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UCLA Cardiac Arrhythmia Center, UCLA Health System, David Geffen School of Medicine at UCLA, Los Angeles, CaliforniaCarol Davila University of Medicine and Pharmacy, Bucharest, Romania
Sinus arrest can be observed during radiofrequency catheter ablation at sites remote from the sinoatrial node (SAN) region.
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Sinus arrest owing to enhanced parasympathetic input to the SAN may result from either direct stimulation of local cardiac ganglionated plexi or activation of afferent cardiac vagal fibers (Bezold-Jarisch-like effect). These 2 mechanisms are distinct from each other.
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SAN damage may occur as a result of direct thermal injury to the SAN artery at sites distant from ablation, including in patients with Kugel anastomoses.
Introduction
Sinus arrest during radiofrequency (RF) ablation at a site distant to the sinoatrial node (SAN) has previously been reported from both right and left atrium, coronary sinus, and pulmonary veins.
We report a case of recurrent sinus arrest during premature ventricular contraction (PVC) RF ablation in the vicinity of the inferoseptal process of the left ventricle (ISP-LV).
Case report
A 70-year-old male patient was referred for ablation of highly symptomatic monomorphic PVCs with a 20% PVC burden. His medical history was notable for presence of ischemic cardiomyopathy with left ventricular (LV) ejection fraction of 40% and coronary artery disease with prior percutaneous coronary interventions and stenting of the left anterior descending artery, left circumflex artery (LCx), and right coronary artery (RCA). A 12-lead electrocardiogram showed q waves in the inferior leads of the intrinsic QRS. PVC had a left bundle branch block morphology with superior axis pattern, QS in the inferior leads with an initial isoelectric component in those leads, and an early precordial R/S transition, suggestive of a basal LV crux exit
(Figure 1A). Coronary angiography showed chronic total occlusion (CTO) of the mid-RCA distal to the stent, and well-developed collateral flow from the LCx and left anterior descending artery to distal RCA branches. SAN artery takeoff was from the LCx (Figure 2A).
Figure 1A: A 12-lead electrocardiogram with morphology of premature ventricular contraction (PVC) targeted for ablation. PVC had a left bundle branch block pattern with early precordial transition and an initial isoelectric component in the inferior leads. B: A 6.5-second sinus arrest occurring about 5 seconds after onset of radiofrequency (RF) energy delivery, preceded by an accelerated idioventricular rhythm with a different morphology than that of targeted PVC. C: Prolongation of sinus rate during another RF lesion; atrial pacing immediately upon cessation of ablation showed intact atrioventricular conduction. Vertical bars mark initiation and cessation of RF energy.
Figure 2A: Selective left coronary angiography, showing supply of the sinoatrial nodal artery from the proximal left circumflex artery as well left coronary artery to distal right coronary artery collateral flow. B: The heart sectioned and viewed from the right anterior oblique direction. The inferoseptal process is the basal inferomedial part of the left ventricular free wall facing to the septal isthmus anterior to the coronary sinus orifice. Note that the epicardial adipose tissue wedges between the inferoseptal process and coronary sinus orifice. This epicardial adipose tissue potentially contains the efferent/afferent autonomic nerve fibers, ganglionated plexi, and atrioventricular nodal artery. C: Electroanatomic maps showing sites of radiofrequency ablation in the vicinity of the inferoseptal process of the left ventricle.
Mapping for earliest local ventricular activation of PVC was performed in the proximal coronary sinus, middle cardiac vein, right ventricle basal septum, and ISP-LV region from the LV endocardium via a transseptal approach. Earliest activation was mapped to the vicinity of the ISP-LV (-30 ms pre-QRS). This correlated with a region of patchy scar. This area was targeted for ablation (Figure 2C). Ablation with an irrigated contact force–sensing ablation catheter (TactiCathTM SE; Abbott Laboratories, Abbott Park, IL) with power 50 watts, contact force 10–15 grams, resulted in repeated sinus bradycardia and sinus arrest 5–6 seconds after onset of energy delivery during multiple RF applications, with longest sinus pause of 6.5 seconds (Figure 1B). Atrial pacing immediately upon cessation of ablation during some ablation session showed intact atrioventricular (AV) conduction (Figure 1C). The patient was under anesthesia and did not elicit any pain response during ablation. Carvedilol was withheld 3 days before the procedure and he had not received any other heart rate–lowering medication. No further PVCs were noted after ablation in this area. He remained free of targeted PVC on a 30-day postablation Holter monitor and no evidence of SAN dysfunction. He endorsed no palpitations on a 3-month follow-up.
Discussion
Though uncommon, sinus arrest and sinus bradycardia have been previously reported during RF ablation at sites remote from the SAN, including anterior right atrium, left atrial roof, vicinity of inferior mitral annulus, pulmonary veins, region of right atrial slow pathway, and right aortic sinus.
These observations had been generally ascribed to neurogenic mechanisms leading to an enhanced parasympathetic effect on the SAN. Three distinct mechanisms—1 involving the intrinsic cardiac nervous system and ganglionated plexi (GP), 1 involving afferent cardiac vagal fibers (Bezold-Jarisch-like reflex), and 1 related to coronary artery circulation and blood supply to the SAN (vasogenic mechanism)—best explain these findings.
Successful ablation of PVCs with atypical left bundle branch block and early precordial transition from the ISP-LV region have been previously reported,
though commonly a right bundle branch block pattern in lead V1 is observed. In the presence of patchy local scar, endocardial ablation at the site of ISP-LV likely affected a critical component of a circuit with an epicardial (LV crux) or midmyocardial exit.
To the best of our knowledge, sinus arrest during ablation at this site has not been reported. ISP-LV (Figure 2B) occupies a unique region in the basal inferomedial LV, given its proximity to (1) cardiac vagal afferent unmyelinated type C fibers, (2) local atrial and ventricular GP, and (3) AV nodal (AVN) artery. The following discussion provides an overview of potential mechanisms for this observation.
Bezold-Jarisch-like reflex mechanism via direct activation of vagal fibers
The Bezold-Jarisch reflex is responsible for parasympathetic stimulation of the heart with complementary sympathetic suppression.
The cell bodies of these neurons are contained within the nodose and jugular ganglia. The central fibers of these bipolar neurons continue to ascend in the vagus nerve and enter the brain stem through the solitary tract, and synapse on neurons in the nucleus of the solitary tract in the medulla (Figure 3).
Figure 3Model of control of the heart by cardiac autonomic nervous system. The intrinsic cardiac ganglia system contains sympathetic and parasympathetic efferents, local circuit neurons, and local afferent neurons. Both the intrinsic cardiac ganglia (cardiac ganglionated plexi) and extracardiac intrathoracic ganglia are modulated by the central nervous system. Bezold-Jarisch reflex (BJR) mechanism involves activation of vagal afferent fibers (neurites) whose cell bodies are contained within the nodose ganglia. The central fibers of these neurons ascend in the vagus nerve and enter the brain stem through the solitary tract, and synapse in the medulla. Red arrows show efferent outputs and blue arrows show afferent inputs. Neurite indicates local afferent neurites embedded in the cardiac walls. β1AR = beta 1 adrenergic receptor; DRG = dorsal root ganglion; GP = ganglionated plexi; M2 = muscarinic acetylcholine receptor type 2; Figure adapted from Fedele and Brand.
Preferential distribution of inhibitory cardiac receptors with vagal afferents to the inferoposterior wall of the left ventricle activated during coronary occlusion in the dog.
Studies have implicated ischemia (this reflex is suggested to be responsible for the hypotension and bradycardia observed during acute inferior myocardial infarction) and reperfusion occurring in similar territory. Both ischemic and perfusion mechanisms are triggered via chemical stimuli, including prostaglandins that serve as a major stimulus to ventricular chemosensitive vagal afferent fibers. Though not directly studied, RF energy or heat may trigger these sensory receptors via similar mechanisms inducing local ischemia, reperfusion, and release of prostaglandins. Proximity of site of ablation (ISP-LV) to these receptors, with a classic parasympathetic effect on the SAN, would render this mechanism as the most plausible. Figure 3 provides a model of the hierarchical control of the heart by cardiac autonomic nervous system, including extracardiac ganglia, intrinsic cardiac GP, and the vagus nerve.
GP mechanism via direct stimulation of intrinsic cardiac nervous system
The cardiac GPs are part of an intrinsic epicardial neural network that comprises multiple ganglia with interconnecting neurons and axons, including afferent sensory fibers and sympathetic and parasympathetic efferents. They serve as the communication conduit between the intrinsic and the extrinsic cardiac nervous system, coordinating the response to afferent and efferent neural trafficking.
have shown that application of high-frequency stimulation to the atrial tissue where GP are presumed to reside induces a bradycardia response, including complete AV block within 2–5 seconds, by stimulating parasympathetic fibers connected to the AVN.
Another study showed that stimulation of cardiac GPs by direct injection of nicotine into tissue hosting them affected sinus rate in all 7 GPs, with an incidence of 50%–95% of the animals among the different GPs.
Bradycardia, when elicited, occurred within few seconds of local nicotine injection. Lastly, endocardial RF application at sites of cardiac GPs infrequently induced a parasympathetic response similar to high-frequency stimulation in a previous study.
Therefore, it is plausible that direct stimulation of local cardiac GPs with RF ablation in the ISP-LV region provoked a parasympathetic effect on the SAN. Such observation is less likely nonetheless, as it would require not only stimulation of local ventricular GP with RF application with either activation or suppression of intrinsic parasympathetic and sympathetic fibers respectively, but also stimulation with a preferential effect on the SAN from the local ventricular GP.
Vasogenic mechanism via direct thermal injury to the SAN artery from a distant site
The SAN artery originates most commonly from the right coronary artery and less frequently from the LCx.
SAN dysfunction, including sinus arrest and sinus bradycardia as a result of direct thermal injury to the SAN artery at a site distant to the SAN region, has been previously described owing to ablation along the LA roof and basal aspect of left atrial appendage.
Although the physiological role of Kugel anastomosis in a setting without coronary artery disease is less important, this artery can work as the critical collateral blood supply to the distal RCA in the setting of CTO of RCA-proximal Kugel anastomosis to reduce the ischemic consequences. In the rare setting when normal blood supply to the SAN artery is compromised (such as the RCA or LCx occlusion proximal to takeoff of the SAN artery), this anastomosis can work as the retrograde collateral source from the AVN artery to the SAN artery if the distal RCA receives other collateral sources. In this setting, damage to the SAN can be expected from the ISP-LV region, as the AVN artery ascends near the region. However, it should also create AVN injury, unless the AVN receives multiple supplies.
In the present case, despite mid-RCA CTO, no Kugel anastomoses was found during selective angiography (Figure 2A). Moreover, the SAN was mainly perfused by the left SAN artery from the LCx, which cannot be affected during the cardiac ablation at the ISP-LV. AVN function was maintained during the sinus arrest. Such findings do not support a vasogenic mechanism as the likely cause for sinus arrest.
Conclusion
This case examines the potential mechanisms of sinus arrest, an uncommon observation during endocardial ablation in the basal LV, and highlights the complexity of cardiac autonomic nervous system as well as coronary circulation in the presence of CTO.
References
Mathuria N.
Bobek J.
Afshar H.
Sinus arrest during radiofrequency ablation of the atrioventricular-node slow pathway: implications and possible mechanisms.
Preferential distribution of inhibitory cardiac receptors with vagal afferents to the inferoposterior wall of the left ventricle activated during coronary occlusion in the dog.
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