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Introduction. Platelet-derived microparticles (PDMPs) measurement adds prognostic implication for ST-elevation acute myocardial infarction (STEMI). The long-term implication of PDMPs in STEMI needs to be corroborated. Methods. The research design was a cohort study. Subjects were STEMI patients and were enrolled consecutively. The PDMPs were defined as microparticles bearing CD41(+) and CD62P(+) markers detected with flow cytometry. The PDMPs were measured on hospital admission and 30 days after discharge. The outcomes were major adverse cardiac events (MACE), i.e., a composite of cardiac death, heart failure, cardiogenic shock, reinfarction, and resuscitated ventricular arrhythmia, occurring from hospitalization until 1 year after discharge. Results. We enrolled 101 subjects with STEMI. During hospitalization, 17 subjects (16.8%) developed MACE. The PDMPs were not different between subjects with MACE and those without (median (IQR): 3305.0/μL (2370.0–14690.5/μL) vs. 4452.0/μL (2024.3–14396.8/μL), p=0.874). Forty-five subjects had increased PDMPs in 30 days after discharge as compared with on-admission measurement. Subjects with increased PDMPs had significantly higher 30-day MACE as compared to subjects with decreased PDMPs 17 (37.8%) vs. 6 (16.7%, p=0.036). There was a trend toward higher MACE in subjects with increased PDMPs as compared to those with decreased PDMPs in 90 days after discharge (48.9% vs. 30.6%, p=0.095) and 1 year after discharge (48.9% vs. 36.1%, p=0.249). Conclusion. The PDMPs level was increased from the day of admission to 30 days after discharge in patients with STEMI. The persistent increase in the PDMPs level in 30 days after the STEMI event was associated with the 30-day postdischarge MACE and trended toward increased MACE during the 90-day and 1-year follow-up.

Objective: Chondroitin sulfate proteoglycans are the primary constituents of the macrophage glycosaminoglycan and extracellular microenvironment. To examine their potential role in atherogenesis, we investigated the biological importance of one of the chondroitin sulfate glycosaminoglycan biosynthesis gene, ChGn-2 (chondroitin sulfate N -acetylgalactosaminyltransferase-2), in macrophage foam cell formation. Approach and Results: ChGn-2-deficient mice showed decreased and shortened glycosaminoglycans. ChGn-2 −/− /LDLr −/− (low-density lipoprotein receptor) mice generated less atherosclerotic plaque after being fed with Western diet despite exhibiting a metabolic phenotype similar to that of the ChGn-2 +/+ /LDLr −/− littermates. We demonstrated that in macrophages, ChGn-2 expression was upregulated in the presence of oxLDL (oxidized LDL), and glycosaminoglycan was substantially increased. Foam cell formation was significantly altered by ChGn-2 in both mouse peritoneal macrophages and the RAW264.7 macrophage cell line. Mechanistically, ChGn-2 enhanced oxLDL binding on the cell surface, and as a consequence, CD36—an important macrophage membrane scavenger receptor—was differentially regulated. Conclusions: ChGn-2 alteration on macrophages conceivably influences LDL accumulation and subsequently accelerates plaque formation. These results collectively suggest that ChGn-2 is a novel therapeutic target amenable to clinical translation in the future.

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Background Previous studies proposed that chronic inflammation in diabetes has a role in abnormal collagen production and elastin degradation, which promotes arterial stiffness. Monocyte-to-High Density Lipoprotein cholesterol ratio (MHR) is a simple measurement associated with inflammation and oxidative stress. However, little is known about the relationship of MHR with arterial stiffness. This study aimed to determine the association of MHR with arterial stiffness in patients with diabetes. Methods A total of 81 patients with type 2 diabetes mellitus were enrolled in a cross-sectional study. Arterial stiffness factor in this study was Cardio Ankle Vascular Index (CAVI). We analyzed complete blood count and lipid profile in all participants, then performed statistical analysis to determine the relationship between MHR and CAVI. Receiver operating characteristic (ROC) analysis was used to estimate the cut-off values of MHR to predict CAVI ≥ 9. Results Median of MHR in this study was 11.91 with the mean of CAVI was 8.13 ± 0.93. Spearman correlation analysis revealed a significant positive correlation between MHR and CAVI (ρ = 0.239, p = 0.031). Multivariate analysis showed the independent association of MHR to arterial stiffness (β = 0.361, 95% CI 0.023–0.093) and to CAVI ≥ 9 (OR 1.181, 95% CI 1.047–1.332). The cut-off values of MHR for predicting CAVI ≥ 9 were identified as ≥ 13 (OR 3.289, 95% CI 1.036–10.441). Conclusion MHR is associated with CAVI in patients with diabetes, irrespective of various potential confounders.

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BACKGROUND: Platelet-derived microparticles (PDMPs) and low-density lipoprotein (LDL) cholesterol are contributing factors to acute myocardial infarction (AMI). However, the association between LDL cholesterol and PDMPs in AMI has not fully discovered. This study assessed the correlation between these two parameters in patients diagnosed with AMI.METHODS: This was an observational cross-sectional study involving 95 subjects with AMI. The blood measurement of PDMPs counts and LDL cholesterol levels were conducted concomitantly within 24 hours of admission. PDMPs count was analyzed by flow-cytometry method, meanwhile the LDL cholesterol was measured with enzymatic and colorimetric methods. For further analysis, subjects were further divided into LDL cholesterol level ≥130 mg/dL and <130 mg/dL. A statistical test was conducted for a correlative and comparative analyses.RESULTS: A correlative analysis to assess the association between PDMPs counts and LDL cholesterol level depicted a low but significant positive correlation (r=0.231, p=0.024). Furthermore, mean PDMPs counts was significantly higher in subjects with LDL cholesterol level ≥130 mg/dL compared to LDL cholesterol level <130 mg/dL (12,499.59 (95% CI: 8,507.44-16,491.74) counts/μL vs. 9,267.23 (95% CI: 4,445.45-14,089.01) counts/μL; p=0.039).CONCLUSION: There was a significant correlation between PDMPs counts and LDL cholesterol levels in AMI. A significantly increased PDMPs counts were found in subjects with LDL cholesterol level ≥130 mg/dL. Therefore, it is recommended to measure PDMPs in patients with high LDL cholesterol levels as both might be significant AMI biomarkers.KEYWORDS: acute myocardial infarction, LDL-cholesterol, platelet microparticles, platelet activation