We developed an isolated rabbit atrial preparation which responds consistently and reproducibly to brief, submaximal stimulation of the autonomic nerves contained in it. In 6 of 11 preparations in the presence of propranolol (1 mg/liter), the time course of changes in the atrial rate following 120 msec vagal stimulation was bimodal. The maximal slowing occurred at 0.64 +/- 0.16 second, and the peak secondary slowing occurred at 2.3 +/- 1.0 seconds. An acceleratory component occurred between the first and second peaks between 0.8 and 1.6 seconds. The total time course of vagal effect lasted for 5.0 +/- 2.0 seconds. These changes in rate could not be explained by shifts in the location of the primary pacemaker. The acceleratory component was due to a 4.7 +/- 2.0 (SD) mV depolarization of the maximum diastolic membrane potential of the primary pacemaker of the sinus node which lasted for 1.8 +/- 0.3 seconds. Following vagal stimulation, there was an increase of 0.2 mM in the activity of potassium in the extracellular space recorded with a potassium-sensitive electrode; this peaked between 1.4 and 2.5 seconds and cleared with an exponential time course. The halftimes for recovery ranged between 2.8 and 4.6 seconds. The initial peak slowing of the bimodal time course and the acceleratory component therefore appear to be direct effects of acetylcholine. The secondary slowing occurs after acetylcholine presumably has been inactivated and occurs coincidently with the accumulation of potassium in the extracellular space.

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Lyme carditis is a rare cardiac manifestation of Lyme disease that occurs when bacterial spirochetes infect the pericardium or myocardium triggering an inflammatory response. The most common electrocardiogram (EKG) findings in these patients include atrioventricular (AV) conduction abnormalities (first, second, and third degree heart block).A 56-year-old male with a history of hypothyroidism, from the Northeastern region of the United States, presented to the emergency department with lightheadedness and chest pain. His EKG revealed sinus bradycardia with a heart rate of 49 beats per minute, without ST segment elevation, T wave inversions, or signs of heart block. An enzyme-linked immunosorbent assay (ELISA) Lyme titer was elevated, and confirmatory Western blot was positive for IgG and negative for IgM. He was treated with intravenous (IV) ceftriaxone; however, he continued to have persistent bradycardia with his heart rate dropping to 20 to 30 beats per minute throughout the night. Additionally, he had several sinus pauses while sleeping, with the longest lasting for 6.1 seconds. A pacemaker and an additional three-week course of IV ceftriaxone was determined to be the best treatment for his resistant bradycardia secondary to Lyme carditis. No symptoms were present at his one month follow-up appointment, as an outpatient, after completing ceftriaxone therapy. The patient follows up with cardiology regularly to have his pacemaker checked.Here we present a unique case of Lyme carditis, without the classical findings of Lyme disease or common EKG findings of AV conduction abnormalities. A high clinical suspicion of Lyme carditis is required when someone from a Lyme endemic region presents with unexplained cardiac symptoms and electrocardiogram abnormalities. This case report aims to add to the knowledge gap between suspicion of Lyme carditis and sinus bradycardia as the only presenting symptom.