Transient Supine-Induced Advanced Heart Block in an Octogenarian

Abstract

Atrioventricular block (AVB) is a conduction disorder that can lead to significant bradyarrhythmias with resultant hemodynamic compromise and cardiogenic shock. While most cases of positional AVB that occur during erect posture are attributed to neurocardiogenic mechanisms, complete AVB occurring exclusively in the supine position is an exceedingly rare phenomenon. We present a case of an 87-year-old Caribbean Black male who presented with symptomatic supine-induced advanced heart block, which transiently resolved during standing with unremarkable comprehensive investigations and subsequently underwent successful dual-chamber permanent pacemaker implantation. The clinician should be cognizant of assessing positional vital signs with telemetric monitoring in patients presenting with idiopathic bradyarrhythmias and presyncope.

Introduction

Atrioventricular block (AVB) occurs when there is a delay or failure in impulse conduction between the atria and ventricles, often resulting in bradycardia. ¹ Complete AVB (third-degree AVB) is characterized by total dissociation between P waves and QRS complexes. ² The underlying causes typically include degenerative fibrosis of the conduction system, acute coronary syndromes, drug-induced effects, metabolic disorders, autonomic dysfunction (AD), neuromuscular disorders, or infiltrative diseases.^3,4

Most positional complete AVB cases occur when a patient moves from a supine to a standing position due to a neurocardiogenic reflex involving vagal tone. ⁵ However, within the existing literature, there is only one other instance where the reverse is described, that is, where the AVB occurs solely while lying and disappears upon standing, highlighting the rarity of this case, its diagnostic work-up, and management. ⁶

We present a rare case of a hypertensive octogenarian patient who demonstrated intermittent advanced heart block when supine, with restoration to normal sinus rhythm upon standing. This case underscores the importance of assessing positional vital signs with telemetry in patients with symptomatic bradycardia.

Case Presentation

An 87-year-old Caribbean Black male with a medical history of controlled hypertension on lisinopril presented to the emergency department with intermittent dizziness occurring, specifically when lying down during the preceding month. He denied experiencing overt syncope, angina, dyspnea, or palpitations. His family observed that he appeared somnolent while reclining but remained alert and responsive when sitting upright or standing. The patient had no prior history of coronary artery disease, cerebrovascular disease, or arrhythmias. He was not prescribed beta-blockers, calcium channel blockers, digoxin, or any other antiarrhythmic drugs. There was no recent history of infections, metabolic derangements, or trauma.

On physical examination, his blood pressure was 122/68 mmHg while supine and 128/75 mmHg when standing. His heart rate in the supine position was 36 beats per minute and increased to 85 beats per minute when standing. Cardiac examination revealed no murmurs, gallops, or signs of heart failure. Neurological assessment demonstrated no focal deficits or postural instability. Carotid sinus massage did not elicit any significant pause or bradycardia. The telemetric evaluation demonstrated complete AVB while supine, with an atrial rate of 70 beats per minute and a ventricular rate of 36 beats per minute with a borderline-wide QRS complex. Upon standing, his electrocardiographic tracing normalized to sinus rhythm at 85 beats per minute, with restored 1:1 AV conduction and no evidence of advanced heart block (Figure 1).

Figure 1.

The patient’s positional 12-lead ECGs. (A) The patient’s ECG when standing illustrating normal sinus rhythm with subtle nonspecific ST-T changes. Some minor motion artifacts were observed (I, aVL). (B) The patient’s ECG when supine demonstrating complete AVB, with an atrial rate of 70 beats per minute and ventricular rate of 36 beats per minute with a borderline-wide QRS complex. AVB, atrioventricular block; ECG, electrocardiogram.

He was admitted to the cardiac ward, where further investigations, including serum electrolytes, thyroid function tests, and cardiac biomarkers, were within normal limits. Transthoracic echocardiography revealed a preserved left ventricular ejection fraction of 60%, with grade 2 diastolic dysfunction, but no overt structural abnormalities, significant valvular disease, pulmonary hypertension, or features suggestive of infiltrative or restrictive cardiomyopathy. An inpatient 48-hour Holter monitor confirmed intermittent complete AVB block occurring exclusively in the supine position, with normal conduction when the patient was upright or ambulating.

Given his symptomatic positional AVB, a dual-chamber pacemaker (DDD mode) was successfully implanted. Following the procedure, the patient remained asymptomatic, with stable AV conduction irrespective of posture. At the 3-month follow-up, he reported no interval recurrent presyncope or syncope.

Discussion

Positional complete AVB is an uncommon phenomenon that poses diagnostic and management challenges. This case highlights an exceedingly rare instance of supine-induced AVB in an octogenarian, warranting an in-depth evaluation of tentative diagnoses with appropriate intervention. The presence of intermittent AVB, which is resolved upon standing, underscores the need for a thorough understanding of the pathophysiology of positional bradyarrhythmias.

Positional AVB is not replete within the electrophysiology literature, but several putative mechanisms have since been postulated. One plausible explanation is enhanced vagal tone in the supine position, which could attenuate AV nodal conduction; however, vagally mediated bradycardia typically results in sinus node suppression rather than complete AVB, making this an improbable etiology.^{7 -9} Another potential pathway is the mechanical compression of the AV node or the His–Purkinje system due to anatomical shifts when supine. Structural abnormalities such as pericardial effusion, cardiac chamber enlargement, and mediastinal or intracardiac masses have been described as abutting or impinging on the native conduction system with resultant positional bradyarrhythmias.^{10 -13} In our case, transthoracic echocardiography ruled out overt lesions, alluding to an alternative pathophysiological mechanism. Our patient, guided by his immediate family, declined further extensive investigations, such as cardiac catheterization and cardiac magnetic resonance imaging. AD can also be implicated, as some patients with autonomic instability exhibit bradyarrhythmias that are modulated by posture. This typically manifests with orthostatic hypotension or sinus node dysfunction as opposed to isolated AV conduction disturbances. ¹⁴ The absence of orthostatic hypotension and preserved chronotropic response to standing in this patient counter this factor as a primary contributor; however, the patient’s ECG did display motion artifact (I, aVL), which could be attributed to muscle contractions or movement disorder disease such as Parkinson’s, the latter of which can be associated with AD.^15,16

Diagnosing positional AVB requires a systematic approach to exclude reversible causes. Medication-induced bradycardia was ruled out in this case due to the absence of pharmacologic agents such as beta-blockers, calcium channel blockers, or digoxin, in addition to the patient’s reported denial of complementary and alternative therapies. ³ Electrolyte derangements and metabolic disturbances, which can contribute to conduction abnormalities, were also excluded through laboratory investigations.^3,17 Continuous ambulatory ECG monitoring played an integral role in confirming the episodic/intermittent nature of the AVB and its robust correlation with supine posture, reinforcing the hypothesis of a position-dependent conduction abnormality. Management decisions for positional AVB should be individualized based on symptom burden and the risk of progression to permanent conduction disease. ³ While some cases may be managed conservatively with positional modifications, the idiosyncratic nature of AVB accentuates the likelihood of major adverse cardiovascular events. Given the patient’s advanced age and symptomatic bradycardia, permanent pacemaker implantation was considered the most appropriate intervention. ⁴ Dual-chamber pacing (DDD mode) was selected to ensure consistent AV synchrony, thereby mitigating symptoms and progression of intrinsic conduction disturbances. ³

This case underscores the importance of recognizing positional AVB as a distinct clinical entity. Although rare, it should be considered in the geriatric subpopulation of patients presenting with unexplained positional dizziness or syncope. Vigilant telemetric monitoring is crucial for detecting transient conduction abnormalities, and complementary cardiac imaging should be performed to exclude structural contributors.

Conclusion

Positional AVB is a rare and underrecognized form of conduction abnormality that can pose significant diagnostic challenges. This case highlights the need for positional telemetric monitoring in patients presenting with unexplained bradyarrhythmia, which is a swift, inexpensive, and noninvasive modality. A comprehensive evaluation assessing the absence of structural heart disease, metabolic derangements, or AD is also warranted, in addition to permanent pacemaker implantation in severe cases. Increased awareness of positional AVB can facilitate timely diagnosis and attenuate unnecessary delays in treatment.