Seth Lessner

Catheter ablation of postinfarction ventricular tachycardia: Ten-year trends in utilization, in-hospital complications, and in-hospital mortality in the United States

BACKGROUND There is a paucity of data regarding the complications and in-hospital mortality after catheter ablation for ventricular tachycardia (VT) in patients with ischemic heart disease. OBJECTIVE The purpose of this study was to determine the temporal trends in utilization, in-hospital mortality, and complications of catheter ablation of postinfarction VT in the United States. METHODS We used the 2002-2011 Nationwide Inpatient Sample (NIS) database to identify all patients ≥18 years of age with a primary diagnosis of VT (International Classification of Diseases, Ninth Edition, Clinical Modification [ICD-9-CM] code 427.1) and who also had a secondary diagnosis of prior history of myocardial infarction (ICD-9-CM 412). Patients with supraventricular arrhythmias were excluded. Patients who underwent catheter ablation were identified using ICD-9-CM procedure code 37.34. Temporal trends in catheter ablation, in-hospital complications, and in-hospital mortality were analyzed. RESULTS Of 81,539 patients with postinfarct VT, 4653 (5.7%) underwent catheter ablation. Utilization of catheter ablation increased significantly from 2.8% in 2002 to 10.8% in 2011 (Ptrend < .001). The overall rate of any in-hospital complication was 11.2% (523/4653), with vascular complications in 6.9%, cardiac in 4.3%, and neurologic in 0.5%. In-hospital mortality was 1.6% (75/4653). From 2002 to 2011, there was no significant change in the overall complication rates (8.4% to 10.2%, Ptrend = .101; adjusted odds ratio [per year] 1.02, 95% confidence interval 0.98-1.06) or in-hospital mortality (1.3% to 1.8%, Ptrend = .266; adjusted odds ratio [per year] 1.03, 95% confidence interval 0.92-1.15). CONCLUSION The utilization rate of catheter ablation as therapy for postinfarct VT has steadily increased over the past decade. However, procedural complication rates and in-hospital mortality have not changed significantly during this period.

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.

Method for differentiating left superior pulmonary vein exit conduction from pseudo-exit conduction.

Electrical isolation of pulmonary vein (PV) conduction from the left atrium (LA) is the cornerstone of successful atrial fibrillation (AF) ablation. Exit block is confirmed by the absence of LA capture during pacing from a circular mapping catheter positioned in the PV; however, far‐field capture of the left atrial appendage (LAA) (pseudo‐pulmonary vein exit conduction) can occur. In this study, we evaluated a methodology for identifying pseudo‐exit conduction.

CATHETER ABLATION OF VENTRICULAR TACHYCARDIA: TEN-YEAR TRENDS IN UTILIZATION, IN-HOSPITAL COMPLICATIONS, AND IN-HOSPITAL MORTALITY IN PATIENTS WITH ISCHEMIC CARDIOMYOPATHY

Catheter ablation has been used to treat incessant ventricular tachycardia (VT) and also to prevent or reduce the frequency of episodes of VT in patients with ischemic cardiomyopathy. However, there are limited data regarding the complications and in-hospital mortality after catheter ablation for

GENDER AND RACIAL/ETHNIC DIFFERENCES IN SURVIVAL AFTER CARDIOPULMONARY RESUSCITATION FOR IN-HOSPITAL CARDIAC ARREST

Data on gender and racial/ethnic differences in survival to hospital discharge after in-hospital cardiac arrest (IHCA) are limited. We used the 2003-2011 Nationwide Inpatient Sample databases to identify all patients aged ≥18 years who underwent cardiopulmonary resuscitation (CPR) (International

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.