The autonomic nervous system and ventricular arrhythmias in myocardial infarction and heart failure

Abstract

Ventricular arrhythmias (VA) can range in presentation from asymptomatic to cardiac arrest and sudden cardiac death (SCD). Sustained ventricular tachycardias/ventricular fibrillation (VT/VF) are a common cause of SCD in the setting of myocardial infarction (MI) and heart failure. A particularly arrhythmogenic cardiac syncytia in these conditions can be attributed to both sympathetic activation and parasympathetic dysfunction, while appropriate neuromodulation has the potential to reduce occurrence of VT/VF. In this review, we outline the components of the autonomic nervous system that play an important role in normal cardiac electrophysiology and function. In addition, we discuss changes that occur in the setting of cardiac disease including adverse neural remodeling and neurohormonal activation which significantly contribute to propensity for VT/VF. Finally, we review neuromodulation strategies to mitigate VT/VF which predominantly rely on increasing parasympathetic drive and blockade of sympathetic neurotransmission.

Paraventricular Nucleus P2X7 Receptors Aggravate Acute Myocardial Infarction Injury via ROS-Induced Vasopressin-V1b Activation in Rats

“…In AMI, both overactivation of the sympathetic nervous system and parasympathetic dysfunction occur [ 37 ]. During AMI, enhanced activity of the cardiac sympathetic afferent reflex (CSAR) transmits afferent input to and stimulates the cardiovascular center.…”

Sympathetic nervous system activation and heart failure: Current state of evidence and the pathophysiology in the light of novel biomarkers

“…These clinical observations were inspired by the previous animal study demonstrating that spontaneous high-amplitude discharge activity from left stellate ganglion was strongly associated with the induction of malignant ventricular arrhythmias[ 166 ]. Modern state-of-the-art neuromodulation strategies that are capable of mitigating VT/VF and atrial arrhythmias are, therefore, focused on increasing parasympathetic drive and inhibiting sympathetic neurotransmission[ 167 , 168 ].…”

Air Pollution and Cardiac Arrhythmias: From Epidemiological and Clinical Evidences to Cellular Electrophysiological Mechanisms

“…ANS can be subdivided into two antagonistic sets of nerves, i.e., the sympathetic nervous system, and the parasympathetic nervous system. The sympathetic stimulation in normal hearts increases the heart rate by enhancing the funny current (I f ), shortens APD, and reduces transmural dispersion of repolarization (54,55). In contrast, in pathological states induced by PM, the dysregulated sympathetic stimulation might enhance the dispersion of repolarization (56,57) and promotes afterdepolarization (58,59).…”