A patient in their 70s was referred to the emergency department for worsening shortness of breath, chest tightness, and episodes of palpitations. The patient’s medical history was remarkable for hypertension and kidney insufficiency. Initial evaluation revealed a heart rate of 53 beats/min, blood pressure of 221/85 mm Hg. Laboratory test results revealed that the patient’s B-type natriuretic peptide level was 838.6 pg/mL (normal level, <300 pg/mL). The initial 12-lead electrocardiogram (ECG) is presented in the Figure, A. Transthoracic echocardiography showed left atrial enlargement (52 mm), normal left ventricular wall thickness, and mild pulmonary hypertension.
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Compared with the QRS complex, the P wave is small, and it is difficult to find abnormalities on the surface electrocardiogram. The normal P wave duration is shorter than 120 milliseconds.3 In the present case, the noteworthy findings on the patient’s initial ECG is prolonged P-wave duration (180 milliseconds) with biphasic morphology in the inferior leads. The P-wave represents normal depolarization that occurs from the right atrium to the left atrium through the Bachmann bundle or region. Bachmann bundle is a muscular bundle composed of aligned myocardial fibers in parallel. Any delay in atrial conduction is pathologically considered as IAB.3 Similarly to atrioventricular block, IAB can be divided into varying degrees of block. The findings shown in the Figure (panel A) may be considered as advanced IAB, which was first described in 1956.2 It is a featured of P-wave duration longer than 120 milliseconds with biphasic P-wave morphology in the inferior limb leads (II, III, and aVF).3 The electrophysiologic mechanism underlying advanced IAB has been explained—the depolarization was completely blocked in the Bachmann region, and activation of the left atrium occurs retrogradely through a zone located close to the coronary sinus, leading to the presence of delay of left atrial depolarization, and forming superior and left deviation of the terminal vector of the P wave. This can explain P-wave prolongation and final negative component of the P wave in the inferior leads, which is different from left atrial enlargement. Cardiac morphological examination (eg, cardiac echocardiography) has confirmed that it may be usually associated with left atrial enlargement, as demonstrated in the present case. At this time, the superior and left deviation of the terminal vector of the P wave generated by IAB can affect the classic V1 pattern of left atrial enlargement, making the negative amplitude of P wave in lead V1 unremarkable (in this case). Therefore, left atrial enlargement cannot be excluded according to the absence of classic V1 pattern. Atrial fibrosis is considered the anatomic substrate of advanced IAB.1,4 Over time the architecture of fibrotic myocardial tissue becomes heterogeneous, thereby affecting intercellular conduction, increasing anisotropy, and contributing to conduction slowing; this development of functional and structural block creates an arrhythmogenic substrate.3,5- 7 The harm of atrial fibrillation has been recognized by clinicians, and several P-wave parameters including P-wave duration, advanced IAB, abnormal P-wave terminal force in V1, low P-wave amplitude in lead I, and abnormal P-wave axis have been associated with increased risk of atrial fibrillation.8 Advanced IAB was found to be independently associated with an increased risk of atrial fibrillation in the ARIC study9 and in the Copenhagen ECG Study.10 Patients older than 60 years with advanced IAB have a 50% risk for developing atrial fibrillation at 6 years; meanwhile, the risk for atrial fibrillation is only 10% among patients who do not have underlying advanced IAB.3 The clinical entity characterized by the association of advanced IAB with atrial fibrillation and other atrial arrhythmias has been named Bayés syndrome.2 An increasing number of cases have demonstrated a link between IAB and the development of left atrial appendage thrombus and embolic stroke in sinus rhythm.3 This patient also finally developed a stroke event 1.5 years later. The clinical treatment of IAB is a hot topic, and the antiarrhythmic medications, cardiovascular risk factor modification, and anticoagulation may be the important investigative treatment modalities.3
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Corresponding Author: Renguang Liu, The Cardiovascular Institute of the First Affiliated Hospital of Jinzhou Medical University, Renmin Street, Jinzhou 121000, Liaoning Province, China (email@example.com).
Published Online: November 21, 2022. doi:10.1001/jamainternmed.2022.4813
Conflict of Interest Disclosures: None reported.
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