Prevention and Treatment of Atrial Fibrillation via Risk Factor Modification.

Atrial fibrillation (AF) is the most common clinically significant arrhythmia, and it increases stroke risk. A preventive approach to AF is needed because virtually all treatments such as cardioversion, antiarrhythmic drugs, ablation, and anticoagulation are associated with high cost and carry significant risk. A systematic review was performed to identify effective lifestyle-based strategies for reducing primary and secondary AF. A PubMed search was performed using articles up to March 1, 2021. Search terms included atrial fibrillation, atrial flutter, exercise, diet, metabolic syndrome, type 2 diabetes mellitus, obesity, hypertension, stress, tobacco smoking, alcohol, Mediterranean diet, sodium, and omega-3 fatty acids. Additional articles were identified from the bibliographies of retrieved articles. The control of hypertension, ideally with a renin-angiotensin-aldosterone system inhibitor, is effective for preventing primary AF and recurrence. Obstructive sleep apnea is a common cause of AF, and treating it effectively reduces AF episodes. Alcohol increases the risk of AF in a dose-dependent manner, and abstinence reduces risk of recurrence. Sedentary behavior and chronic high-intensity endurance exercise are both risk factors for AF; however, moderate physical activity is associated with lower risk of AF. Recently, sodium-glucose cotransporter-2 inhibitors and glucagon-like peptide-1 agonists have been associated with reduced risk of AF. Among overweight/obese patients, weight loss of ≥10% is associated with reduced AF risk. Lifestyle changes and risk factor modification are highly effective for preventing AF.

How to implant a phrenic nerve stimulator for treatment of central sleep apnea?

BACKGROUND: Central sleep apnea (CSA) is a breathing disorder caused by the intermittent absence of central respiratory drive. Transvenous phrenic nerve stimulation is a new therapeutic option, recently approved by the FDA , for the treatment of CSA. OBJECTIVE: To describe the technique used to implant the transvenous phrenic nerve stimulation system (the remede System, Respicardia, Inc). METHODS: The remede System is placed in the pectoral region, typically on the right side. A single stimulation lead is placed in either the left pericardiophrenic vein (PPV) or the right brachiocephalic vein (RBC). A sensing lead is placed into the azygous vein to detect respiration. RESULTS: In the remede System Pivotal trial, 147 of 151 (97%) patients were successfully implanted with the system. Sixty-two percent of stimulation leads were placed in the PPV and 35% in the RBC. Mean procedure time was 2.7 ± 0.8 hours and 94% of patients were free from implant-related serious adverse events through 6 months. CONCLUSION: In patients with CSA, transvenous phrenic nerve stimulation is an effective and safe therapy with an implant procedure similar to that of cardiac implantable electronic devices.

Delayed-enhanced MR scar imaging and intraprocedural registration into an electroanatomical mapping system in post-infarction patients.

Post-infarction arrhythmias are most often confined to scar tissue. Scar can be detected by delayed-enhanced cardiac magnetic resonance. The purpose of this study was to assess the feasibility of pre-procedural scar identification and intraprocedural real-time image registration with an electroanatomical map in 23 patients with previous infarction and ventricular arrhythmias (VAs). Registration accuracy and cardiac magnetic resonance/electroanatomical map correlations were assessed, and critical areas for VA were correlated with the presence of scar. With a positional registration error of 3.8 ± 0.8 mm, 86% of low-voltage points of the electroanatomical map projected onto the registered scar. The delayed-enhanced cardiac magnetic resonance-defined scar correlated with the area of low voltage (R = 0.82, p < 0.001). All sites critical to VAs projected on the registered scar. Selective identification and extraction of delayed-enhanced cardiac magnetic resonance defined scar followed by registration into a real-time mapping system are feasible and help to identify and display the arrhythmogenic substrate in post-infarction patients with VAs.

Mapping and ablation of epicardial idiopathic ventricular arrhythmias from within the coronary venous system.

BACKGROUND: The prevalence of epicardial idiopathic ventricular arrhythmias that can be ablated from within the coronary venous system (CVS) has not been described. METHODS AND RESULTS: In a consecutive group of 189 patients with idiopathic ventricular arrhythmias referred for ablation, the site of origin (SOO) of ventricular tachycardia and/or premature ventricular contractions was determined by activation mapping and pace mapping. Mapping was performed within the CVS if endocardial mapping did not reveal an SOO. Venography of the CVS and coronary angiography were performed before ablation in the CVS. In 27 of 189 patients (14%+/-5%; 95% confidence interval), the SOO of the ventricular arrhythmia was identified from within the coronary venous system, either in the great cardiac vein (n=26) or the middle cardiac vein (n=1). The mean activation time at the SOO was -29+/-8 ms. Twenty of 27 patients (74%) underwent successful ablation within the CVS. Epicardial ventricular arrhythmias displayed a broader R wave in V(1) compared with arrhythmias in the control group (85 ms [interquartile range, 40] versus 65 ms [interquartile range, 95]; P<0.01). Two patients had recurrent premature ventricular contractions within 2 weeks after ablation, and no recurrences occurred in the remaining patients during a median follow-up of 13 months (range, 25). In the 7 patients with unsuccessful ablation, failure was because the ablation catheter could not be advanced to the SOO within the great cardiac vein (n=4), inadequate power delivery at the SOO (n=1), proximity to the phrenic nerve (n=1), or proximity of the SOO to a major coronary artery (n=1). Transcutaneous epicardial ablation was effective in 1 of 2 patients in whom it was attempted. CONCLUSIONS: Almost 15% of idiopathic ventricular arrhythmias have an epicardial origin. ECG characteristics help to differentiate epicardial arrhythmias from endocardial ventricular arrhythmias. The SOO of epicardial arrhythmias can be ablated from within the CVS in approximately 70% of patients.

Assessment of radiofrequency ablation lesions by CMR imaging after ablation of idiopathic ventricular arrhythmias.

OBJECTIVES: To identify and characterize ablation lesions after radiofrequency (RF) catheter ablation of ventricular arrhythmias in patients without prior myocardial infarction and to correlate the ablation lesions with the amount of RF energy delivered and the clinical outcome. BACKGROUND: Visualization of RF energy lesions after ablation of ventricular arrhythmias might help to identify reasons for ablation failure. METHODS: In a consecutive series of 35 patients (19 women, age: 48 +/- 15 years, ejection fraction: 0.56 +/- 0.12) without structural heart disease who were referred for ablation of ventricular arrhythmias, cardiac magnetic resonance imaging with delayed enhancement was performed before and after ablation. Ablation lesions were sought in the post-ablation cardiac magnetic resonance images. The endocardial area, depth, and volume of the lesions were measured. Lesion size was correlated with the type of ablation catheter used and the duration of RF energy delivered. RESULTS: In 25 of 35 patients (71%), ablation lesions were identified by delayed enhancement a mean of 22 +/- 12 months after the initial ablation procedure. The mean lesion volume was 1.4 +/- 1.4 cm(3), with a mean endocardial area of 3.5 +/- 3.0 cm(2). The largest lesions (mean volume of 2.9 +/- 2.1 cm(3) with an endocardial area of 6.4 +/- 3.4 cm(2)) were identified in patients in whom the arrhythmias originated in the papillary muscles. Ablation duration correlated with lesion size (r = 0.67, p < 0.001). There was no difference in lesion volume with irrigated versus nonirrigated ablation catheters (1.0 +/- 0.73 vs. 2.0 +/- 2.1 cm(3), p = 0.09). Identification of ablation lesions in patients with a failed procedure identified the sites where ineffective RF energy lesions were created. CONCLUSIONS: RF ablation lesions can be detected long term after an ablation procedure targeting ventricular arrhythmias in patients without previous infarction. Lesion size correlates with the amount of RF energy delivered and is largest when a targeted arrhythmia originates in a papillary muscle.