Pre-Operative Stellate Ganglion to Prevent Post-Operative Atrial Fibrillation

BACKGROUND AND RATIONALE Post-operative atrial fibrillation (POAF) is a widely recognized problem after cardiac surgery. Atrial fibrillation is the most common arrhythmia to occur after cardiac surgery. The reported incidence after coronary artery bypass grafting (CABG) is 15-40%, 37-50% after valve surgery, and up to 60% after CABG and valve surgery1-3. Most POAF episodes occur by day three2. Postoperative AF is associated with increased risk of postoperative stroke (3.3% versus 1.4%), increased length of hospital stay (ICU stay 5.7 versus 3.4 days, floor stay 10.9 versus 7.5 days), increased incidence of ventricular arrhythmias (9.2% versus 4.0%), increased need for permanent pacemaker implant (3.7% versus 1.6%), and increased mortality3-5.

Multiple therapies have been proposed to prevent POAF in order to reduce hospital length of stay and possibly the risk of stroke and death. Beta blockers, sotalol, amiodarone, atrial pacing, and antioxidant vitamins have all been shown to lower risk of POAF6-11. Beta blockers are the most frequently used medications owning to safety, ease of use, cost-effectiveness, and familiarity. Long-term beta blocker therapy is indicated in many patients undergoing cardiac surgery anyway due to underlying cardiac conditions (coronary artery disease, cardiomyopathy, etc). The other interventions are associated with increased adverse effects and/or unclear added benefit in addition to beta blockers12.

Cardiac sympathetic innervation arises from the stellate ganglion. The stellate ganglia can be temporarily anesthetized by percutaneous injection of local anesthetic (such as lidocaine, bupivacaine, or ropivacaine). This procedure can be done at bedside with ultrasound guidance. Stellate ganglion block (SGB) can reduce sympathetic output to the heart with minimal system effect. The post ganglionic fibers from the stellate ganglion release not only norepinephrine (the target of beta blockers) but several additional neurotransmitters (including neuropeptide Y and galanin) that modulate adrenergic signaling13,14. SGB provides added benefit in addition to both beta blockers and antiarrhythmics (such as amiodarone) for the suppression of refractory ventricular tachycardia15. The effect of SGB on arrhythmia suppression can last up to several weeks, the longer duration of efficacy relative to drug half-life is likely due to alterations in neuro-transmission and neural processing.

While SGB has been most widely applied to refractory ventricular arrhythmias, there are antiarrhythmic effects in the atrial also. In a canine model stellate ganglion stimulation facilities AF induction and worsened atrial electrical properties (shortened atrial effective refractory period (ERP) and increased dispersion of the atrial ERP). SGB reduced AF initiation16. This effect is similar in humans; SGB prolongs atrial ERP, reduces atrial inducibility, and in those with inducible AF, shortens AF duration17. One study evaluating pre-operative SGB to reduce the risk of radial artery spasm when the radial artery was used as a coronary bypass conduit found a significantly lower incidence of post-operative atrial fibrillation, inotropic agent use, and ST segment depression in those who received SGB18. SGB may have a similar or complimentary effect to low level vagal nerve stimulation, which has been shown to reduce POAF in cardiac surgery patients19.

B. OBJECTIVES