The connection concerning the autonomic nervous system and coronary spasm during the systole is multifaceted. An augmentation in sympathetic activity, due to pain caused by angina and the several transient ischemic episodes may origin an augment in noradrenaline, the neurotransmitter of efferent sympathetic fibers, triggering more vasoconstriction by stimulating vascular smooth muscle cells, besides may lead the cardiac hypertrophy. Based on these concepts we aim to find a role to renal sympathetic denervation in patients with symptomatic myocardial bridging refractory to standard clinical treatment and ventricular arrhythmias. In conclusion, our findings suggest that RSD can be a role in myocardial bridging treatment, augmenting the LVEF, diminishing the LV mass and the number of transient ischemic segments measured by CMRI, besides to reduce the number of individuals presenting symptoms, the mean of NSVT recorded by 24-hour-Holter monitoring, and the number of patients with SVT inducible by the EPS. Perhaps such benefits are due to the decrease in the LV mass and sympathetic cardiac activity, consequently, there being less constriction of the arteries with myocardial bridges and less ventricular arrhythmias.We report preliminary data on 6 patients with controlled hypertension, with normal renal function, with symptomatic myocardial bridging refractory to clinical treatment and ventricular arrhythmias who underwent a pilot renal sympathetic denervation (RSD) procedure. At baseline, the 6 (100%) patients presented symptoms while 6 months after RSD only 1 (17%) subject still complained of the symptoms (P=0.0152). Our findings suggest that RSD can play a role in myocardial bridging treatment, augmenting LVEF, diminishing LV mass and the number of transient ischemic segments measured by CMRI.
6-Month Outcomes in Patients With Implantable Cardioverter-Defibrillators Undergoing Renal Sympathetic Denervation for the Treatment of Refractory Ventricular Arrhythmias
