Cardiac vagal afferent neurotransmission in health and disease: review and knowledge gaps

The meticulous control of cardiac sympathetic and parasympathetic tone regulates all facets of cardiac function. This precise calibration of cardiac efferent innervation is dependent on sensory information that is relayed from the heart to the central nervous system. The vagus nerve, which contains vagal cardiac afferent fibers, carries sensory information to the brainstem. Vagal afferent signaling has been predominantly shown to increase parasympathetic efferent response and vagal tone. However, cardiac vagal afferent signaling appears to change after cardiac injury, though much remains unknown. Even though subsequent cardiac autonomic imbalance is characterized by sympathoexcitation and parasympathetic dysfunction, it remains unclear if, and to what extent, vagal afferent dysfunction is involved in the development of vagal withdrawal. This review aims to summarize the current understanding of cardiac vagal afferent signaling under in health and in the setting of cardiovascular disease, especially after myocardial infarction, and to highlight the knowledge gaps that remain to be addressed

Thoracic Epidural Anesthesia Can Be Effective for the Short‐Term Management of Ventricular Tachycardia Storm

Background Novel therapies aimed at modulating the autonomic nervous system, including thoracic epidural anesthesia (TEA), have been shown in small case series to be beneficial in treating medically refractory ventricular tachycardia (VT) storm. However, it is not clear when these options should be considered. We reviewed a multicenter experience with TEA in the management of VT storm to determine its optimal therapeutic use.Methods and Results Data for 11 patients in whom TEA was instituted for VT storm between July 2005 and March 2016 were reviewed to determine the clinical characteristics, outcomes, and role in management. The clinical presentation was incessant VT in 7 (64%), with polymorphic VT in 3 (27%) and monomorphic VT in 8 (73%). The underlying conditions were nonischemic cardiomyopathy in 5 (45%), ischemic cardiomyopathy in 3 (27%), and hypertrophic cardiomyopathy, Brugada syndrome, and cardiac lipoma in 1 (9%) each. Five (45%) had a complete and 1 (9%) had a partial response to TEA; 4 of the complete responders had incessant VT. All 4 patients with a documented response to deep sedation demonstrated a complete response to TEA.Conclusions More than half of the patients with VT storm in our series responded to TEA. TEA may be effective and should be considered as a therapeutic option in patients with VT storm, especially incessant VT, who are refractory to initial management. Improvement in VT burden with deep sedation may suggest that sympathoexcitation plays a key role in perpetuating VT and predict a positive response to TEA

European Heart Rhythm Association (EHRA)/Heart Rhythm Society (HRS)/Asia Pacific Heart Rhythm Society (APHRS)/Latin American Heart Rhythm Society (LAHRS) expert consensus on risk assessment in cardiac arrhythmias: use the right tool for the right outcome, in the right population.

In clinical practice and for scientific purposes, cardiologists and primary care physicians perform risk assessment in patients with cardiac diseases or conditions with high risk of developing such. The European Heart Rhythm Association (EHRA), Heart Rhythm Society (HRS), Asia Pacific Heart Rhythm Society (APHRS), and the Latin American Heart Rhythm Society (LAHRS) set down this expert consensus statement task force to summarize the consensus regarding risk assessment in cardiac arrhythmias. Objectives were to raise awareness of using the right risk assessment tool for a given outcome in a given population, and to provide physicians with practical proposals that may lead to rational and evidence-based risk assessment and improvement of patient care in this regard. A large variety of methods are used for risk assessment and choosing the best methods and tools hereof in a given situation is not simple. Even though parameters and test results found associated with increased risk of one outcome (e.g. death) may also be associated with higher risk of other adverse outcomes, specific risk assessment strategies should be used only for the purposes for which they are validated. The work of this task force is summarized in a row of consensus statement tables

Cardiac Parasympathetic Neural Remodeling and Electrophysiological Effects of Vagal Nerve Stimulation

The autonomic nervous system regulates cardiac excitability and genesis of ventricular tachyarrhythmias (VT/VF). Myocardial infarction leads to sympathetic activation and parasympathetic dysfunction, which act in concert to increase risk of sudden death due to VT/VF. The mechanism behind parasympathetic dysfunction and the electrophysiological effects of vagal nerve stimulation are poorly characterized. The vago-symapthetic trunks carries both efferent cardiomotor as well as cardiac afferent fibers that transduce mechano-chemical changes. To better delineate and compare their functional effects, in normal porcine hearts in vivo, right and left vagal nerve stimulation (VNS) was performed and hemodynamic parameters and activation recovery interval mapping (ARI) performed. ARI is a validated surrogate of local action potential duration. Subsequently, role of afferent fiber activation during VNS on efferent control of cardiac function was assessed by transection of right and/or left, and ispilateral, contralateral, and/or bilateral trunks. Finally, mechanism behind neural parasympathetic remodeling due to myocardial infarction (MI) and the anti-arrhythmic effects of VNS were assessed in a chronic porcine infarct model.In normal porcine hearts, right and left VNS significantly decreased heart rate and dP/dt max and prolonged regional ARI. No anterior-posterior-lateral ventricular regional differences in prolongation of ARI were found. However, endocaridal ARI increased more than epicardial ARI, and apical ARI more than basal ARI, during right and left VNS. With regards to afferent fiber activation during VNS, an augmentation in hemodynamic and electrophysiological effects of right VNS after ipsilateral vagal nerve transection was observed. Similar changes were suggested by left VNS after left vagal nerve transection, however, contralateral vagal nerve transection did not modify VNS response. Finally, measurement of regional acetylcholine, the primary neurotransmitter of cardiac parasympathetic neurons, showed that this neurotransmitter is primarily preserved in infarcted hearts. However, direct neural recordings from intrinsic cardiac ganglia showed significant alterations in the basal activity of parasympathetic efferent neurons that receive input from the left vagal trunk, suggesting a decrease in central parasympathetic drive. Augmentation of parasympathetic drive with VNS reduced ventricular tachy-arrhythmia inducibility by decreasing dispersion of repolarization in border zone regions of infarcted hearts. In conclusion, both right and left vagi provided significant innervation to the ventricular myocardium, modulating both cardiac electrical and mechanical function. VNS activated both afferent and efferent fibers in the ispilateral vagal trunk, and afferent fiber activation reduced efferent physiological effects. Myocardial infarction led to significant neural remodeling and alteration in the behavior of parasympathetic neurons in the cardiac ganglia, changes that were suggestive of decreased central parasympathetic drive. VNS restored this drive and electrically stabilized infarct border zones, reducing ventricular arrhythmias