Right atrial compartmentalization may alter the substrate for AF, thus improving the efficacy of previously ineffective antiarrhythmic drugs. Because it is relatively safe, it may be a reasonable adjunctive intervention to maintain sinus rhythm in patients with drug-refractory AF.

A case is presented of an 18-year-old male who had been resuscitated following an episode of sudden death due to ventricular fibrillation. The patient was noted to have an abnormal deflection in the terminal QRS on surface ECG and an abnormal signal-averaged ECG demonstrating a late potential coincident with the terminal QRS abnormality on the ECG. The patient had easily inducible polymorphic ventricular tachycardia during electrophysiologic study, which was suppressed by quinidine but not by procainamide or beta blockers. The surface ECG and signal-averaged ECG also were normalized by quinidine but not by procainamide or beta blockers. The patient had no further arrhythmias on quinidine for 6 years until he inexplicably discontinued his medication and died suddenly shortly thereafter. The present case may represent a unique familial sudden death syndrome or possibly a variant of the sudden death syndrome associated with right bundle branch block and ST elevation in V1 through V3. Currently available data suggest that, in such patients, an implantable cardioverter defibrillator may provide better protection from sudden death than does antiarrhythmic drug therapy.

INTRODUCTION: Thyroid crisis is a rare and life-threatening endocrine emergency characterized by exaggerated clinical manifestations of hyperthyroidism with cardiovascular manifestations being the most severe. Rhythm disturbances, sinus tachycardia and atrial fibrillation, are the commonest cardiac manifestations of severe thyrotoxicosis; however, asystole remains a very atypical and uncommon presentation. We present a case of thyrotoxicosis due to Grave’s disease complicated by multiple episodes of asystole. CASE PRESENTATION: A 65-year-old female recently diagnosed with Grave’s disease presented to the hospital with recurrent episodes of syncope. Her hospital course was significant for atrial fibrillation with subsequent progression to sinus pauses and asystole spontaneously reverting to atrial fibrillation. Her thyroid hormone levels were found to be markedly elevated at the time of presentation. She was initially managed with a temporary pacemaker but ultimately transitioned to a permanent dual-chamber pacemaker, in addition to concurrent anti-thyroid treatment with propylthiouracil and prednisone. She made an uneventful recovery and was discharged from hospital a few days later with scheduled outpatient follow-up. CONCLUSION: Asystole due to hyperthyroidism remains a very uncommon presentation of severe thyrotoxicosis, and in rarer situations can occur in hyperthyroid patients without any associated predisposing conditions such as infection, inflammation or medication use as previously reported. The mechanisms underlying this rhythm disturbance remain elusive, nevertheless, its management may require a permanent pacemaker placement in addition to concurrent medical treatment of the underlying cause and the thyroid hormone disturbance using standard hyperthyroid medications.