry were evaluated. Results: Arterial stiffness was elevated in subjects with MetS when compared with nonMetS subjects. PWV, especially afPWV increased progressively with increasing number of MetS risk factors (r = 0.322, P <0.001). We also found that the frequency distribution of the rs1333049 genotypes is significantly associated with the afPWV (P <0.05). In multivariate analyses, there was an association between homozygous C allele and afPWV (Odds ratio (OR), 8.16; 95% confidence interval (CI), 1.91 to 34.90; P = 0.005), while the GC genotype was not related to afPWV (OR, 1.79; 95% CI, 0.84 to 3.77; P = 0.129) when compared with the GG genotype. Conclusions: Our findings demonstrate for the first time that arterial stiffness is associated with genetic polymorphism in 9p21 and metabolic risk factors in a Thai population.

Background: It has been known that hypertension is an independent risk factor for cardiovascular disease (CVD). CVD is the major cause of morbidity and mortality in developed and developing countries. Elevation of blood pressure (BP) increases the adverse effect for cardiovascular outcomes. Prevention of increased BP plays a crucial role in a reduction of those outcomes, leading to a decrease in mortality. Therefore, the purpose of this study was to investigate the effects of dietary black sesame meal on BP and oxidative stress in individuals with prehypertension. Methods: Twenty-two women and eight men (aged 49.8 ± 6.6 years) with prehypertension were randomly divided into two groups, 15 subjects per group. They ingested 2.52 g black sesame meal capsules or placebo capsules each day for 4 weeks. Blood samples were obtained after overnight fasting for measurement of plasma lipid, malondialdehyde (MDA) and vitamin E levels. Anthropometry, body composition and BP were measured before and after 4-week administration of black sesame meal or a placebo. Results: The results showed that 4-week administration of black sesame meal significantly decreased systolic BP (129.3 ± 6.8 vs. 121.0 ± 9.0 mmHg, P < 0.05) and MDA level (1.8 ± 0.6 vs. 1.2 ± 0.6 μmol/L, P < 0.05), and increased vitamin E level (29.4 ± 6.0 vs. 38.2 ± 7.8 μmol/L, P < 0.01). In the black sesame meal group, the change in SBP tended to be positively related to the change in MDA (R = 0.50, P = 0.05), while the change in DBP was negatively related to the change in vitamin E (R = -0.55, P < 0.05). There were no correlations between changes in BP and oxidative stress in the control group. Conclusions: These results suggest the possible antihypertensive effects of black sesame meal on improving antioxidant status and decreasing oxidant stress. These data may imply a beneficial effect of black sesame meal on prevention of CVD.