The autonomic nervous system and the origins of neurocardiology.

Following new concepts by Bichat in the early 19th century, of organic and animal life centered around the ganglionic nervous system, over 100 years of anatomic studies and physiologic experimentation eventually resulted in Gaskell's 1916 book entitled "The Involuntary Nervous System" and Langley's 1921 book entitled "The Autonomic Nervous System." Neurology and cardiology emerged as specialties of medicine in the early 20th century. Although neurology made several prominent discoveries in neurophysiology during the first half of the 20th century, cardiology developed coronary care units and cardiac catheterization in the 1960s. Programmed electrical stimulation of the heart and noninvasive ambulatory monitoring provided new methodologies to study clinical cardiac arrhythmias. Experimentally, direct cardiac nerve stimulation of sympathetic nerve endings, as well as parasympathetic control of the atrioventricular node, provided the background to new detailed autonomic studies of the heart. Neurocardiology, perhaps initially more directed towards our understanding of sudden cardiac death, ultimately embraced an even significantly more complex scheme of local circuit neurons and near-endless loops of interconnecting neurons in the heart. Intrathoracic extracardiac and intracardiac ganglia have been recharacterized, both anatomically and physiologically, laying the groundwork for potential new therapies of cardiac neuromodulation.

The reuse of cardiac pacemakers and defibrillators: A convoluted history in an era of global health.

Following the development of permanent transvenous cardiac pacing in the 1960s, the costs of pacemakers quickly led to their reuse in both developed countries and in low-and middle-income countries (LMIC). Legal, ethical, and industrial factors gradually resulted in the termination of reuse in developed countries. Without health care budgets to pay for costly pacemaker technologies, nongovernmental organizations (NGOs), and other groups have provided support to physicians and hospitals treating patients with heart block in LMICs. Multiple other academic and private groups have also assisted such patients in LMICs. Pacemaker companies have provided physicians and hospitals with new devices (that have an expired package date or through charitable donations). Greater care of preparing and cleaning refurbished devices have demonstrated overwhelmingly the safety and effectiveness of reused devices. More recently, cardiac resynchronization therapy and implantable cardioverter-defibrillators have also been reused in patients in LMICs. While the globalization of noncommunicable diseases continues, patients with rhythm disorders in LMICs can no longer be left behind. While patients in developed countries only receive new devices to treat rhythm disorders, the practice of reused cardiac implantable electronic devices will expand in LMICs, until equal access to device technologies be made available to all.

Prevalence of left atrial appendage thrombus detected by transoesophageal echocardiography before catheter ablation of atrial fibrillation in patients anticoagulated with non-vitamin K antagonist oral anticoagulants.

AIMS: There is ongoing controversy about the need for routine transoesophageal echocardiography (TOE) prior to atrial fibrillation (AF) ablation. Recently, the debate was reignited by the publication of a large series of patients showing a prevalence of left atrial appendage thrombus (LAAT) on TOE of 4.4%. We sought to assess the prevalence of LAAT on TOE before AF ablation at our institution. METHODS AND RESULTS: Consecutive patients scheduled for AF ablation at our institution between January 2009 and December 2016 were included. All patients were on oral anticoagulation for at least 4 weeks prior to TOE. Transoesophageal echocardiographies were performed 3-5 days prior to scheduled AF ablation. Data were collected utilizing a prospective database. In all, 668 patients and 943 AF ablation procedures were included. Mean age was 64 ± 11 years, 72% were male, average CHADS2 score was 1.0 ± 1.0, and 72% of the patients had paroxysmal AF. At the time of ablation, 496 (53%) were on non-vitamin K antagonist oral anticoagulants (NOACs) and 447 (47%) were on Warfarin. There were three cases with LAAT (3/943, 0.3%), all of whom had persistent AF and were on Warfarin. Two patients underwent surgical ablation and the third patient did not undergo ablation. CONCLUSION: In our experience, the prevalence of LAAT in patients on anticoagulation therapy undergoing TOE before catheter ablation of AF is 0.3%, which was much lower than recently reported. None of the patients with paroxysmal AF or on NOACs were found to have LAAT. Rather than routine use of TOE prior to AF ablation, a risk-based approach should be considered.

Contact force mapping and voltage thresholds during high-frequency stimulation of human cardiac ganglionated plexuses†.

AIMS: The intrinsic cardiac nervous system consists of ganglionated plexuses (GPs) localized epicardially to specific regions of the left atrium (LA). The relation between voltage thresholds and endocardial contact force associated with autonomic effects during stimulation of GPs has not previously been evaluated. METHODS AND RESULTS: Sixteen patients with symptomatic atrial fibrillation (AF) underwent mapping of GPs prior to radiofrequency ablation of AF. Pre-acquired computed tomographic images were merged with 3D non-fluoroscopic electroanatomic mapping of the LA. Using high-frequency stimulation (HFS), the voltage thresholds of GPs was obtained while patients received conscious sedation. At each location, the contact force measurement from the catheter was correlated with the voltage applied during HFS at 5, 10, or 15 V to obtain an autonomic effect, usually associated with asystole, or marked bradycardia. There were 192 applications of HFS, resulting in GP identification in all patients (mean 3.4 per patient, range 1-5). During HFS, an autonomic response was significantly more likely to occur at 10 V as compared with 5 V (P < 0.008). There was no significant relation between the measured contact force and the likelihood of obtaining an autonomic response. When performing HFS at 15 V, a sudden overshoot with maximal values of contact force of up to 100 g was also observed. High-frequency stimulation was well tolerated, without associated adverse events. CONCLUSION: An autonomic response during HFS was significantly more likely to occur at 10 V as compared with 5 V. Although the GPs are epicardial structures, significant contact force was not required for their localization.

A prospective placebo controlled randomized study of caffeine in patients with supraventricular tachycardia undergoing electrophysiologic testing.

INTRODUCTION: Patients with cardiac arrhythmias are generally instructed to avoid caffeine intake. A comprehensive evaluation of the electrophysiological effects of caffeine on atrial and ventricular tissues in humans has not previously been performed. METHODS AND RESULTS: Eighty patients (31 men, mean age 49 ± 14 years) with symptomatic supraventricular tachycardia (SVT) undergoing an electrophysiologic study (EPS) prior to catheter ablation were randomized to receive oral caffeine or placebo. Caffeine at a dosage of 5 mg/kg (moderate intake) or placebo tablets were administered orally at a mean time of 57 ± 13 minutes prior to the EPS. The median (IQR) caffeine level in patients receiving caffeine was 7.4 µg/mL (4.7-8.7), as compared with 0.15 (0.00-0.61) in patients receiving placebo, P < 0.0001. Caffeine was associated with a significant increase in resting systolic and diastolic blood pressures as compared with placebo, while the resting heart rate was not significantly different between both groups. Caffeine was not associated with significant effects on the effective refractory period of the atrium or ventricle, as well as on AV node conduction. SVT was induced in all but 3 patients; there was no significant difference between groups receiving placebo or caffeine on SVT inducibility or the cycle length of induced tachycardias. CONCLUSIONS: Caffeine, at moderate intake, was associated with significant increases in systolic and diastolic blood pressures, but had no evidence of a significant effect on cardiac conduction and refractoriness. Furthermore, no effect of caffeine on SVT induction or more rapid rates of induced tachycardias was found.