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Background: Coronary artery disease (CAD) develops as a result of atherosclerosis. Atherosclerosis is a condition that leads to clogged arteries and can be caused by a variety of factors. Several studies have shown that various factors contribute to the development and progression of CAD. The aim of this study was to investigate the serum levels of MBL-2, TNC and TAC in patients with CAD and the relationship between these biochemical parameters and the progression of CAD., Methods: In this study, 60 serum samples were obtained from CAD patients as the case group and 20 healthy serum samples as the control group. Serum levels of MBL-2 and TNC were measured by the ELISA method. Serum TAC level was determined by calorimetry (spectrophotometry). In addition, MDA serum level was measured by reaction with thiobarbituric acid (TBA)., Results: The mean age in the case and control groups was 58.4 ± 9.5 years and 85 ± 9.8 years, respectively. There was no significant difference in age, sex and family history in patients with CAD (p > 0.05), but there was a significant difference in blood pressure and smoking history (p > 0.05). Serum cholesterol, triglyceride, and LDL levels were significantly increased in the case group compared to the control group, while serum HDL-C levels were significantly decreased in the case group. Serum levels of MBL-2, TNC, and MDA were significantly increased in the case group compared to the control group. The serum level of TAC was significantly lower in the case group than in the control group., Conclusion: This study suggests that it is possible to diagnose patients with coronary artery disease (CAD) in the early stages of their disease and take preventive measures by measuring these parameters in serum. However, more research is needed before these serum parameters can be considered diagnostic biomarkers or therapeutic targets., (© 2021 The Authors. Journal of Clinical Laboratory Analysis published by Wiley Periodicals LLC.)

Myocardial injury following elective percutaneous coronary intervention (PCI) occurs in about one-third of patients and is associated with mortality. Platelet aggregation, thrombosis formation, and inflammation are the main causes of cardiac injury during PCI. Vitamin D plays a key role in the cardiovascular system by exerting antiplatelet, anticoagulant, and anti-inflammatory properties. There is no published study that investigated the effect of vitamin D in the prevention of cardiac injury following elective PCI. In a randomized clinical trial, 99 patients admitted for elective PCI were randomized into vitamin D (n = 52) and control (n = 47) groups. The intervention group received 300 000 IU vitamin D orally 12 hours before PCI. The cardiac biomarkers were checked at baseline, 8 and 24 hours after PCI. hs-CRP was also measured at baseline and after 24 hours. The increase in CK-MB was documented in 20 patients (42%) in the control group and 18 patients (34.6%) in the intervention group (P = .417). Furthermore, the increase in cTnI occurred in 4 patients (8%) and 2 patients (3.3%) in the control and intervention groups, respectively (P = .419). No significant changes were noted in the level of cardiac biomarkers. In the vitamin D group, the mean difference in CK-MB between 8 and 24 hours was significantly lower (P = .048). The mean difference in hs-CRP was significantly lower in the vitamin D group (P = .045). This study could not show a clear effect of vitamin D in the prevention of cardiac injury during elective PCI. Further outcome-based studies are needed to describe the role of vitamin D in the prevention of periprocedural myocardial injury., (© 2017, The American College of Clinical Pharmacology.)

Cell death following acute myocardial infarction (MI) is the hallmark pathology of cardiovascular disease, leading to considerable mortality and morbidity. Platelet and neutrophil activation and inflammatory cytokines, prominently TNF-α, play an important role in the development of cell death. Because pentoxifylline inhibits platelet and neutrophil activation and reduces TNF-α, this study was performed to assess the potential benefit of pentoxifylline in the reduction of myocardial injury following acute MI. In this randomized clinical trial, 98 patients with acute MI were randomly divided into 2 groups. The intervention group received an oral dose of 1200 mg of pentoxifylline immediately before thrombolytic therapy (TLT). All patients received the same standard protocol for treatment of MI. Cardiac enzymes were checked over 48 hours. ST resolution was measured over 90 minutes. Then all patients were followed up for a 1-month period to assess major adverse cardiac effects (MACEs). There were no significant differences in peak levels of CPK (P = .18) and CK-MB (P = .33) between the 2 groups, whereas peak level of troponin I was significantly lower in the pentoxifylline group (16.8 ± 10.4 vs 21.3 ± 11.6; P = .048). No significant change between the groups was observed in biomarkers levels, ST segment resolution, cardiac ejection fraction, and MACEs. The results showed that pentoxifylline significantly reduced the peak value of troponin I in patients with acute MI receiving TLT. No significant change was observed in the other studied parameters. Further outcome-based studies are needed to show the clinical relevance of differences between the groups in troponin peak., (© 2017, The American College of Clinical Pharmacology.)