In patients with stable coronary artery disease (CAD), secretory phospholipase A2 (sPLA2) is commonly increased and acts as a good prognosticator for the future cardiovascular events.1,2 Even a single test of plasma sPLA2 activity in those with acute coronary syndromes (ACS) would indicate an important scientific information regarding prediction for the next cardiovascular events.3 Phospholipase A2 enzymes hydrolyze phospholipids at the sn-2 position to produce lysophospholipids and fatty acids. 4 This enzyme produces isoprostanes, a prostaglandin-like compound formed in vivo from the free radical-catalyzed peroxidation of essential fatty acids, which has strong mitogenic activity. It induces thrombocyte aggregation and vasoconstriction 5 and possibly stimulates acute inflammatory response. In the future, a promising inhibitor of this enzyme activity would be an evolving new therapy in atherosclerosis. Serum amyloid-A (SAA) is a family of proteins that form a major component of the acute-phase inflammatory Keywords ► acute coronary syndromes ► secretory phospholipase A2 ► myeloperoxidase ► serum amyloid-A ► coronary heart disease ► case-control study ► odds ratio AbstractIn coronary heart disease (CHD), levels of secretory phospholipase A2 (sPLA2) are commonly increased. Serum amyloid-A (SAA) is increased in acute coronary syndromes (ACS) as well. It is needed to verify the hypotheses that sPLA2 is associated with the odds of ACS through elevation of SAA. We conducted a case-control study with 57 male patients with ACS and 30 controls matched by gender category. Levels of sPLA2, SAA, and myeloperoxidase (MPO) were measured by immunoreactive assay on the basis of a double-antibody sandwich technique. Levels of sPLA2, MPO, and SAA were significantly higher in patients than those in controls (11,359.0 AE 10,372.4 pg/mL vs. 1,320.5 AE 654.5 pg/mL, p ¼ 0.00; 438.6 AE 310.7 ng/mL vs. 271.1 AE 176.8 ng/mL, p ¼ 0.01; 10,995.2 AE 2,842.6 ng/mL vs. 3,861.7 AE 3,173.5 ng/mL, p ¼ 0.00). There were significant correlations between age, visceral obesity, MPO, sPLA2, and SAA (r ¼ 0.43; p ¼ 0.00; r ¼ 0.30; p ¼ 0.00; r ¼ 0.28; p ¼ 0.00 and r ¼ 0.53; p ¼ 0.00). On multivariate logistic regression analyses, there were significant and independent associations between sPLA2 and SAA with odds of ACS [OR (95% CI) ¼ 14.2 (2.1 to 98.6), p ¼ 0.00; OR (95% CI) ¼ 44.9 (6.9 to 328.4), p ¼ 0.00]. Our findings suggest that sPLA2 may be associated with the odds of ACS compared with controls through increased inflammation, represented by elevated SAA.
Obesitas saat ini telah menjadi masalah kesehatan di dunia karena merupakan salah satu faktor bagi timbulnya penyakit seperti dislipidemia, stroke, penyakit jantung koroner dan lain-lain. Salah satu prediktor yang spesifik untuk menilai risiko terjadinya Penyakit Jantung Koroner (PJK) adalah dengan mengukur Indeks Aterogenik Plasma (IAP). IAP dihitung dengan menggunakan rumus Log(TG/HDL). Penelitian ini bertujuan untuk mengetahui hubungan antara obesitas dengan profil High Density Lipoprotein (HDL), trigliserida (TG) dan IAP serta melihat risiko terjadinya PJK berdasarkan Indeks Aterogenik Plasma. Penelitian ini merupakan penelitian observasional dengan desain cross sectional. Subjek penelitian adalah wanita dewasa muda yang obes dan non obes dengan teknik pengambilan subjek menggunakan teknik purposive sampling. Hasil penelitian menunjukkan adanya hubungan antara lingkar perut dengan kadar TG, HDL dan IAP (p<0,05). Pada subjek obes terjadi peningkatan kadar TG, penurunan kadar HDL dan peningkatan nilai IAP. Dari hasil penelitian ini dapat disimpulkan bahwa berdasarkan nilai IAP subjek obes memiliki risiko PJK 4,472 kali lebih besar dibandingkan dengan subjek non obes. Kata Kunci : obesitas, trigliserida, high density lipoprotein, indeks aterogenik plasma ABSTRACTObesity is a health problem in the world because it can be a risk factor for other diseases such as dyslipidemia, stroke, coronary heart disease (CHD), and others. One of the specific CHD risk predictors is the Atherogenic Index of Plasma (AIP). AIP is calculated by using Log(TG/HDL). The purpose of this research is to investigate the relationship between obesity and HDL profile, TG and AIP, as well as to see the chance of having CHD based on AIP. This research was conducted using a descriptive observational method with a cross-sectional design. The subject of this research is the young women who are obese and not obese. The data collection method is a purposive sampling method. The result of this research showed that there is a relationship between abdominal circumference and triglycerides, HDL and AIP (p<0.05). Obese subjects have higher triglycerides, a decrease of HDL and an increase of AIP. From this result, it concludes that based on AIP, obese subjects tend to have CHD 4.472 times higher than non-obese subjects.
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BACKGROUND: Inflammation is a central feature of the atherosclerotic process particularly in obesity. hsCRP, a marker of inflammation, may be directly involved in all phases of atheroslerosis by complement activation, apoptosis, vascular cell activation, monocyte recruitment, lipid accumulation and thrombosis. Inflammation has a causal relationship with cysteine proteases including cathepsin S. Therefore, cathepsin S is considered as a molecular link between obesity and atherosclerosis. An imbalance between elastolytic cysteine proteases, cathepsin S and its inhibitor, cystatin C, is involved in the pathogenesis of atherosclerosis. Some studies have shown that increased circulating levels of cathepsin S, hsCRP and cystatin C in inflammatory conditions contribute to atherosclerosis. This study was conducted to investigate the associations between ox-LDL and cathepsin S, and cystatin C and hsCRP in men with central obesity.METHODS: This was a cross-sectional study involving 71 male subjects with central obesity (waist circumference ≥90 cm), with no renal dysfunction, aged 30-60 years.RESULTS: Cathepsin S did not have a significant correlation with ox-LDL (r=0.158, p=0.096). ox-LDL had positive correlation with cystatin C (r=0.156; p=0.029) and hsCRP (r=0.204; p=0.045), and cathepsin S/cystatin C ratios (r=0.360; p=0.024) at level >91 U/L (median ox-LDL).CONCLUSIONS: There were associations between ox-LDL and cystatin C, hsCRP and cathepsin S/cystatin C ratios in men with central obesity.KEYWORDS: obesity, inflammation, atherosclerosis, hsCRP, cystatin C, cathepsin S, ox-LDL
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