The association between apelin-12 levels and paroxysmal supraventricular tachycardia.

AIMS: Our aim was to investigate the apelin-12 levels in patients with atrioventricular tachyarrhythmias and compare with those in patients with lone atrial fibrillation. METHODS: Forty four patients with supraventricular tachycardia as atrial fibrillation, 44 patients with paroxysmal supraventricular tachycardia (P-SVT) as atrioventricular tachyarrhythmias, including atrioventricular nodal reentrant tachycardia or atrioventricular reentrant tachycardia, and 30 age- and sex-matched healthy individuals were included in the study. RESULTS: The apelin-12 levels were significantly lower in both atrial fibrillation and P-SVT groups than control group. In post-hoc analysis, there was no significant difference in apelin-12 levels between atrial fibrillation and P-SVT groups (P = 0.9). Patients in atrial fibrillation group and patients in P-SVT group had significantly lower apelin-12 levels than control group, separately (P < 0.001 and P < 0.001, respectively). The sensitivity and specificity values of the apelin-12 levels for predicting SVT, including both atrial fibrillation and atrioventricular reentrant tachycardia or atrioventricular nodal reentrant tachycardia were 64.77 and 90%, respectively (cut-off value was 0.87). The area under the receiver operator characteristic curve was 0.834 for the apelin-12 levels (P = 0.0001). CONCLUSION: Apelin-12 levels are lower in patients with atrial fibrillation and P-SVT than control groups. Lower apelin levels in patients with atrial fibrillation and P-SVT would be expected to result in a decrease in the conduction velocity.

The effect of nesfatin-1 levels on paroxysmal supraventricular tachycardia.

BACKGROUND: Nesfatin-1 was originally identified as a neuropeptide of the hypothalamus, which is a key integration area of the brain, where numerous neuropeptides and transmitters are released to participate in the control of essential body functions. In the literature, there are no studies showing the relationship between the nesfatin-1 level and paroxysmal supraventricular tachycardia. We hypothesize that the circulating levels of nesfatin-1 may increase during supraventricular tachycardia, to engage the vagal stimulation to terminate by the inhibition of neuropeptide-Y, and may activate oxytocin and the corticotropin-releasing hormone. MATERIALS AND METHODS: This study includes 120 cases (80 patients and 40 controls). Patients with paroxysmal supraventricular tachycardia were compared with the control group with regard to sex, nesfatin-1 level, comorbid diseases, serum renal function values, and patients' vital findings. RESULTS: The nesfatin-1 levels were significantly higher in the paroxysmal supraventricular tachycardia group than in the control group and positively correlated highly with heart rate (r = 0.634; P < 0.001). The area under the receiver operating characteristic curve was 0.644 for the nesfatin-1 levels (P = 0.0051). The sensitivity and specificity values of the nesfatin-1 levels were 41.2% and 95%, respectively (cutoff value >1743.7 pg/mL). CONCLUSION: At the end of this study, a statistically significant correlation was found between the serum nesfatin-1 level and supraventricular tachycardia. Although multifactorial causes may explain the relationship, we based our hypothesis on the relationship of the antagonistic effects of nesfatin-1 on the neuropeptide-Y and activated oxytocin.