Reversal of left bundle branch block–induced cardiomyopathy by His bundle pacing

Introduction

Whether left bundle branch block (LBBB) is a cause or consequence of deterioration of left ventricular function is difficult to determine because both conditions are often identified concomitantly in clinical practice. We herein describe the correction of LBBB by His bundle pacing (HBP) and subsequent normalization of a low left ventricular ejection fraction (LVEF) in a patient previously diagnosed with dilated cardiomyopathy and LBBB. The right bundle branch (RBB) was injured during the procedure and recovered during follow-up. The evidence of LBBB-induced cardiomyopathy and possible causes of RBB block (RBBB) are discussed.

Case report

A 61-year-old woman presented with a 4-year history of severe dyspnea and bilateral pedal edema. She had repeatedly been admitted to a local hospital for dilated cardiomyopathy with heart failure. The LVEF had fluctuated between 18% and 28%. An electrocardiogram (ECG) and the results of 24-hour Holter monitoring, recorded at admission, showed complete LBBB with a QRS duration of 172 ms (Figure 1(a)). Echocardiography revealed a left ventricular end-diastolic diameter (LVEDD) of 69 mm, severe left ventricular dysfunction (LVEF of 15%), and decreased left ventricular wall motion. Computed tomography–coronary angiography showed no evidence of coronary artery disease. Intensive medical treatment was administered to the patient but was ineffective. Therefore, we decided to attempt HBP with an aim to recruit the left bundle branch (LBB) and restore synchronization.

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Figure 1.

Twelve-lead electrocardiogram and intracardiac electrogram recorded by the 3830 lead. (a) Electrocardiogram at admission showed sinus rhythm with complete left bundle branch block and QRS duration of 172 ms (57 beats per minute). (b) The intracardiac electrogram showed a 2:1 atrioventricular block (red arrows indicate the P wave and blue arrows indicate the QRS complex). (c) The intracardiac electrogram revealed His bundle–ventricular block.

A SelectSecure 3830 lead (Medtronic, Inc., Minneapolis, MN, USA) was placed through a C315 sheath (Medtronic, Inc.) and guided to the atrioventricular septum. During His bundle mapping, 2:1 atrioventricular conduction occurred (Figure 1(b)), and an intracardiac electrogram showed His bundle–ventricular (HV) block (Figure 1(c)). A temporary pacemaker was inserted into the right ventricle to avoid a progressive atrioventricular block. At a low pacing frequency of about 60 beats per minute, HBP corrected the LBBB and decreased the QRS duration to 120 ms with an acute threshold of 1.0 v/0.4 ms. However, the QRS morphology presented RBBB even with a higher voltage and pulse width during the procedure. The unipolar and bipolar impedance was 886 and 593 Ω, respectively. We managed to screw the lead in the exact site (Figure 2(a), (b)). The post-procedural ECG showed RBBB (Figure 3(a)). The symptoms of heart failure had been reversed by the 1-month post-procedure follow-up. A repeat ECG showed recovery of the RBB injury with rate-dependent RBBB (Figure 3(b)), which may have existed before HBP although the results of the 24-hour Holter monitoring, recorded at admission, did not show rate-dependent RBBB. Repeat echocardiography revealed a decreased LVEDD of 53 mm and an improved LVEF of 38%. The patient showed significant improvements 3 months later: the LVEDD had decreased to 51 mm and the LVEF had increased to 50%.

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Figure 2.

Lead position determined by fluoroscopy in the (a) left anterior oblique (LAO) view and (b) anteroposterior (AP) view. The red arrows show the 3830 His lead.

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Figure 3.

Twelve-lead electrocardiogram. (a) Twelve-lead electrocardiogram during His pacing showed right bundle branch block (red arrow) with a QRS duration of 120 ms. (b) Twelve-lead electrocardiogram 1 month after the procedure showed recovery of the right bundle branch injury with rate-dependent right bundle branch block (red arrow).

Discussion

The present case suggests that HBP offers a more physiological means and can significantly improve the long-term prognosis and quality of life in patients with heart failure, which is in accordance with the results of several clinical trials.^1,2 In addition, the severe heart dysfunction in our patient recovered to absolute normality after the correction of LBBB by HBP, which implies the presence of LBBB-induced cardiomyopathy instead of primary cardiomyopathy in this patient. Similarly, Vaillant et al. ³ reported that six patients with isolated LBBB developed nonischemic cardiomyopathy characterized by a decreased LVEF and left ventricular enlargement after 11 years of follow-up, and all patients were hyper-responders to cardiac resynchronization therapy, indicating that LBBB can cause severe heart failure. Moreover, Auffret et al. ⁴ reviewed the evidence of LBBB-induced cardiomyopathy and implied that LBBB might be the best explanation for the subsequent progression to cardiomyopathy in patients who exhibit an excellent response to cardiac resynchronization therapy. However, a large-cohort study with prospective follow-up is required.

In the present case, 2:1 atrioventricular conduction occurred during His bundle mapping, and the intracardiac electrogram showed HV block. After HBP, the LBBB was corrected; however, RBBB occurred with a QRS duration of 120 ms. We inferred that the RBB had been injured by the lead. The HBP procedure runs the risk of damaging the normal conduction system of the heart. Vijayaram et al. ⁵ reported the incidence of His bundle injury during permanent HBP in patients with no evidence of His-Purkinje disease. In total, 28 of 358 patients had His bundle injury in the form of third-degree atrioventricular block (n = 4), RBBB (n = 21), and LBBB (n = 3). All patients with third-degree atrioventricular block, all patients with LBBB, and 12 of 21 patients with RBBB completely recovered from their injury within 1 minute to 1 hour. However, the remaining 9 of the 21 patients with RBBB did not recover, even during the follow-up period. Most cases of RBBB occurred during fixation of the His bundle electrode, and a few occurred during the process of electrical mapping. ⁵ In the current case, RBBB occurred during the process of electrical mapping to identify the appropriate site of the His bundle. The RBB had not recovered from this injury within 72 hours, whereas it had finally recovered by the 1-month follow-up. Because the ventricular escape beats occurred before the RBBB occurred, we inferred that the cause of the RBBB may be related to mechanical injury of the distal RBB during mapping, suggesting that a temporary pacemaker is necessary during the HBP procedure for patients with LBBB.

In conclusion, we have herein reported a case in which a patient, initially diagnosed with dilated cardiomyopathy, presented with heart failure and LBBB that were eventually reversed by HBP. This case provides evidence for the clinical presence of LBBB-induced cardiomyopathy and shows that the use of temporary pacemakers is essential during HBP procedures in patients with LBBB. Moreover, the recovery period for the intraoperative mechanical injury to RBB conduction may be delayed.