Abstract | December 19, 2022
When is Sinus Bradycardia Pathologic?
Learning Objectives
- This case serves as a review of coronary artery anatomy, the differential diagnosis for syncope, SA and AV node pacing rates, and clinical manifestations of SN dysfunction. In addition to the review of these important foundational concepts, physicians and medical learners should take away the importance of interrogating the root cause of symptomatic sinus bradycardia.
Introduction: Approximately 40% of adults will experience an episode of syncope in their lifetime. Less common etiologies of syncope, such as a myocardial infarction (MI), should be considered when syncope is accompanied by bradycardia and hypotension. The existing literature consists of case reports describing prolonged sinus arrest due to obstruction of the sinus nodal artery (SNA) following a percutaneous coronary intervention of the Right Coronary Artery (RCA). To our knowledge, no cases have been published describing sinus nodal (SN) ischemia presenting as isolated syncope with preserved SN pacing. This case reinforces foundational concepts of coronary artery anatomy, pacing rates, and sinus bradycardia, in addition to raising questions about when sinus bradycardia should be suspected to be pathologic.
Case Presentation: A 70 y.o. male presented to the emergency department with a one-day history of multiple syncopal episodes. The patient denied chest pain, shortness of breath, or a prior history of syncope. Syncope workup revealed sinus bradycardia with a rate in the 30s and hypotension with a BP of 76/55. CXR showed no acute cardiopulmonary processes. CT Brain without contrast was negative for acute intracranial pathology. Due to the patient’s abnormal sinus heart rate, a repeat EKG and cardiac enzymes were ordered, revealing ST-T wave abnormalities consistent with an inferior infarct and upward trending HS Troponin I. Emergent coronary angiography revealed a proximal RCA to mid-RCA lesion with 100% stenosis. Export thrombectomy and RCA stenting were successfully performed. Upon discharge, the patient’s hypotension had resolved, and he was in junctional bradycardia with a pulse in the 60s. He was scheduled for cardiology follow up.
Conclusion: This patient’s sinus node retained its pacemaking capabilities at a rate of 30 beats-per-minute upon presentation. Acute disturbances of SN function caused by myocardial infarction is driven by both ischemia and neural reflex effects from mechanical or chemoreceptors in the ventricular wall. This case raises the question of why this patient’s pacemaking system had a delay in switching from sinus rhythm to atrioventricular (AV) pacing. Possible explanations include chronic ischemia with the development of collaterals that sustained a suboptimal but functional sinus pace rate.
References:
- Sathnur N, Ebin E, Benditt DG. Sinus Node Dysfunction. Card Electrophysiol Clin. 2021 Dec;13(4):641-659. doi: 10.1016/j.ccep.2021.06.006. Epub 2021 Sep 23. PMID: 34689892.
- Shimizu R, A. R., Ishikawa J, Harada K. (2021). Prolonged sinus arrest due to the obstruction of a sinus node branch after percutaneous coronary intervention of the right coronary artery. Journal of Cardiology Cases, 25(5), 319-322. doi:10.1016/j.jccase.2021.11.014.
