Concomitant measurements of serum annexin A5 levels and hematological indices as markers in recent and old myocardial infarction with low ejection fraction: A preliminary study.

BACKGROUND: Serum annexin A5 (anxA5) level is significantly increased in patients with acute coronary syndrome. Hematological indices are significantly increased in patients with ischemic heart disease. This study aimed to demonstrate the changes in the distribution of blood cells and the levels of anxA5 in patients presented with significant low ejection fraction ST-elevation acute myocardial infarction (STEMI) in comparison with corresponding patients with ischemic heart disease. METHODS: Patients with low ejection fraction presenting at Hospital of Diyala University of Iraq were enrolled. Electrocardiograph (ECG), echocardiograph, hematological indices, serum annexin V (anxV) levels and the determinants of the cardio-metabolic risk factors were performed. Based on clinical examination, ECG findings and laboratory tests, patients were divided into healthy subjects (n=20); patients with acute MI (n=40) and with chronic MI (n=12). RESULTS: Acute MI has significant high levels of serum triglyceride, uric acid and high mean value of red cell distribution width (RDW) compared with healthy subjects and chronic MI. Platelet distribution width (PDW) is significantly reduced in patients of acute MI and chronic MI compared with healthy subjects, whereas the plateletcrit (PCT) is significantly higher in acute MI compared with healthy subjects. There is an insignificant difference between the means of serum anxA5 levels of acute MI (35.6±7.2ng/ml) and chronic MI (32.4±8.9ng/ml), but significantly higher than the cutoff level of the healthy subjects (5ng/ml). CONCLUSIONS: Measurement of serum annexin level is a useful diagnostic marker of acute or chronic MI with low ejection fraction.

Endothelial microparticles reduce ICAM-1 expression in a microRNA-222-dependent mechanism.

Endothelial microparticles (EMP) are released from activated or apoptotic endothelial cells (ECs) and can be taken up by adjacent ECs, but their effect on vascular inflammation after engulfment is largely unknown. We sought to determine the role of EMP in EC inflammation. In vitro, EMP treatment significantly reduced tumour necrosis factor-α-induced endothelial intercellular adhesion molecule (ICAM)-1 expression on mRNA and protein level, whereas there was no effect on vascular cell adhesion molecule-1 expression. Reduced ICAM-1 expression after EMP treatment resulted in diminished monocyte adhesion in vitro. In vivo, systemic treatment of ApoE-/- mice with EMP significantly reduced murine endothelial ICAM-1 expression. To explore the underlying mechanisms, Taqman microRNA array was performed and microRNA (miR)-222 was identified as the strongest regulated miR between EMP and ECs. Following experiments demonstrated that miR-222 was transported into recipient ECs by EMP and functionally regulated expression of its target protein ICAM-1 in vitro and in vivo. After simulating diabetic conditions, EMP derived from glucose-treated ECs contained significantly lower amounts of miR-222 and showed reduced anti-inflammatory capacity in vitro and in vivo. Finally, circulating miR-222 level was diminished in patients with coronary artery disease (CAD) compared to patients without CAD. EMPs promote anti-inflammatory effects in vitro and in vivo by reducing endothelial ICAM-1 expression via the transfer of functional miR-222 into recipient cells. In pathological hyperglycaemic conditions, EMP-mediated miR-222-dependent anti-inflammatory effects are reduced.

Assessment of Serum Cystatin C Levels in Newly Diagnosed Acute Myocardial Infarction at the Onset and at the Time of Hospital Discharge.

BACKGROUND: Cystatin C (Cys-C) is a marker of renal damage. Higher serum levels of Cys-C were observed in cardiovascular disease. This study aimed to test the null hypothesis that Cys-C levels in newly diagnosed acute myocardial infarction (AMI) may remain high in the survival and the impact of the cardiometabolic risk factors is small. METHODS: Forty patients with AMI are enrolled in this study. The cardiometabolic factors including the anthropometric measurements, blood pressure and lipid profile were determined. The diagnosis of AMI is based on the electrocardiograph, cardiac enzymes and positive troponin-c (cTn) test. Quantitative determination of serum high sensitive C-reactive protein (hs-CRP) and Cys-C was carried out, at the time of admission and at the time of the discharge, using the enzyme-linked immunosorbent assay (ELISA) technique. RESULTS: Serum Cys-C levels significantly increased at the time of the admission (1,296 ± 431.8 ng/mL) and at the time of the discharge (1,244.6 ± 482 ng/mL) compared with the reference levels (0.7 ± 0.2 ng/mL) of the healthy subjects. Non-significant differences were found between Cys-C levels in respect to the presence or absence of the cardiometabolic risk factors at the times of admission and discharge. Significant decrease of Cys-C levels was found in patients who have negative cTn at the time of discharge compared with corresponding levels at the time of admission. CONCLUSIONS: We conclude that AMI patients have significant high serum levels of Cys-C at the time of admission and the levels significantly decreased in patients with negative cTn test within few days indicating an association between infarct size and the levels of Cys-C.