Serum and saliva sialic acid in periodontitis patients with and without cardiovascular disease.

Serum total sialic acid (sTSA) has recently been shown to be a cardiovascular risk factor. However, there is little information about the role of sTSA and TSA in saliva in periodontitis, a chronic and inflammatory disease known to be a risk factor for cardiovascular disease (CVD). We aimed to investigate the changes in sTSA and TSA levels in saliva in patients having both periodontitis and CVD versus periodontitis patients without diagnosed CVD. The study group consisted of 26 patients with proven periodontitis and 26 controls with no diagnosed systemic disease but periodontitis. sTSA and saliva TSA levels were determined by the thiobarbituric acid method, and C-reactive protein (CRP) was evaluated by the nephelometric method. The severity of periodontitis has been determined by the community periodontal index of treatment needs (CPITN). TSA in blood and saliva and CRP levels in blood were significantly increased in CVD patients compared with the control group. CPITN ranged from 2 to 4 in both groups. Significant and positive correlations were found between sTSA and saliva SA levels in patients and controls and between tooth loss and TSA both in blood and saliva. Therefore, TSA in saliva may be a useful marker similar to sTSA in CVD patients.

The relation between plasma tissue factor and oxidized LDL levels in acute coronary syndromes.

AIM: Tissue factor (TF) is a low-molecular-weight glycoprotein responsible for the initiation of the coagulation cascade. The relation between oxidized low-density lipoprotein (Ox-LDL), that has been shown to be involved in atherogenesis, and TF has not been evaluated before in circulating plasma. The aim of this study was to determine plasma levels of TF and Ox-LDL in acute coronary syndrome (ACS) and stable coronary artery disease (SCAD). METHODS: The study group consisted of 41 patients with ACS and 26 patients with SCAD. Among the ACS patients, 12 were diagnosed with unstable angina pectoris (UAP) and 29 were diagnosed with acute myocardial infarction (AMI). The control group consisted of 30 healthy volunteers. TF and Ox-LDL levels were evaluated by ELISA kits. RESULTS: Ox-LDL levels were significantly higher in UAP and AMI patients compared with the control (p < 0.001) and SCAD (p < 0.01 and p < 0.001, respectively) groups. TF levels were significantly higher in the UAP, AMI and SCAD groups compared with the control group (p < 0.001, p < 0.001 and p < 0.01, respectively). In the AMI group a significant increase was observed in TF levels when compared with the SCAD group (p < 0.01). Plasma Ox-LDL levels were significantly and positively correlated with TF levels in the UAP and AMI groups (p < 0.05, r = 702, and p < 0.0001, r = 0.679, respectively). CONCLUSION: The potential link between Ox-LDL and TF in circulating blood in ACS may strengthen the evidence supporting a relationship between oxidant stress, lipids and thrombosis and consequently may contribute to understanding the mechanism through which Ox-LDL and TF may mediate the pathogenesis of CAD.

Assessment of valvulopathy in Parkinson's disease patients on pergolide and/or cabergoline.

OBJECTIVE: To assess the effect of ergot derivatives on cardiac valves in patients with Parkinson's disease (PD). MATERIALS AND METHODS: Echocardiography was performed on 46 PD patients who used either pergolide or cabergoline (MonoPD) or both (MixPD) for a minimum of 1 year and 49 age-matched healthy controls. Valvular regurgitation was graded as mild, moderate and severe. MonoPD and MixPD groups were compared with regard to demographic features, drug profile and valvulopathy. RESULTS: The PD group had a mean age of 63 years, agonist duration of 3.8 years and agonist equivalent dose of 3.5mg/day. Moderate regurgitation in all three valves was significantly more common in the PD group than the controls. Severe valvular regurgitation was not observed in either group, with the exception of one PD patient. The frequency of valvulopathy and doses of agonists did not differ between MixPD and MonoPD groups. CONCLUSION: PD patients on dopamine ergot agonists are prone to moderate valvular regurgitation more than age-matched controls. However, the frequency of valvulopathy was similar in patients who used either one or more agonists.

Galectin-3 and plasma cytokines in patients with acute myocardial infarction.

OBJECTIVE: To investigate the concentrations of plasma cytokines and Galectin-3 (Gal-3) as inflammatory markers in patients with acute myocardial infarction (AMI). METHODS: The study population consisted of 29 patients with AMI and 29 healthy control subjects. We measured Gal-3, tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6) levels in plasma using enzyme-linked immunosorbent assays (ELISAs). We measured levels of C-reactive protein (CRP) via the nephelometric method. RESULTS: Patients with AMI showed significantly higher plasma Gal-3, TNF-α, and IL-6 levels compared with controls. Gal-3 levels were positively and significantly correlated with plasma IL-6, TNF-α, and CRP levels in the control and patient groups. CONCLUSION: Our findings suggest that Gal-3 can be a new circulating biomarker of inflammation associated with AMI.

Apelin in ST segment elevation and non-ST segment elevation acute coronary syndromes: a novel finding.

BACKGROUND: Apelin is a novel endogenous peptide with inotropic and vasodilatory properties. AIM: To investigate the role of apelin in the prognosis of acute coronary syndromes (ACS) and to assess the relationship between apelin and other diagnostic and prognostic markers. METHODS: Seventy-six patients with ACS (mean age 62.1 ± 10 years) were evaluated in terms of their plasma apelin-36 concentrations, ejection fraction (EF), high sensitivity C-reactive protein (hsCRP), creatine kinase (CK), CK-MB and troponin I levels. The study group consisted of 35 ST elevation myocardial infarction (STEMI) and 41 non-ST elevation (NSTE) ACS patients. Patients were followed up for one year for cardiovascular outcomes. RESULTS: There was no significant relationship between apelin and TIMI, GRACE, GENSINI scores, hsCRP and EF in STEMI and NSTE-ACS groups (p > 0.05). Apelin showed positive correlations with CK, CK-MB and troponin I in patients with NSTE-ACS, but a negative correlation in patients with STEMI (p < 0.05). There were no statistically significant differences between patients reaching the composite end point at one year with regard to apelin levels. CONCLUSIONS: Apelin was positively correlated with cardiac biomarkers in patients with NSTE-ACS but negatively correlated in patients with STEMI. In STEMI, generally larger amounts of myocardial cells are subjected to infarction compared to NSTE-ACS, which may explain why apelin levels decrease with increasing CK, CK-MB and troponin levels in STEMI patients.

Short-term effects of rilmenidine on left ventricular hypertrophy and systolic and diastolic function in patients with essential hypertension: comparison with an angiotensin converting enzyme inhibitor and a calcium antagonist.

The short-term (three months) effects of rilmenidine on systemic hypertension induced left ventricular hypertrophy (LVH) and left ventricular systolic and diastolic functions in comparison with those of perindopril and nifedipine-slow release (SR) formulation were studied. The short-term effects of rilmenidine on biochemical parameters and lipid profiles were evaluated. Sixty patients (39 men, 21 women) with a mean age of 59 +/- 14 years and with mild to moderate systemic arterial hypertension were enrolled in three groups. The first group received 1 mg/day of rilmenidine, the second group 4 mg/day of perindopril, and the third group 20 mg/day of nifedipine SR. All drugs induced a similar decrease in systolic and diastolic blood pressure (BP) values. Left ventricular mass (LVM) and LVM index decreased equally in all groups associated with a significant increase in the E/A ratio. The ratio between the reduction in LVM and decrease in mean arterial pressure (LVM/mmHg) was higher in groups 1 and 2. Negative correlations between LVM and LVMI. E/A, and the dv/dt ratio were obtained. Rilmenidine did not change the blood chemistry and lipid profile values. Despite its neutral effect on lipid profile and biochemical parameters. rilmenidine is as effective as perindopril and nifedipine in controlling hypertension and decreasing left ventricular hypertrophy.

Interleukin-8, nitric oxide and glutathione status in proliferative vitreoretinopathy and proliferative diabetic retinopathy.

PURPOSE: To evaluate interleukin-8 (IL-8), nitric oxide (NO) and glutathione (GSH) profiles in vitreous humor and blood samples in patients with proliferative diabetic retinopathy (PDR) and in patients with proliferative vitreoretinopathy (PVR) and to compare the levels with those of controls. PATIENTS AND METHODS: NO concentrations were determined by using the Greiss reaction in plasma and vitreous humor samples. GSH levels were determined in both blood and vitreous humor samples, using DTNB, a disulfide chromogen. Vitreous IL-8 were assayed by ELISA. Twenty-three patients with PDR, 18 patients with PVR and 21 cadavers as the control group were included in the study. RESULTS: Plasma and vitreous NO levels were found to be 25.6 +/- 2.1 and 36.9 +/- 3.0 micromol/l in patients with PDR, 27.0 +/- 4.7 and 34.3 +/- 2.9 micromol/l in patients with PVR and 17.4 +/- 2.7 and 15.9 +/- 1.4 micromol/l in controls, respectively. Vitreous humor and plasma NO levels did not show any statistically significant difference between PDR and PVR groups. However, the values for vitreous in both groups were significantly higher than those of controls (p < 0.0001). Although IL-8 levels in vitreous samples of patients with PDR were not significantly different (79.6 +/- 9.7 pg/ml) from those of patients with PVR (42.2 +/- 7.3 pg/ml) (p = 0.06), the levels in both groups were significantly higher than those of controls (19.0 +/- 3.9 pg/ml) (p < 0.0001 and p < 0.05, respectively). Blood and vitreous GSH levels were found to be 5.3 +/- 0.4 micromol/g. Hb and 0.58 +/- 0.16 micromol/l in patients with PDR and 8.4 +/- 0.5 micromol/g. Hb and 15.7 +/- 2.2 micromol/l in patients with PVR and 12.0 +/- 1.1 micromol/g. Hb and 0.26 +/- 0.03 mmol/l in controls, respectively. Vitreous and blood GSH levels were significantly lower in patients with PDR compared to those with PVR (p < 0.0001 for both). CONCLUSION: Elevated levels of vitreous and plasma NO and vitreous IL-8 in PDR and PVR implicate a role for these parameters in the proliferation in these ocular disorders. GSH concentrations both in vitreous and blood samples of the PVR and PDR patients were much less than those observed in the control group. Lower GSH concentrations detected in PDR in comparison with those in PVR in vitreous humor and to a lesser degree in blood may play an important role in pathogenesis of new retinal vessel formation in patients with PDR. This also suggests that oxidative stress may be involved in the pathogenesis of PVR and particularly that of PDR.