Jeffrey H. Chung

Time course of adenosine-induced pulmonary vein reconnection after isolation: implications for mechanism of dormant conduction.

Background: Adenosine (ADO) has been proposed to reconnect isolated pulmonary veins (PVs) postablation through hyperpolarization of damaged myocytes in an animal model. However, PV reconnection can occur via ADO‐mediated sympathetic activation. We sought to determine the mechanism of ADO‐induced PV reconnection in the clinical setting by characterizing its time course and location in patients undergoing PV isolation.

Differential Effects of Adenosine on Pulmonary Vein Ectopy After Pulmonary Vein Isolation Implications for Arrhythmogenesis

Background— The mechanism of pulmonary vein (PV) triggers of atrial fibrillation remains unclear. We performed adenosine (ADO) testing after PV isolation to characterize spontaneous dissociated PV rhythm and ADO-induced PV ectopy. Methods and Results— Seventy-four patients (61 men; age, 61±10 years) undergoing PV isolation for atrial fibrillation were studied. For each isolated PV, dissociated ectopy was recorded and ADO was administered. After isolation of 270 PVs, 50 PVs with dissociated ectopy were identified. In 42 PVs exhibiting PV rhythm, ADO resulted in PV rhythm suppression in 35 (83%) PVs, with all occurring during ADO-induced bradycardia, and in PV rhythm acceleration in 13 (31%) PVs, with all occurring after resolution of ADO-induced bradycardia. In 11 PVs, both ADO-induced PV rhythm acceleration and suppression were seen. Among 220 electrically silent PVs, ADO induced PV ectopy in 28 (13%) veins. The timing of ADO-induced PV ectopy with respect to ADO effects on heart rate varied. ADO induced PV ectopy during the early phase of ADO effect only in 12 PVs, during the late phase of ADO effect only in 8 PVs, and during both early and late phases of ADO effect in 8 PVs. Conclusions— The mechanism of spontaneous PV rhythm after isolation is likely automaticity, given the close association of ADO effects on PV rhythm with its chronotropic and dromotropic effects. However, ADO can induce PV ectopy in electrically silent PVs in a manner not closely tied to its effects on heart rate and may be because of the activation of autonomic triggers.

Adenosine-Induced Atrial Fibrillation: Insights Into Mechanism

Atrial fibrillation (AF) is a potential adverse effect of intravenous administration of adenosine.1,2 Although the mechanism is not known, this phenomenon is thought to be mediated by adenosine’s effects on shortening atrial action potential duration and refractoriness. Because adenosine has little effect on atrial conduction velocity, the net effect of adenosine, therefore, is to shorten the wavelength of activation, thereby potentiating AF. On a cellular level, these effects are caused by activation of the inward rectifying K+ current I KAdo. However, adenosine has other effects that may promote arrhythmogenesis. For example, adenosine has sympathoexcitatory effects mediated through baroreflex activation and chemoreceptor stimulation. Adenosine can also hyperpolarize dormant pulmonary vein myocytes and increase excitability,3 as well as trigger pulmonary vein ectopy.4 We report on a possible alternative mechanism of adenosine-induced AF, on the basis of findings during a pulmonary vein isolation procedure. These findings may have broader implications for understanding vagally mediated AF. A 67-year-old woman with a history of hypertension, hyperlipidemia, transient ischemic attack, and symptomatic persistent AF, which was medically refractory, underwent radiofrequency catheter ablation to electrically isolate the pulmonary veins. She developed multiple episodes of paroxysmal AF after the initial procedure and 3 months later presented for a second catheter ablation procedure. An electroanatomic map of the left atrium and all 4 pulmonary veins were constructed. Interrogation of the left superior pulmonary vein with a circular mapping catheter (CMC) showed persistent entrance block with far-field signals from the left atrial appendage (confirmed by pacing the left atrial appendage with the ablation catheter). Exit block was confirmed with circumferential pacing with the CMC. Intravenous adenosine (12 mg) was administered, which resulted in AF coincident with adenosine-induced transient atrioventricular nodal block (Figure 1A). The left superior pulmonary vein remained electrically quiescent during AF. …

Differential Effects of Adenosine on Pulmonary Vein Ectopy After Pulmonary Vein IsolationClinical Perspective: Implications for Arrhythmogenesis

Background— The mechanism of pulmonary vein (PV) triggers of atrial fibrillation remains unclear. We performed adenosine (ADO) testing after PV isolation to characterize spontaneous dissociated PV rhythm and ADO-induced PV ectopy. Methods and Results— Seventy-four patients (61 men; age, 61±10 years) undergoing PV isolation for atrial fibrillation were studied. For each isolated PV, dissociated ectopy was recorded and ADO was administered. After isolation of 270 PVs, 50 PVs with dissociated ectopy were identified. In 42 PVs exhibiting PV rhythm, ADO resulted in PV rhythm suppression in 35 (83%) PVs, with all occurring during ADO-induced bradycardia, and in PV rhythm acceleration in 13 (31%) PVs, with all occurring after resolution of ADO-induced bradycardia. In 11 PVs, both ADO-induced PV rhythm acceleration and suppression were seen. Among 220 electrically silent PVs, ADO induced PV ectopy in 28 (13%) veins. The timing of ADO-induced PV ectopy with respect to ADO effects on heart rate varied. ADO induced PV ectopy during the early phase of ADO effect only in 12 PVs, during the late phase of ADO effect only in 8 PVs, and during both early and late phases of ADO effect in 8 PVs. Conclusions— The mechanism of spontaneous PV rhythm after isolation is likely automaticity, given the close association of ADO effects on PV rhythm with its chronotropic and dromotropic effects. However, ADO can induce PV ectopy in electrically silent PVs in a manner not closely tied to its effects on heart rate and may be because of the activation of autonomic triggers.

Differential Effects of Adenosine on Pulmonary Vein Ectopy After Pulmonary Vein IsolationClinical Perspective

Background— The mechanism of pulmonary vein (PV) triggers of atrial fibrillation remains unclear. We performed adenosine (ADO) testing after PV isolation to characterize spontaneous dissociated PV rhythm and ADO-induced PV ectopy. Methods and Results— Seventy-four patients (61 men; age, 61±10 years) undergoing PV isolation for atrial fibrillation were studied. For each isolated PV, dissociated ectopy was recorded and ADO was administered. After isolation of 270 PVs, 50 PVs with dissociated ectopy were identified. In 42 PVs exhibiting PV rhythm, ADO resulted in PV rhythm suppression in 35 (83%) PVs, with all occurring during ADO-induced bradycardia, and in PV rhythm acceleration in 13 (31%) PVs, with all occurring after resolution of ADO-induced bradycardia. In 11 PVs, both ADO-induced PV rhythm acceleration and suppression were seen. Among 220 electrically silent PVs, ADO induced PV ectopy in 28 (13%) veins. The timing of ADO-induced PV ectopy with respect to ADO effects on heart rate varied. ADO induced PV ectopy during the early phase of ADO effect only in 12 PVs, during the late phase of ADO effect only in 8 PVs, and during both early and late phases of ADO effect in 8 PVs. Conclusions— The mechanism of spontaneous PV rhythm after isolation is likely automaticity, given the close association of ADO effects on PV rhythm with its chronotropic and dromotropic effects. However, ADO can induce PV ectopy in electrically silent PVs in a manner not closely tied to its effects on heart rate and may be because of the activation of autonomic triggers.

Differential Effects of Adenosine on Pulmonary Vein Ectopy Following Pulmonary Vein Isolation: Implications for Arrhythmogenesis

Background— The mechanism of pulmonary vein (PV) triggers of atrial fibrillation remains unclear. We performed adenosine (ADO) testing after PV isolation to characterize spontaneous dissociated PV rhythm and ADO-induced PV ectopy. Methods and Results— Seventy-four patients (61 men; age, 61±10 years) undergoing PV isolation for atrial fibrillation were studied. For each isolated PV, dissociated ectopy was recorded and ADO was administered. After isolation of 270 PVs, 50 PVs with dissociated ectopy were identified. In 42 PVs exhibiting PV rhythm, ADO resulted in PV rhythm suppression in 35 (83%) PVs, with all occurring during ADO-induced bradycardia, and in PV rhythm acceleration in 13 (31%) PVs, with all occurring after resolution of ADO-induced bradycardia. In 11 PVs, both ADO-induced PV rhythm acceleration and suppression were seen. Among 220 electrically silent PVs, ADO induced PV ectopy in 28 (13%) veins. The timing of ADO-induced PV ectopy with respect to ADO effects on heart rate varied. ADO induced PV ectopy during the early phase of ADO effect only in 12 PVs, during the late phase of ADO effect only in 8 PVs, and during both early and late phases of ADO effect in 8 PVs. Conclusions— The mechanism of spontaneous PV rhythm after isolation is likely automaticity, given the close association of ADO effects on PV rhythm with its chronotropic and dromotropic effects. However, ADO can induce PV ectopy in electrically silent PVs in a manner not closely tied to its effects on heart rate and may be because of the activation of autonomic triggers.

MECHANISM AND LOCATION OF ADENOSINE-INDUCED PULMONARY VEIN-LEFT ATRIAL RECONNECTION FOLLOWING PULMONARY VEIN ISOLATION

Results: In 9 (30%) pts, ADO-induced PV conduction occurred in 13/106 (12%) PVs. Transient ADO-induced PV conduction was seen with 10 PVs (mean duration 14 ± 5 s) while sustained PV reconnection was seen with 3 PVs. Onset of ADO-induced PV conduction (mean 13 ± 6 s post bolus) occurred prior to sinus slowing or AV block in 7 (54%) PVs, during sinus slowing and/or AV block in 6 (46%) PVs, and in none during the sinus tachycardia phase. PV reconnection was most commonly seen at the left atrial appendage-PV ridge of the left superior PV (23% of all reconnected PVs).