Mesenchymal stem cells derived from epicardial adipose tissue reverse cardiac remodeling in a rabbit model of myocardial infarction.

OBJECTIVE: Myocardial infarction (MI) is one of the most important causes of death. MI-related tissue loss and cardiac remodeling may result in heart failure. Intramyocardial injection of mesenchymal stem cells derived from adipose tissues, in acute MI animal models, has shown promising regenerative capabilities. This study aimed to investigate the myocardial regenerative capacity of epicardial adipose tissue-derived mesenchymal stem cells (ADSCs) in a rabbit model of MI. MATERIALS AND METHODS: A rabbit model of MI was performed in three groups: a sham-operated group, a control group, and a treatment group. MI was induced by coronary artery ligation via thoracotomy in the first operation. Four weeks after the first operation, intramyocardial injections of phosphate-buffered saline (PBS; control group) or ADSCs (10×106 in 100 µL; treatment group) were performed in the peri-infarct zone. Four weeks after the second operation, rabbits were sacrificed for further analysis. RESULTS: A significant increase in ejection fraction (p<0.0001) was detected in the treatment group, along with a significant increase in vascular density (p<0.001) and a significant decrease in infarct size (p<0.05) compared to the control group. CONCLUSIONS: Epicardial adipose tissue is a rich source of mesenchymal stem cells, which can differentiate into cardiomyocytes, as well as having neoangiogenic properties. Due to its potential to ameliorate chronic ischemic changes in the heart, it may be preferable in cardiac regenerative cell therapies.

Paricalcitol counteracts the increased contrast induced nephropathy caused by renin-angiotensin-aldosterone system blockade therapy in a rat model.

OBJECTIVE: The effect of vitamin D and renin-angiotensin-aldosterone system blockade medications in pathophysiology of contrast induced nephropathy (CIN) is controversial. The effects of paricalcitol (active vitamin D analogue) and losartan treatments in an experimental model of CIN were investigated in this study. MATERIALS AND METHODS: Thirty-six male Wistar albino rats were examined in five treatment groups. Placebo group (Group A; n = 4) received no active medication; control group (Group B; n = 8) received only contrast media (CM); Group C (n = 8) received paricalcitol; Group D (n = 8) received losartan and Group E (n = 8) received paricalcitol plus losartan. CIN was induced by NG-nitro-L-arginine methyl ester and indomethacin before iohexol injection. Renal histopathological findings were categorized and renal immunohistochemical examinations by caspase-3 rabbit primary antibody were performed. RESULTS: Creatinine and cystatin C levels significantly increased in the treatment groups, compared to Group A. However, creatinine levels were not significantly increased in Groups C, D and E compared to Group B. Compared to Group B, a significant increase of cystatin C levels was observed in Group D (p < 0.01). In Group E, when paricalcitol treatment was added to losartan treatment, cystatin C levels were similar to Group B (p = 1.00). In histopathological and immunohistochemical examination frequency of Grade 2/3 tubular necrosis and renal caspase 3 activity scores were significantly higher in the losartan treatment group compared to the other treatment groups. The histopathological effects related to losartan treatment were found to be reversed when paricalcitol treatment was combined. CONCLUSIONS: Our findings suggest that paricalcitol treatment counteracts increased contrast induced nephropathy caused by losartan. These findings warrant further clinical studies to investigate the benefit of paricalcitol in CIN prophylaxis.

The relationship between antibeta 2 glycoprotein antibodies and SYNTAX score in patients undergoing coronary artery by-pass graft surgery.

OBJECTIVE: The SYNTAX Score was recently developed to characterize the coronary vasculature with respect to the number of lesion's location, complexity, and functional impact and it is a quantitative scoring system to assist with patient selection for optimal revascularization strategy between percutaneous coronary intervention (PCI) and coronary artery by-pass surgery (CABG). b2-glycoprotein I (b2GPI), a plasma protein that binds cardiolipin, acts as a modulator of platelet aggregation and coagulation. Antibodies to b2GPI may have a role in atherosclerosis by inducing endothelial cell activation. We investigated the relationship between anti beta 2 GPI and severity of coronary artery stenosis by calculating the SYNTAX Score among patients undergoing CABG surgery. PATIENTS AND METHODS: We prospectively investigate 612 patients who undergo elective coronary angiography between September 2012 and June 2013. Patients were evaluated for blood chemistry and anti-b2GPI IgA, IgM and IgG. Ninety seven patients with complete biochemical analysis including anti Beta 2 GPI antibodies and undergone CABG have been enrolled in this study. We divided patients in to 2 groups according to the SYNTAX scores. Group 1 included 48 patients with low SYNTAX scores (<23) and group 2 included 49 patients with intermediate and high SYNTAX scores (>23). RESULTS: There was significant correlation between elevated anti b2GPI IgG levels and higher SYNTAX score which indicate advanced and complex CAD. In this study, lesion complexity increased progressively with increasing anti-b2GPI-IgG type of antibody levels. According to this findings, anti-b2GPI-IgG is a strong predictor of higher SYNTAX score. CONCLUSIONS: In addition to the traditional risk factors for atherosclerosis, the proinflammatory and procoagulant activities of antiphospholipid antibodies appear to be important risk factors for atherosclerotic occlusive disease.