The antiangiogenic effects of levosimendan in a CAM assay.

BACKGROUND: There is a physiological balance between the stimulatory and inhibitory signals for blood vessel growth. In many symptomatic patients with peripheral artery disease, coronary artery disease, and ischemic chronic wounds, there is a pathological insufficiency of angiogenesis. Therefore, determining the angiogenic or antiangiogenic effects of molecules currently used in cardiovascular treatment is crucial. Although levosimendan is the most well studied calcium sensitizer in preclinical and clinical practice, to the best of our knowledge, there are no previous studies investigating its angiogenic or antiangiogenic effects. In the present study, we aimed to investigate the effects of levosimendan on angiogenesis. METHODS: The antiangiogenic efficacy of levosimendan was examined in vivo in the chick chorioallantoic membrane (CAM) model by using 20 fertilized eggs and drug solutions of 1 and 10 µmol/L concentrations. Decreases in the density of the capillaries were assessed and scored. RESULTS: Significant antiangiogenic effects were observed at 1 and 10 µmol/L concentrations of levosimendan. The antiangiogenic scores of levosimendan at 1 and 10 µmol/L concentrations were 0.6 and 1.10, respectively. The antiangiogenic score of bevacizumab, used as a positive control, was 0.95 at 1.0 µmol/L concentration. No significant difference was found between the antiangiogenic scores of levosimendan and bevacizumab (p=0.54). CONCLUSIONS: Our results indicate that levosimendan has antiangiogenic effects on the chorioallantoic membrane. However, these findings must be confirmed in future studies on humans.

[Investigation of Chlamydophila pneumoniae seropositivity and risk factors in patients with atherosclerotic vascular disease in Sivas, Turkey]. / Sivas Yöresinde Aterosklerotik Damar Hastaligi Olan Kisilerde Chlamydophila pneumoniae Seropozitifligi ve Risk Faktörleri ile Iliskisi.

The role of various microorganisms including Chlamydophila (formerly Chlamydia) pneumoniae, have been frequently investigated in the pathogenesis of atherosclerosis. In our study, the relationship between C.pneumoniae seropositivity and risk factors for atherosclerosis have been evaluated. A total of 90 atherosclerotic patients (71 of them were male; age range: 45-87 years; mean age: 65.3 ± 8.7 years) and 90 control subjects without coronary diseases (41 of them were male; age range: 42-84 years; mean age: 61.6 ± 9.6 years) were included in the study. Both groups were also evaluated for the presence of risk factors such as age, gender, smoking, hypertension, diabetes, obesity, dyslipidemia, familial history and the high levels of ferritin, cholesterol (total, HDL and LDL) and HS (high sensitive)-CRP. The presence of C.pneumoniae IgG, IgM and IgA antibodies were investigated by micro-immunofluorescence (MIF) and ELISA methods using commercial kits (Euroimmun, Germany). The total antibody seropositivity rate was found 100% (90/90) in patient group by both MIF and ELISA methods, while this rate in control group was 94% (85/90) by MIF and 92% (83/90) by ELISA. When MIF test results were taken into consideration (since it is accepted as the reference method for C.pneumoniae serology), IgG, IgM and IgA positivity rates in patient and control groups were found as 100% (90/90) and 89% (80/90); 70% (63/90) and 59% (53/90); 3% (3/90) and 2% (2/90), respectively. Statistically significant difference between patient and control groups was detected only for IgG positivity (p< 0.05) and for total antibody positivities (100% and 94%, respectively) (p< 0.05). The evaluation of the risk factors revealed that age, hypertension, dyslipidemia and HS-CRP levels exhibited statistically significant differences between patient and control groups (p< 0.05 for each parameter tested). Statistically significant relation was detected only between high HS-CRP levels and C.pneumoniae seropositivity (p< 0.05). It was concluded that in areas with high C.pneumoniae infection prevalence, early diagnosis and specific treatment of C.pneumoniae infections, may prevent establishment of chronic infection and eliminate a risk factor for the development of atherosclerosis.

Replacement of the Native Mitral Valve Due to Endocarditis Caused by Stenotrophomonas Maltophilia.

We report a case of a 59-year-old female patient with vegetative native mitral valve endocarditis caused by Stenotrophomonas maltophilia (SM). She had hemodialysis-dependent chronic renal failure, but no immunosuppressive disease. Echocardiography showed mobile vegetation on her native mitral valve. Right femoral artery embolectomy and mitral valve replacement were performed simultaneously. She awakened from anesthesia, but she passed away due to septic shock complications. To the best of our knowledge, this was the first case in whom native mitral valve endocarditis caused by SM was observed (despite of absence of any immunosuppressive event) and needed to undergo valve replacement.

Replacement of the native mitral valve due to endocarditis caused by stenotrophomonas maltophilia

Abstract We report a case of a 59-year-old female patient with vegetative native mitral valve endocarditis caused by Stenotrophomonas maltophilia (SM). She had hemodialysis-dependent chronic renal failure, but no immunosuppressive disease. Echocardiography showed mobile vegetation on her native mitral valve. Right femoral artery embolectomy and mitral valve replacement were performed simultaneously. She awakened from anesthesia, but she passed away due to septic shock complications. To the best of our knowledge, this was the first case in whom native mitral valve endocarditis caused by SM was observed (despite of absence of any immunosuppressive event) and needed to undergo valve replacement.

Comparison of the antiangiogenic effects of heparin sodium, enoxaparin sodium, and tinzaparin sodium by using chorioallantoic membrane assay.

Unfractionated heparin (UFH) and low molecular weight heparins have been used as anticoagulation agents in cardiovascular clinics for decades. However, these molecules also have potent antiangiogenic effects. Whereas, angiogenesis may be the most crucial determinant of the prognosis of cardiovascular diseases, and except some special situation, antiangiogenic effect is not desirable in the most of the cardiovascular disease. In this study, we aimed to compare the antiangiogenic potency of UFH, enoxaparin, and tinzaparin. The antiangiogenic efficacies of UFH, enoxaparin, and tinzaparin were examined in vivo by using the chick chorioallantoic membrane (CAM) model. Twenty fertilized eggs were used for each studied drug. Drug solutions were prepared in 10 and 1 IU/10 µl concentrations. Decreases in the density of the capillaries were assessed and scored. All three drugs showed antiangiogenic effects on the chick CAM at the 10 IU/10 µl concentration. However, the antiangiogenic score of the UFH was significantly higher than that of enoxaparin and tinzaparin at 1 and 10 IU/10 µl concentrations. UFH had stronger and antiangiogenic potential than enoxaparin and tinzaparin. However, tinzaparin showed dose-dependent antiangiogenic effects. We think that an anticoagulant molecule with a less and dose-dependent antiangiogenic effect, as in the case of tinzaparin, may be more desirable in case of cardiovascular disease related with insufficient angiogenesis.