The Role of Adenosine and Its Degradation Enzymes - Adenosinedeaminase and Adenosinekinase in Pathogenesis of Vasovagal Syncope.

INTRODUCTION: Adenosine is mediator regulating physiological and pathological processes in organism. It probably plays a role in pathogenesis of vasovagal syncopes (VVS), too. Adenosine, its receptors and degradation enzymes- adenosinedeaminase (ADA) and adenosinekinase (ADK), are called the adenosinergic system. AIM: We aimed to evaluate serum levels of adenosine, ADA and ADK in patients with tilt-induced VVS and compare them to tlit-negative controls. Secondary aim was to compare the levels between the types of VVS and correlate them with hemodynamic parameters. SUBJECTS AND METHODS: Altogether 132 individuals were involved in this study (age 39,88±15,64 years, 51 males). All patients underwent head up tilt test (HUTT) in differential diagnosis of syncope. Blood sampling was performed before and after HUTT. Baseline and stimulated serum levels of adenosine, ADA and ADK were evaluated by ELISA method. RESULTS: HUTT was positive in 91 patients (HUTT+), 41 individuals were negative (HUTT-). HUTT+ patients had higher baseline and stimulated adenosine levels, when compared to HUTT- population. The rise in adenosine was higher in HUTT+ group. On the other hand, the increase of ADA was significantly higher in HUTT- subjects. Among HUTT+ group, the highest adenosine was found during vasodepressoric VVS. CONCLUSION: Adenosinergic system may play role in pathogenesis of VVS. Patients with VVS have higher adenosine levels, that may be caused by attenuated degradation. Adenosine seems to be involved predominantly in vasodepressoric type of VVS. Further research evaluating complex function of adenosinergic system in these patients is needed.

Adenosine, adenosine- deaminase and implantable recorder outcome in syncopal patients.

BACKGROUND: Adenosine test was proposed as a tool for identification of syncopal patients who benefit from pacemaker implantation. Aim of the study was to assess the relationship between adenosine levels, the outcome of adenosine test and results of implantable loop recorder (ILR) monitoring in patients with syncope. METHODS: In 29 patients (mean age 59 ± 11 years, 15 men, 14 women) with unexplained syncope ILR was implanted. In addition, adenosine test (intravenous injection of 20 mg adenosine bolus) and assays of plasmatic adenosine and adenosine-deaminase were performed. RESULTS: Adenosine test was positive in 15 patients and negative in 14 patients. Patients with positive adenosine test had lower adenosine levels compared to patients with negative test (8.86 ± 2.07 ng/ml vs. 15.18 ± 2.14 ng/ml, p = .04). No difference was observed in adenosine deaminase levels (16.35 ± 2.20 IU/l vs. 13.20 ± 2.48 IU/l, p = .40). There was a negative correlation between adenosine level and AVB duration during adenosine test (p = .04; R2  = 0.22). Patients with positive adenosine test had more frequent asystole during ILR monitoring than patients with negative test (9 pts vs. 1 pt, p = .005). Adenosine levels were lower in patients with asystolic syncope on ILR compared to vasodepressor syncope 8.20 ± 2.86 ng/ml versus 13.27 ± 7.26 ng/ml, p = .05). CONCLUSIONS: Patients with positive adenosine test have decreased production of endogenous adenosine compared to patients with negative adenosine test. Positivity of adenosine test and low adenosine level in the peripheral blood were associated with more frequent asystolic episodes during ILR monitoring.

Effects of continuous positive airway pressure on cardiovascular risk profile in patients with severe obstructive sleep apnea and metabolic syndrome.

BACKGROUND: The increased risk of atherosclerotic morbidity and mortality in patients with obstructive sleep apnea (OSA) has been linked to arterial hypertension, insulin resistance, systemic inflammation, and oxidative stress. We aimed to determine the effects of 8 weeks of therapy with continuous positive airway pressure (CPAP) on glucose and lipid profile, systemic inflammation, oxidative stress, and global cardiovascular disease (CVD) risk in patients with severe OSA and metabolic syndrome. METHODS: In 32 patients, serum cholesterol, triglycerides, high-density lipoprotein cholesterol, fibrinogen, apolipoprotein A-I, apolipoprotein B (ApoB), high-sensitivity C-reactive protein, interleukin-6, tumor necrosis factor (TNF)-alpha, leptin, malondialdehyde (MDA), and erythrocytic glutathione peroxidase (GPx) activity were measured at baseline and after 8 weeks of CPAP. The insulin resistance index (homeostasis model assessment [HOMA-IR]) was based on the homeostasis model assessment method, the CVD risk was calculated using the multivariable risk factor algorithm. RESULTS: In patients who used CPAP for > or = 4 h/night (n = 16), CPAP therapy reduced systolic BP and diastolic BP (p = 0.001 and p = 0.006, respectively), total cholesterol (p = 0.002), ApoB (p = 0.009), HOMA-IR (p = 0.031), MDA (p = 0.004), and TNF-alpha (p = 0.037), and increased erythrocytic GPx activity (p = 0.015), in association with reductions in the global CVD risk (from 18.8 +/- 9.8 to 13.9 +/- 9.7%, p = 0.001). No significant changes were seen in patients who used CPAP for < 4 h/night. Mask leak was the strongest predictor of compliance with CPAP therapy. CONCLUSIONS: In patients with severe OSA and metabolic syndrome, good compliance to CPAP may improve insulin sensitivity, reduce systemic inflammation and oxidative stress, and reduce the global CVD risk.