Successful use of Closed Loop Stimulation pacemaker for carotid sinus syndrome due to infiltrating neck cancer

Abstract

A 64-year-old male with oropharyngeal carcinoma experienced recurrent syncope and hypotension due to neoplastic compression of the right carotid space. Despite initial treatment with atropine and fluid resuscitation, the patient continued to experience presyncope and hypotensive events. After treatment with a conventional dual-chamber pacemaker failed, the use of closed-loop stimulation (CLS) successfully resolved the syncope episodes. This case highlights the efficacy of CLS pacing in managing reflex syncope caused by extrinsic neoplastic compression of the carotid sinus. The CLS algorithm, by detecting pre-syncopal phases and increasing heart rate proactively, offers a significant advantage over conventional pacing in preventing syncope.

1. Introduction

Carotid sinus syndrome (CSS) is typically triggered by pressure on the carotid sinus and is characterized by hypotension and bradycardia, potentially resulting in syncope. In rare cases, compression of the carotid sinus by a progressive or invasive tumor may lead to CSS [1]. Although cardiac pacing is an established treatment option for patients with CSS [2], there are no reports describing the benefit of dual-chamber pacing using the closed-loop stimulation (CLS) algorithm (Biotronik, SE & CO, Berlin, Germany) in patients with cancer-related CSS. We present a case of CSS due to extrinsic neoplastic compression, in which the CLS algorithm played a critical role in eliminating syncopal episodes.

2. Case report

We present the case of a 64-year-old man, with a past medical history of hypertension, obesity, smoking, hypercholesterolemia, and a recent diagnosis of oropharyngeal spinocellular carcinoma, awaiting initiation of chemotherapy.

The patient presented to the emergency department after experiencing multiple episodes of presyncope over the past few weeks, and after 3 syncopal events in the last two days. Each episode was preceded by a visual obnubilation and discomfort, with cranial trauma and lacerated wound after the last episode. Upon arrival of the emergency care team, the patient was markedly hypotensive (arterial blood pressure 75/40 mmHg) and bradycardic, and the electrocardiogram showed sinus bradycardia with heart rate of 25 bpm (Fig. 1). Administration of atropine (0.5 mg) and intravenous fluids led to an increase in blood pressure and heart rate. The patient was admitted to the intensive care unit for continuous monitoring. Echocardiography revealed a left ventricle of normal size and thickness, normal contractility, and preserved systolic function (56 %), with normal size of right sections. Mild mitral and tricuspid regurgitation and normal aortic valve were observed. During hospitalization, continuous monitoring revealed frequent episodes of sinus bradycardia with sinus arrest lasting up to 3 seconds (Fig. 2a) and the emergence of a junctional rhythm (Fig. 2b), accompanied by marked hypotension (drop of systolic blood pressure from 130 mmHg to 75 mmHg), reappearance of feeling faint and partial presyncope. A neck computed tomography (CT) scan was performed showing neoplastic invasion of the right carotid space (Fig. 3a–d). The observed irregular mass encompassed the right internal and external carotid arteries with thrombotic obliteration of the right internal jugular vein. After the diagnosis of CSS due to extrinsic neoplastic compression, patient underwent a dual chamber pacemaker implant without complications. During the first two months of follow up, the device was programmed in DDD mode (basic rate: 60 bpm) with the CLS algorithm inactive. The patient experienced sporadic presyncope episodes and one transient loss of consciousness on a hypotensive basis. At the 3-month device follow-up, proper functioning of the pacemaker was confirmed (atrial threshold: 0.5 V × 0.4ms; sensing: 2.5 mV; pacing impedance: 650 Ω; ventricular threshold: 0.6 V × 0.4ms; sensing: 12 mV; pacing impedance: 680 Ω) and device was reprogrammed to DDD-CLS mode at the same base rate (60 bpm). Following CLS activation, no further episodes of loss of consciousness occurred. Chemotherapy was initiated without resulting in a reduction of the mass volume which remained unchanged on the CT scan performed 6 months after pacemaker implantation. At a 9-month follow-up, with pacemaker programmed in DDD-CLS mode for 7 months (72 % of atrial pacing and 14 % of ventricular pacing), the patient remained free from syncope and continued oncological treatments.

Fig. 1.

Electrocardiogram from recent medical history showing sinus bradycardia with heart rate of 25 bpm.

Fig. 2.

Electrograms collected during the hospital stay showing (a) sinus bradycardia with sinus arrest lasting up to 3 sec and (b) emergence of junctional rhythm.

Fig. 3.

Axial (a), coronal (b) and sagittal (c) computed tomography (CT) scans showing thrombotic obliteration of the right internal jugular vein. Three-dimensional reconstruction of the neck vessels (d) showed neoplastic compression on surrounding structures (particularly right carotid space).

3. Discussion

This clinical case shows how CLS allows to correct recurrent and disabling syncopal episodes in a patient suffering from a severe and atypical form of CSS caused by tumor infiltration of the carotid glomus.

Increased pressure or stretch of the carotid sinus causes an abnormal carotid baroreflex response which leads to vasodilatation, bradycardia (cardioinhibition), and hypotension resulting in loss of consciousness in patients with CSS [3]. In some cases, the effects of hyperstimulation of the carotid sinus by extrinsic masses are so intense to induce hypotensive cardiac arrests, with the need for cardiopulmonary resuscitation [4]. In the presented case, hyperstimulation of the carotid sinus resulted in recurrent syncopal episodes linked to a double hypotensive and cardioinhibitory mechanism. To reduce the compression of the carotid sinus, neurectomy or surgical debulking of the tumor [5] were considered, but these treatments were deemed unfeasible in this case. Chemotherapy may be beneficial for long-term treatment of the underlying cause of CSS; hence, the patient was started on neoadjuvant chemotherapy. Radiotherapy, which could relieve symptoms of CSS in tumor-related encasement of the carotid artery in a palliative setting, was also considered [6] but the risk of tumor blowout was deemed too high. Pacemakers with CLS have been demonstrated to be an effective option of treatment for patients with neurally-mediated (reflex) syncope helping to reduce syncope recurrences or alleviate symptoms [7]. In our case, after the implantation of a dual-chamber pacemaker, simple DDD stimulation corrected the cardioinhibition, but the patient remained symptomatic due to hypotensive presyncope on a vasodepressive basis. Pacemaker programming in CLS rate-adaptive mode made it possible to mitigate this problem. This could be explained considering the compensatory mechanism underlying reflex syncope. Indeed, reflex syncope is characterized by a decrease in cardiac output and blood pressure due to peripheral venous blood pooling [7]. These effects trigger a subsequent increase in sympathetic tone by the baroreceptor reflex which leads to increased heart rate and inotropism (pre-syncopal phase). In vasovagal syncope, increased myocardial contraction activates the mechanoreceptors of the left ventricle inhibiting the sympathetic system and triggering the vasovagal reaction. Increased vagal tone leads to a vasodilation and/or bradycardia with a marked drop of arterial blood pressure (syncopal phase). In this scenario, syncope prevention is possible only with the detection of pre-syncopal rather than late syncopal mechanisms and with an early reaction with a rate increase. Unlike other pacing modalities, CLS can detect changes in myocardial contraction dynamics and adapt the pacing rate to counteract the drop in blood pressure with an increase of the heart rate (Fig. 4). Recently, Brignole et al. [8] investigated the temporal relationship between haemodynamic changes and CLS activation during tilt-induced vasovagal syncope. This study showed that onset of CLS pacing occurred early during the pre-syncopal phase in most patients who underwent tilt-test under video recording, 1.7 minutes before the expected heart rate (HR) drop at the time of maximum vasovagal effect (i.e. loss of consciousness or minimum blood pressure). Furthermore, during the pre-syncopal phase, the CLS algorithm further increased HR from 88 bpm (CLS pacing rate at onset) to a maximum of 105 bpm and CLS pacing persisted, albeit attenuated, at the time of maximum vasovagal effect. This finding supports the additional benefit of CLS on DDD pacing in maintaining cardiac output and preventing syncopal recurrences. In line with previous studies which showed the benefit of an early activation of CLS pacing in patients with reflex syncope, our case clearly confirms how programming a pacemaker in DDD-CLS mode could be decisive in the treatment of recurrent syncopal episodes in a complex cancer patient.

Fig. 4.

Functional scheme of the CLS feature [1]. With each systole, CLS measures right ventricular impedance which reflects contraction dynamics around the lead tip. Impedance trends depend on blood and myocardial muscle volumes surrounding the lead tip. First, a resting reference curve (patient's rest state) is constructed [2]. CLS monitors the impedance trend during each ventricular contraction and compares it against the resting reference curve. The pacing rate is adjusted based on the difference in the area under the curves—the greater the difference, the higher the pacing rate [3]. CLS translates variations in myocardial contraction dynamics into a pacing rate that the patient's own cardiovascular control system adjusts. Too high pacing rates activate baroreceptors due to elevated arterial pressure, inducing reflex downregulation of contractility and subsequent pacing rate reduction. If the pacing rate is too low, the system reacts in the opposite direction. ANS = Autonomic nervous system; CLS = Closed Loop Stimulation.

Consent statement

Written informed consent was obtained from the patient.

Data statement

Data available within the article.

Ethical Statement

Written informed consent was obtained from the patient(s) for publication of this case report and any accompanying images.

Declaration of competing interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.