A case report of an S-ICD–recorded asystole due to SMART pass deactivation in a patient with non-obstructive hypertrophic cardiomyopathy

Abstract

Background

The SMART pass (SP) algorithm of the subcutaneous implantable cardioverter-defibrillator (S-ICD; Boston Scientific Emblem) uses a high-pass filter to reduce inappropriate shocks due to signal oversensing. In cases of small to no R-wave amplitude, the SP algorithm is automatically deactivated, and an electrocardiogram (ECG) is recorded.

Case Summary

A 63-year-old patient with hypertrophic cardiomyopathy (HCM) without left ventricular outflow tract obstruction underwent implantation of an S-ICD. When the patient reported syncope months later, device interrogation revealed SP deactivation due to a 22-second asystole, consistent with the timing of the syncope. Prior to the event, there was no indication of future pacing requirement. The patient had a stable two-vessel coronary artery disease as well as unaltered echocardiographic findings, including preserved left ventricular ejection fraction. The S-ICD was replaced by a transvenous dual-chamber implantable cardioverter-defibrillator.

Discussion

Although bradycardia detection is not available in the S-ICD system, in our case, it was enabled due to ECG recording performed during SP deactivation, which outlines the importance of careful investigation. Since bradyarrhythmia in HCM is considered rare, it has been studied far less extensively than atrial and ventricular tachyarrhythmia. There is substantial evidence that myocardial fibrosis is a significant predictor of ventricular tachycardia and sudden cardiac death. However, more extended research is required to further investigate the association between myocardial fibrosis and bradyarrhythmia in patients with HCM, as well as to evaluate the potential of magnetic resonance imaging-based screening to identify patients at risk requiring future pacing.

Learning points.

• It is of utmost importance to carefully review every SP deactivation event, not only as a predictor of inappropriate shocks but also as a potential indicator of bradyarrhythmia and asystole.

• There is a need for additional screening strategies to identify, prior to S-ICD implantation, patients at risk of requiring anti-bradycardia pacing in the future.

Introduction

The subcutaneous implantable cardioverter-defibrillator (S-ICD) is designed to detect and treat ventricular arrhythmias, including ventricular tachycardia and ventricular fibrillation, by delivering a high-voltage shock. Owing to its inability to provide anti-bradycardia pacing, it is indicated for patients at low risk of bradyarrhythmia.¹

The SMART pass (SP) algorithm (Boston Scientific Corporation, Marlborough, MA) uses a high-pass filter to reduce inappropriate shocks due to cardiac signal oversensing. When undersensing is suspected, the SP algorithm is automatically deactivated as the filter may also reduce the S-ICD telemetry–recorded QRS complex amplitude. The following criteria, derived from the subcutaneous electrocardiogram (ECG), are applied and resulted in permanent deactivation and associated episode storage: Asystole lasting at least 10 s, or seven consecutive signals with amplitudes ≤0.25 mV accompanied by five consecutive interval measurements, including two of five intervals ≥1.4 s.²

Monkhouse et al. found that, in most cases, SP deactivation is caused by a small R-wave or an arrhythmia with a periodic axis shift. Less than 1% of cases involved true asystole as the underlying cause.³

Summary figure

Case presentation

A 63-year-old patient with hypertrophic cardiomyopathy (HCM) without left ventricular outflow tract (LVOT) obstruction and an estimated 5.57% risk of sudden cardiac death according to the ESC HCM SCD risk calculator underwent implantation of an S-ICD (Boston Scientific Emblem) in March 2025, after careful evaluation. The decision in favour of a subcutaneous device was supported by the patient’s previous history of mitral valve endocarditis. The resting ECG prior to implantation showed sinus rhythm with a normal heart rate, right bundle branch block, and normal atrioventricular conduction. Echocardiography demonstrated concentric left ventricular hypertrophy without left ventricular dilatation, with a maximal wall thickness of 1.7 cm and preserved left ventricular ejection fraction.

During a routine appointment in November 2025, the patient reported syncope that had occurred 3 months earlier. The episode occurred at home while the patient was seated and was not preceded by prodromal symptoms. When interrogated, the device showed an SP deactivation at the time of the syncope. An ECG was recorded, revealing a 22-second asystole (Figure 1). The resting ECG was unchanged compared with previous recordings (Figure 2). Apart from low-dose bisoprolol 2.5 mg once daily, the patient was not on any other bradycardia-inducing medication.

Figure 1.

Device-recorded ECG showing 22-second asystole.

Figure 2.

Resting 12-lead ECG prior to implantation.

Prior to the event, there was no indication of bradycardia or asystole in the patient’s history. Two 24-hour Holter ECG recordings performed prior to S-ICD implantation showed no tachyarrhythmias or bradyarrhythmias. He is known to have two-vessel coronary artery disease; however, the most recent coronary angiography, performed in February 2025, showed stable disease with no indication for further intervention. A follow-up echocardiographic evaluation confirmed stable findings, with no LVOT obstruction, no wall motion abnormalities, and a preserved left ventricular ejection fraction.

Due to the new requirement for pacing, the S-ICD was replaced by a transvenous dual-chamber implantable cardioverter-defibrillator. The patient has remained asymptomatic since device replacement.

Discussion

Although bradycardia detection is not available in the S-ICD system at present, ECG recording performed during SP deactivation in our case enabled the documentation of an episode of asystole.

Because SP deactivation has a strong predictive value for inappropriate shocks, it is recommended that every episode of deactivation be investigated carefully. As most SP deactivations are not attributable to true pauses, a thorough evaluation of the recorded ECG, along with correlation to the clinical presentation, is required.³

Prior to this report, only a few cases of asystole detected by an S-ICD through SP deactivation have been described. In most cases, the condition leading to S-ICD implantation was either ischaemic cardiomyopathy or myocarditis.^4–6

However, in our case, the patient underwent implantation because of non-obstructive hypertrophic cardiomyopathy. To date, the literature has largely focused on atrial fibrillation and ventricular tachyarrhythmia in patients with HCM.^7,8 Since bradyarrhythmia is considered rare, it has been studied far less extensively.^9,10 Nevertheless, the literature suggests that up to a quarter of HCM patients suffer from bradyarrhythmia due to sinus node dysfunction, atrioventricular block, or both.⁹ Nakasuka et al. discovered that around 8% of their study cohort had bradyarrhythmia requiring pacing therapy.¹⁰

Numerous studies provide evidence that myocardial fibrosis, as part of the arrhythmic substrate, plays a significant role in ventricular tachycardia and ventricular fibrillation as well as atrial arrhythmias.^11,12 It has also been shown to be a predictor for sudden cardiac death in patients with HCM.¹³ Moreover, myocardial fibrosis is also believed to be a central contributor to bradyarrhythmia in postinfarct patients; however, only a few authors have described a correlation between myocardial fibrosis and primary bradycardia in patients with HCM.^14,15 Additional research is required to fully characterize the association between myocardial fibrosis and bradyarrhythmia in patients with HCM as well as to further investigate the potential of MRI-based risk stratification with regard to a future need for cardiac pacing.

In conclusion, this case highlights two central points: on the one hand, the importance of carefully reviewing every SP deactivation event, not only as a predictor of inappropriate shocks but also as a potential indicator of bradyarrhythmia and asystole; on the other hand, it underlines the need for additional screening strategies to identify patients at risk requiring future pacing prior to S-ICD implantation.

Lead author biography

Philipps-Universität Marburg: Medical Degree (10/2010–11/2016); Bürgerhospital Frankfurt am Main: Department of Gastroenterology; Department of Pneumology, Cardiology, and Mechanical Ventilation (08/2017–06/2019); Jüdisches Krankenhaus Berlin: Department of Cardiology; Intensive Care Unit; Department of Angiology, Title: Specialist in Internal Medicine (04/2020–05/2023); since 05/2023 Jüdisches Krankenhaus Berlin: Fellow in the Department of Cardiology; Training in Rhythmology (Invasive Electrophysiology and Active Heart Rhythm Implants), Title: Specialist in Internal Medicine and Cardiology (02/2026).

Author contributions

M.L. drafted the manuscript. All authors revised the manuscript critically.

Marie Lajos (Conceptualization, Data curation, Formal analysis, Investigation, Methodology, Visualization, Writing—original draft [lead]), Wim Rother (Conceptualization, Supervision [supporting]), Thomas Hucko (Investigation, Methodology [supporting]), Kristof Graf (Supervision [supporting]), and Sebastian Spencker (Conceptualization, Data curation, Project administration [equal], Supervision [lead], Writing—review & editing [supporting])

Consent: Written consent, in line with the COPE guidelines, for the submission and publication of this case was obtained from the patient.

Funding

None declared.

Data availability

Data regarding this case are available upon reasonable request.