Symptomatic Junctional Bradycardia Due to Untreated Hypothyroidism After Beta-Blocker Discontinuation: A Case Report.

Hypothyroidism is known to cause bradycardia, but there are no direct comparisons of the level of thyroid-stimulating hormone (TSH) to heart rate (HR) to assist in therapeutic hormonal management. This case presents a patient who developed symptomatic junctional bradycardia and underwent serial TSH testing to attempt to improve her HR while minimizing systemic toxicity from levothyroxine. The patient had a history of paroxysmal atrial fibrillation on beta-blocker therapy and hypothyroidism and developed symptomatic junctional bradycardia following a lapse in her thyroid supplementation. Upon initiation of hormonal replacement therapy, serial TSH levels were assessed as she continued to have episodic bradycardia with severe hypertension. Given the lack of evidence correlating TSH levels to HR, this case report calls for further studies to be conducted to create reliable guidelines in therapeutic management to prevent bradycardia events while minimizing systemic levothyroxine toxicity.

Influence of drive cycle length on initiation of ventricular fibrillation during implantable cardioverter defibrillator threshold testing.

BACKGROUND: Programmed electrical stimulation of the heart as a method to induce tachyarrhythmias has been described since the 1960s. To date, no study has examined optimal drive cycle length in the induction of ventricular fibrillation (VF) during defibrillation threshold testing after implantable cardioverter-defibrillator placement. We hypothesized that longer drive cycle length, by means of the longer action potential duration, would promote intramyocardial phase 2 reentry and facilitate induction of VF. METHODS: Fifty consecutive implants were randomized in a prospective crossover format for this study. The group consisted of 40 men and 10 women, with each patient receiving either a 400 or 600 ms initial drive train prior to 1.2 J internal shock on the T wave with a goal to induce ventricular fibrillation. The timing of the T wave shock was determined by measuring the interval from the beginning of the QRS to the apex of the T wave in lead II. Successful inductions were defibrillated via the cardioverter defibrillator. Patients were then crossed over and the protocol repeated. RESULTS: Twenty of 23 (87%) patients were successfully induced into VF in the initial 400 ms drive train arm whereas 22 of 27 (81%) were successfully induced in the 600 ms arm. Thus, a total of 44 (88%) patients were successfully induced at 400 ms, 41 (82%) patients were successfully induced at 600 ms, and 2 (4%) patients were not inducible at either cycle length, but were inducible with 50 Hz ventricular stimulation. However, no significant difference was noted between the two groups. CONCLUSION: No investigation to date has questioned whether a relationship exists between drive cycle length and initiation of ventricular fibrillation. Our study addresses this question, though negative for difference between 400 and 600 ms drive trains. Further research into optimal strategies for inducing ventricular fibrillation will minimize patient sedation time and discomfort while undergoing defibrillator threshold testing.