Biomedical subjects

Serdar Aksoyek

Publications and source records attributed to Serdar Aksoyek.

6 recordsLinked to original sources

PubMed2006

Plasma soluble osteopontin concentrations are increased in patients with rheumatic mitral stenosis and associated with the severity of mitral valve calcium.

Although the severity of valvular calcification is an important prognostic indicator, the cellular mechanisms of the calcification process are unknown. Osteopontin modulates inflammation and biomineralization, and increased osteopontin expression has been demonstrated in calcified degenerative or rheumatic cardiac valves. The present study evaluated soluble plasma osteopontin in 32 patients with echocardiographically determined rheumatic mitral stenosis and compared the results to those of a control group of 22 healthy patients. Patients were evaluated with routine echocardiographic techniques, Wilkins scoring, and 2-dimensional echocardiographic calcium scoring. Patients with rheumatic involvement other than in the mitral valve were excluded. Plasma osteopontin and high-sensitivity C-reactive protein levels in patients with mitral stenosis were significantly higher those of the control group (p = 0.006 and p = 0.0001, respectively). A significant correlation was found between plasma osteopontin levels and the severity of mitral valve calcification (p = 0.003) and also between high-sensitivity C-reactive protein levels and Wilkins score (p = 0.009). There was a stepwise and statistically significant increase in soluble plasma osteopontin levels in association with the severity of mitral valve calcification. In conclusion, increased osteopontin levels were correlated with the severity of mitral valve calcification in patients with rheumatic mitral stenosis, suggesting an important role of osteopontin in the modulation of valvular calcification. Elevated levels of high-sensitivity C-reactive protein concentrations suggest the presence of ongoing inflammation in those patients.

Adult↗

PubMed2006

Simvastatin treatment improves endothelial function and increases fibrinolysis in patients with hypercholestrolemia.

OBJECTIVES: Statins reduce cardiovascular events by cholesterol-lowering as well as nonlipid-related actions. Thrombin activatable fibrinolysis inhibitor (TAFI) is a recently identified independent risk factor of thrombosis. Endothelial dysfunction is also a strong predictor of cardiovascular events. The aim of this study was to assess the effects of simvastatin treatment on circulating TAFI concentrations and endothelial function in patients with hypercholesterolemia. METHODS: Thirty-five patients (19 female, mean age 48 +/- 7 years) with hyperlipidemia were recruited into the study. Simvastatin was administered, 40 mg daily, for eight weeks to all subjects. Study subjects did not receive any medication except for lipid-lowering therapy during the follow-up period. Endothelial function was evaluated by flow-mediated dilation (FMD) from the brachial artery of the patients. Plasma lipid parameters, TAFI levels and endothelial function were measured before and after simvastatin treatment. RESULTS: Treatment with simvastatin showed a significant decrement in plasma total cholesterol, LDL cholesterol and triglyceride levels (p<0.05). Plasma TAFI levels were also significantly decreased after simvastatin treatment [median 17.0 (range 0.4-93.7) mcg/mL versus median 6.9 (range 0.8-63.0) mcg/mL, p<0.001]. Mean FMD was measured 7.7 +/- 2.5% at baseline and significantly improved after treatment (13.0 +/- 1.4%) (p=0.001). CONCLUSION: Our findings of decreased TAFI levels may reflect the beneficial effect of simvastatin treatment on fibrinolysis, and improved endothelial function may suggest the improved future cardiovascular events in hyperlipidemic patients.

Anticholesteremic Agents↗

PubMed2005

Immediate effects of fluvastain on circulating soluble endothelial protein C and free tissue factor pathway inhibitor in acute coronary syndromes.

BACKGROUND: Statins promptly lower rates of adverse cardiovascular events in patients with acute coronary syndromes (ACS). These therapeutic properties may be mediated by the effects of statins on key hemostatic factors. This study examined the immediate effects of fluvastatin on plasma free tissue factor pathway inhibitor (fTFPI) and soluble endothelial protein C receptor (sEPCR) concentrations in patients with unstable angina or non-ST segment elevation myocardial infarction. METHODS: We studied 57 patients consecutively admitted to our emergency department and randomly assigned to placebo (n = 29) versus fluvastatin, 80 mg, p.o. (n = 28). All patients were treated with aspirin and metoprolol p.o., nitroglycerin i.v., and subcutaneous enoxaparin. Venous blood was sampled as soon as possible upon admission, before and 6 h after administration of study drug and standard anti-ischemic therapy. RESULTS: Mean sEPCR concentrations decreased significantly in patients treated with fluvastatin (-8.1 +/- 6.7% from baseline) and was unchanged in the placebo group (-2.3 +/- 14.4%, P = 0.007 vs. fluvastatin). Though fTFPI increased significantly after the administration of both fluvastatin and placebo, the mean increase after fluvastatin (450+/-436%) was significantly greater than after placebo (155+/-141%, P = 0.001). CONCLUSIONS: Treatment with fluvastatin significantly modified key hemostatic factors toward an antithrombotic effect within 6 h. These properties may, in part, explain the early salutary effects of fluvastatin in patients with ACS.

Acute Disease↗

PubMed2005

Increased soluble glycoprotein V concentration during the acute onset of unstable angina pectoris in association with chronic cigarette smoking.

Platelet hyperactivity is important in the pathobiology of acute coronary syndromes. Glycoprotein V (GPV) is an integral membrane protein of platelets in the function of the GPIb-V-IX receptor for vWf/shear-dependent platelet adhesion in arteries. Soluble GPV is a novel marker of platelet activation. The aim of this study is to assess circulating soluble GPV levels in unstable angina pectoris (UA). Twenty-one patients (15 men, six women, aged 52+/-7 years) with UA pectoris were studied. The inclusion criteria were angina at rest lasting >20 min during the preceding 6 h, with transient ST segment depression and/or T wave inversion and no evidence of myocardial infarction detected with the use of cardiac troponin-T. Coronary artery stenosis was angiographically confirmed in all patients. Twenty age- and sex-matched healthy adults (14 men, six women, aged 48+/-7 years) served as controls. There were no significant differences among the studied groups with respect to age, sex, obesity, smoking, total cholesterol, LDL-cholesterol, HDL-cholesterol, triglyceride and platelet counts. Plasma-soluble GPV concentrations were higher in the UA patient group (126+/-46 ng/ml) than those in the healthy controls (82+/-15 ng/ml) (P=0.001). There was a significant correlation only between plasma-soluble GPV levels and smoking (r=0.526, P=0.0001). Smoker UA patients had higher levels of soluble GPV than the non-smoker patients (139+/-40 vs. 113+/-50 ng/ml, respectively, P=0.02). However, soluble GPV levels were similar in smoker and non-smoker healthy controls (P=0.2). It is concluded that soluble GPV concentrations are significantly increased during the acute clinical course of unstable angina pectoris, indicating that soluble GPV may be useful marker of platelet activation in those patients. The level of the molecule is significantly affected from smoking in those patients.

Acute Disease↗

PubMed2005

Melatonin levels decrease in type 2 diabetic patients with cardiac autonomic neuropathy.

The present study has been designed to determine melatonin levels in type 2 diabetic patients and test the relationship between the autonomic nervous system and melatonin dynamics. Thirty-six type 2 diabetic patients and 13 age-matched healthy subjects were recruited for the study. Circadian rhythm of melatonin secretion was assessed by measuring serum melatonin concentrations between 02:00-04:00 and 16:00-18:00 hr. Melatonin dynamics were re-evaluated with respect to autonomic nervous system in diabetic patients with autonomic neuropathy who were diagnosed by the cardiovascular reflex tests, heart rate variability (HRV), and 24-hr blood pressure monitoring. Nocturnal melatonin levels and the nocturnal melatonin surge were low in the diabetic group (P = 0.027 and 0.008 respectively). Patients with autonomic neuropathy revealed decreased melatonin levels both at night and during day when compared with healthy controls (P < 0.001 and 0.004 respectively) while the melatonin dynamics were similar to controls in patients without autonomic neuropathy. Nocturnal melatonin level was positively correlated with nocturnal high and low frequency components of HRV (P = 0.005 and 0.011 respectively) and systolic and diastolic blood pressures at night (P = 0.002 and 0.004 respectively) in patients with autonomic neuropathy. We found a negative correlation between nocturnal melatonin levels and the degree of systolic blood pressure decrease at night (r = -0.478, P = 0.045). As a conclusion this study has shown that circadian rhythm of melatonin secretion is blunted in type 2 diabetic patients and there is a complex relationship between various components of autonomic nervous system and melatonin secretion at night. Among the patients with autonomic neuropathy those with more preserved HRV and the systolic nondippers (<10% reduction in blood pressure during the night relative to daytime values) have more pronounced melatonin surge at night.

Autonomic Nervous System Diseases↗

PubMedDate not supplied

Patients with paroxysmal atrial fibrillation but not paroxysmal supraventricular tachycardia display evidence of platelet activation during arrhythmia.

It is well known that chronic atrial fibrillation (CAF) and paroxysmal atrial fibrillation (PAF) are associated with hypercoagulable state. However, pathological hemostatic changes during the paroxysmal supraventricular tachycardia (PSVT) have not yet been elucidated. To determine platelet activity in patients with PSVT, PAF and CAF, we examined the levels of beta-thromboglobulin (BTG) and platelet factor 4 (PF4) during tachyarrhythmia attacks. We measured the levels of BTG and PF4, as an index of platelet activation in 15 patients with PAF (9 men, mean age 45+/-11), and 14 patients with PSVT (8 men, mean age 40+/-10). Levels were compared to 22 age and sex matched healthy controls in sinus rhythm and with 25 patients with CAF (16 men, mean age 51+/-12). Blood samples were taken during arrhythmia and 24 hours after conversion to sinus rhythm. Patients taking medications or have clinical conditions that may affect the BTG and PF4 levels were excluded. In patients with PAF, BTG and PF4 levels were significantly higher than in controls (p<0.009, and p=0.002, respectively), and in patients with PSVT (p<0.004, and p=0.009, respectively), however, BTG and PF4 levels were significantly lower than CAF patients (p=0.002, and p=0.02, respectively). Moreover, BTG and PF4 levels were significantly decreased 24 hours after conversion to sinus rhythm (p<0.0001), and p=0.004, respectively). Although BTG and PF4 levels in patients with PSVT were significantly lower than in patients with PAF (p=0.04, and p=0.009, respectively) and CAF (p=0.0001, and p=0.0001, respectively), BTG and PF4 levels were similar to controls and did not change significantly after recovery to sinus rhythm (p=NS for all). These results indicate that there was no platelet activation in patients with PSVT during tachyarrhythmia but significantly increased platelet activity in PAF and CAF patients. There was a significant decrement of the platelet activity to a level of control subjects twenty-four hours after cardioversion of PAF.

Adult↗