Neuromodulation of Cardiac Dysfunction

Publisher Summary This chapter focuses on the neuromodulation of cardiac dysfunction. The mechanical causes of morbidity and mortality of cardiac dysfunction are a result of loss of contractile tissue and pump dysfunction. The electrical consequences of cardiac dysfunction are a result of the development of abnormal electrical conduction leading to substrate for reentrant arrhythmias and ventricular tachycardia and sudden cardiac death. The neurohormonal activation that occurs in CHF has inspired some to assess the effects of direct neuromodulation on cardiac function. Vagal nerve stimulation prevents inflammation and inhibits the release of cytokines such as TNF. The discovery that cholinergic neurons inhibit acute inflammation suggests a selective approach of neuromodulation to down regulate the inflammation associated with CHF. The possibility of selective stimulation of neural inputs that specifically modulate inotropic function of the myocardium could theoretically acutely, and perhaps chronically, impact on the long-term survival of the patients. Moreover, the device-based modulation of inotropic function could offer the potential of reestablishing a circadian rhythm within the heart, which is not achievable with pharmacological therapy. Neuromodulation for the treatment of cardiac arrhythmia has been applied in two distinct ways, which include suppressing the sympathetic nerve activity and augmenting the parasympathetic nerve activity. During sympathetic nerve stimulation, there is an increase in heart rate and LV pressure that can alter cardiac vulnerability and predispose the heart to ventricular fibrillation.