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Kusumoto et al 2018 Bradycardia Clinical Practice Guidelines

August 20, 2019 Circulation. 2019;140:e382–e482. DOI: 10.1161/CIR.0000000000000628 e404

CLINICAL STATEMENTS AND GUIDELINES 4.3.2. Electrophysiology Study in Patients With Documented or Suspected Bradycardia or Conduction Disorders

Recommendation for Electrophysiology Testing in Patients With Documented or Suspected Bradycardia or Conduction Disorders Referenced studies that support the recommendation are summarized in Online Data Supplement 7.

COR LOE Recommendation

IIb C-LD 1.  In patients with symptoms suspected to be attributable to bradycardia, an electrophysiology study (EPS) may be considered in selected patients for diagnosis of, and elucidation of bradycardia mechanism, if initial noninvasive evaluation is nondiagnostic.S4.3.2-1–S4.3.2-5

Synopsis

An EPS is an invasive, catheter-based procedure that can be used to test the integrity of cardiac conduction system and to assess potential inducibility of various cardiac tachyarrhythmias. EPS are well tolerated and the risk of serious procedural complications such as cardiac tamponade and life-threatening ventricular arrhythmia is minimal.S4.3.2-2,S4.3.2-5 The goal of an EPS in the context of bradycardia evaluation is to identify the presence of abnormal sinus node function or atrioventricular conduction, and the anatomic location of any conduction disorder. Pharmacologic drugs are sometimes administered during an EPS as a part of study protocol to modulate the autonomic tone or to “stress” the sinus node, atrioventricular conduction, and intraventricular conduction. An EPS in a patient thought to have bradycardia may uncover possible tachycardia mechanisms for symptoms. An EPS is generally not performed as the first-line diagnostic assessment in patients with suspected bradycardia. Most patients who undergo an EPS have already undergone a series of noninvasive cardiac evaluations, such as ECG, tilt table testing, echocardiogram, and/or ambulatory electrocardiographic monitoring, which may have been inconclusive. EPS have been performed almost exclusively in patients with unexplained syncope or presyncope, and some of these cases were found to be bradycardia mediated.S4.3.2-1–S4.3.2-4

Recommendation-Specific Supportive Text

1.	The diagnostic yield of EPS in symptomatic patients with suspected bradycardia has been shown to vary widely (range, 12%–80%), depending on the patient population studied.S4.3.2-1,S4.3.2-3 In 1 study of patients presenting with unexplained syncope, those who had history of heart disease (eg, coronary artery disease, hypertension, mitral valve prolapse) had a higher incidence of an abnormal EPS compared with patients who had a structurally normal heart.S4.3.2-5 In addition, the likelihood of an abnormal EPS was greater in patients who had an abnormal ECG at baseline (eg, bundle branch block or prior myocardial infarction [MI]).S4.3.2-4 In most cases, the cause of symptomatic bradycardia can be established without invasive evaluation. The use of an EPS has almost exclusively been examined in patients with syncope or presyncope, and is generally an adjunctive tool in the evaluation of patients in whom bradycardia is suspected but has not been documented after noninvasive evaluation.S4.3.2-6 Although correlation between symptoms and rhythm remain the cornerstone for management of patients with syncope, EPS may be a reasonable approach in a patient with syncope associated with trauma who also has a high pretest probability for significant conduction disease (eg, LBBB).S4.3.2-6–S4.3.2-8 EPS may also be performed when the patient is undergoing an invasive procedure such as an endomyocardial biopsy.

5 BRADYCARDIA ATTRIBUTABLE TO SND

5.1 Pathology/Pathophysiology/Etiology

of SND

The pathophysiology of SND is varied and usually involves complex electrophysiologic and structural remodeling. The sinoatrial node is comprised of a complex matrix of pacemaker cells, transitional cells, endothelial cells, fibroblasts, and extracellular scaffolding, and is characterized by a unique ion channel and connexin expression profile that results in chronotropic automaticity.S5.1-1 Genomewide association analyses have identified multiple loci in ion channel and channel interacting proteins related to normal and abnormal resting heart rates, providing insight into mechanisms controlling heart rate that may someday translate to new therapeutic targets.S5.1-2–S5.1-7 The specialized cardiomyocytes of the sinus node are surrounded by strands of connective tissue that electrically insulate the pacemaker cells from atrial myocardial tissue; this structural support appears to be essential for normal functioning as it protects pacemaker cells from the suppressive effects of hyperpolarization from adjacent myocytes.S5.1-8 Collagen content of the heart increases with age, however, and this increased fibrosis is correlated with slower heart rate and slower sinoatrial conduction times (SACT).S5.1-8 A histopathologic study of 111 patients with both normal rhythm, SND and atrial arrhythmias demonstrated an association between more extensive fibrosis and subjects with SND or tachybrady syndrome.S5.1-9 Notably, fibrosis of the sinus node was also associated with fibrosis in the atrioventricular node.S5.1-1,S5.1-8–S5.1-10 Asymptomatic sinus bradycardia has not been associated with adverse outcomes.S5.1-11,S5.1-12 However, patients with symptoms attributable to SND have a high risk of

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