Cardioneuroablation is one of the emerging therapies in vasovagal syncope. In this study, we present a simple method of cardioneuroablation performed via a right-sided approach, targeting anterior-right and right-inferior ganglionated plexi, along with procedural and follow-up data. Patients who had underwent cardioneuroablation between March 2018 and September 2019 with vasovagal syncope in 2 clinics were enrolled in the study. All patients underwent radio-anatomically guided radiofrequency ablation targeting anterior-right ganglionated plexi and right-inferior ganglionated plexi. Syncope and symptom burden, 24-hour ambulatory electrocardiogram data at presentation, and at follow-up were assessed along with procedural data. A total of 23 patients underwent modified right-sided cardioneuroablation. Mean basal cycle length decreased significantly from 862.3 ± 174.5 ms at the beginning of the procedure 695.8 ± 152.1 ms following the final radiofrequency ablation (P < .001). Mean 24-hour ambulatory heart rate increased significantly from 66.4 ± 10.7 bpm at baseline to 80 ± 7.6 bpm at follow-up (P < .001). Only 1 patient had 1 episode of syncope following the procedure at the mean follow-up period of 10 ± 2.9 months. The same patient had recurrent presyncope. The right-sided cardioneuroablation approach was found to be an effective treatment for vasovagal syncope and may be regarded as a default initial cardioneuroablation technique.

Left atrial scar is an important entity in the atrial fibrillation substrate. P wave dispersion (PWD) is an indicator of slow and inhomogeneous conduction in the atria. In this study, we aim to investigate the relation between PWD and left atrial scars identified by electroanatomical mapping. Patients who had an electroanatomical map obtained during sinus rhythm as well as at least one electrocardiogram in sinus rhythm prior to the procedure were included in the study. Left atrial scar (defined as <0.5 mV) area was calculated on the electroanatomical map. Maximum and minimum P wave duration and PWD were compared between patients with and without left atrial scar. A total of 224 patients were enrolled in the study. Of them, 47.9% of the patients were female. On the electroanatomical map, left atrial scar was identified in 103 patients, and no scar was present in 121 patients. PWD was significantly increased in patients with left atrial scar when compared to the no-scar group (46 ms ± 20 vs. 38 ms ± 15, respectively, p < 0.001). Similarly, PWD was significantly increased in patients with moderate-to-severe scar, when compared to patients with mild scar (50 ms ± 19 vs. 41 ms ± 19, respectively, p = 0.026). PWD was found not to be a good predictor of left atrial scar with an AUC of 0.625 for scar vs. no scar. PWD is significantly increased in patients with left atrial scar identified by electroanatomical mapping, however, the receiver operating characteristic analysis showed that PWD is not a good predictor of presence of left atrial scar.

Background: Ventricular fibrillation (VF) is a poorly understood arrhythmia that is one of the main mechanisms of sudden cardiac death in patients with structural heart disease (SHD). Fascicular and Purkinje tissue (FPT) has been implicated in VF. Objective: In this study, we sought to analyze the involvement of FPT colocalized with the scar area of SHD. Additionally, we aimed to investigate outcomes of FPT and scar substrate ablation in SHD VF patients and compare outcomes with VT ablation patients. Methods: This is a retrospective observational study. Clinical and procedural data were collected. Results: Sixteen patients undergoing VF ablation were assigned to the VF group, and their outcomes were compared to those of 170 patients who underwent structural VT ablation. In 15 patients, FPT targets colocalized with low voltage area, LPs, and/or LAVAs. Septal Purkinje and left posterior fascicle were most commonly involved. Procedural metrics were similar with patients undergoing VT ablation. During median follow‐up of 5.5 months (interquartile range [IQR]: 3.5–10), VF recurred in two patients. Conclusion: This study has shown frequent colocalization of FPT with electrophysiologic substrate (late potentials [LPs], low voltage area, etc.) in patients with SHD and VF. We have shown the feasibility of FTP and substrate ablation with good mid‐term outcomes in a small group of patients. Larger studies are necessary for definitive evidence.

Carotid sinus syndrome (CSS) is a rare condition leading to recurrent syncope. Permanent pacemaker implantation is the mainstay treatment of cardioinhibitory CSS. In this report, we present a CSS patient with reproducible atrioventricular block during carotid massage, who was treated with cardioneuroablation.

The relationship between coronary tortuosity (CorT) and tissue-level myocardial perfusion is not clear. We investigated tissue perfusion in myocardial territories supplied by tortuous coronary arteries. Among patients who had undergone coronary angiography, patients with reported CorT, those with ≥1 coronary artery were included in the study group (100 patients). The control group included patients with normal coronary arteries (100 patients). Thrombolysis In Myocardial Infarction frame count (TFC) and myocardial blush grade (MBG) were calculated for each coronary artery. Mean TFC was significantly higher in tortuous right coronary artery (RCA), left anterior descending (LAD) artery, and circumflex (Cx) artery compared to their non-tortuous counterparts (28.81 ± 6.463 vs 21.94 ± 3.328, P = .009; 43.28 ± 5.698 vs 36.17 ± 3.875, P = .006; 29.35 ± 4.111 vs 23.821 ± 2.639; P < .001, respectively). Mean MBG was also significantly lower in tortuous RCA, LAD, and Cx, compared to their normal counterparts (2.78 ± 0.417 vs 2.98 ± 0.155, P < .001; 2.74 ± 0.483 vs 2.97 ± 0.164, P < .001; 2.92 ± 0.277 vs 2.99 ± 0.110, P < .001, respectively). For each tortuous coronary artery, TFC was similar for every MBG category. Tortuous coronary arteries have higher TFC and lower MBG, suggesting impaired epicardial and microvascular coronary flow, when compared to normal coronary arteries.