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Background: No existing criteria unequivocally differentiate focal atrial tachycardia (AT) caused by microreentry, triggered activity, or enhanced automaticity. Although macroreentrant AT is readily diagnosed based on entrainment criteria, the smaller circuit dimension associated with microreentrant AT makes it challenging to validate the presence of reset with fusion. An algorithm was, therefore, developed that is independent of entrainment but which reliably identifies specific mechanisms of focal AT.Methods and Results: Fifty-nine patients with AT underwent adenosine testing after mapping of tacycardia. Ten ATs had nonfocal activation, with ≥90% of tachycardia cycle length identified with electroanatomical mapping, findings consistent with macroreenty. All ATs were insensitive to adenosine. Forty-nine patients had focal AT with centrifugal activation. In 32/49 (67%) ATs, electrograms were nonfractionated, and <50% of tachycardia cycle length could be mapped. Based on programmed stimulation, 26/32 (81%) of these ATs were classified as due to triggered activity and 6/32 (19%) as due to enhanced automaticity. Adenosine terminated 100% of triggered ATs and transiently slowed or suppressed 100% of automatic ATs. The remaining 17 focal ATs had localized fractionated electrograms (≥35% of tachycardia cycle length) at the site of successful ablation and were classified as microreentrant. Adenosine had no effect in these ATs. The response to adenosine accurately differentiated all subtypes of focal AT, P<0.05.Conclusions: Adenosine-sensitivity (termination or transient slowing/suppression) in response to adenosine was 100% sensitive and specific for identifying focal AT mechanisms due to triggered activity or automaticity, respectively. Absence of adenosine effect on focal AT identifies tachycardia due to microreentry. [ABSTRACT FROM AUTHOR]

Background: Idiopathic ventricular arrhythmias of left bundle branch block inferior axis morphology are usually localized to the right ventricular outflow tract (RVOT), presumably below the pulmonic valve (PV). However, the PV location is usually not confirmed by direct visualization. Methods and Results: Intracardiac echocardiography was used to visualize and tag the PV annulus, which was then integrated with 3-dimensional voltage maps of the RVOT. Distances were measured from the furthest extent of myocardial signal (bipolar voltage ≥1.5 mV) to the PV annulus. This was performed in 24 control patients and 24 prospective patients with RVOT arrhythmias. Myocardial signal beyond the PV was found in 92% of controls and 88% of RVOT arrhythmia patients (P=1.000). Average myocardial extension was further on the septal side than on the free wall side for control patients (5.6 mm; interquartile range [IQR], 3.6-7.7, versus 1.7 mm; IQR (-)0.1 to (+)4.0; P=0.002) and RVOT arrhythmia patients (5.7 mm; IQR, 2.7-7.7, versus 1.4 mm; IQR, (-)0.8 to (+)4.8; P=0.004). Eleven (46%) RVOT arrhythmia foci were localized beyond the valve in the pulmonary artery (median 8.2 mm above PV; IQR, 6.6-10.3 mm); these locations were confirmed as supravalvular by direct intracardiac echocardiography visualization. Conclusions: Myocardial voltage extension into the pulmonary artery in humans is ubiquitous and can be demonstrated in vivo using 3-dimensional integrated intracardiac echocardiography to localize the PV. These extensions frequently serve as origins of presumed RVOT arrhythmias; intracardiac echocardiography localization of the PV allows reclassification of these as pulmonary arterial arrhythmias. [ABSTRACT FROM AUTHOR]

The article describes atrial tachycardia (ATs) that occur after superior transseptal incision in mitral valve surgery (MVS) and proposes methods to verify lines of block as an end point for catheter ablation. Findings revealed that the optimal endpoint for ablating ATs after MVS is to establish lines of block that can be recognized by patterns of activation in the lateral right atrium (RA). Identifying late activated corridor in the RA is also a new criterion for lateral conduction block.

The article discusses a study which conducted adenosine (ADO) testing after pulmonary vein (PV) isolation to characterize spontaneous dissociated PV rhythm and ADO-induced PV ectopy. The study involved 74 patients undergoing PV isolation for atrial fibrillation (AF) and found that the mechanism of spontaneous PV rhythm after isolation is likely automaticity. ADO's ability to induce PV ectopy in electrically silent PVs in a way not closely tied to its effects on heart rate is also noted.

[Figure: see text]. [ABSTRACT FROM AUTHOR]

Background: Patients undergoing catheter ablation of myocardial infarction-associated ventricular tachycardia (VT) have significant comorbidities that can increase the risks of adverse outcomes. The rates of readmissions after VT ablation are unknown. We sought to examine in-hospital outcomes, costs, and 30-day readmissions after catheter ablation of myocardial infarction-associated VT.Methods: Using the Nationwide Readmissions Database, we evaluated 4109 admissions for catheter ablation of myocardial infarction-associated VT occurring between 2010 and 2015. On the basis of International Classification of Diseases, Ninth Revision, Clinical Modification and Clinical Classification Software codes, we identified comorbidities, procedural complications, 30-day readmissions, and costs associated with VT ablation.Results: The index admission in-hospital mortality rate and procedural complication rate after VT ablation were 2.7% and 11.5%, respectively. Independent predictors of mortality included pulmonary hypertension, lung disease, obesity, and coagulopathy. Following discharge after VT ablation, the 30-day readmission rate was 19.2% with a median time to readmission of 10.0 days (IQR, 3.8-17.6 days) and an in-hospital mortality rate of 2.9%. Cardiac causes accounted for 74% of readmissions, with VT and congestive heart failure constituting 41% and 14% of all readmissions, respectively. Pulmonary hypertension, congestive heart failure, smoking, chronic pulmonary disease, and prolonged index hospitalization were significant independent predictors of 30-day readmission. After adjustment, 30-day readmissions were associated with a 38.9% increase in cumulative hospitalization costs.Conclusions: Thirty-day readmissions after catheter ablation of VT occur in nearly 1 out of 5 cases, with the majority of readmissions being caused by recurrent VT or congestive heart failure. Baseline comorbidities are significant predictors of procedural mortality, complications, and readmissions. Strategies to reduce recurrent VT postablation by improving procedural success, optimizing postablation heart failure treatment, and ensuring close postdischarge follow-up may help reduce readmissions and healthcare costs. [ABSTRACT FROM AUTHOR]

Background: The mechanisms underlying paroxysmal atrial flutter/atrial fibrillation initiation by ectopic foci from various locations are unclear., Methods and Results: We used parallel computational techniques to study an anatomically accurate 3-dimensional atrial structure incorporating a detailed ionic-current model of an atrial myocyte. At the single-cell level, upregulation of the L-type Ca2+ current I(Ca,L) steepened restitution curves of action potential duration and conduction velocity compared with the control. Spontaneous firings of ectopic foci, coupled with sinus activity, produced dynamic spatial dispersions of repolarization, including discordant alternans, which caused conduction block and reentry only for the elevated I(Ca,L) case. For each foci location, a vulnerable window for atrial flutter/atrial fibrillation induction was identified as a function of the coupling interval and focus cycle length. For ectopic foci in the pulmonary veins and left atrium, the site of conduction block and reentry gradually shifted, as a function of coupling interval, from the right atrium to the interatrial area and finally to the left atrium. The size of the vulnerable window was largest for pulmonary vein foci, becoming markedly smaller for right atrial foci, especially those near the sinoatrial node., Conclusions: These findings suggest that a mechanism of dynamically induced repolarization dispersion, especially discordant alternans, underlies the induction of atrial flutter/atrial fibrillation by atrial ectopic foci. The sites and likelihood of reentry induction varied according to ectopic focus location and timing, with the largest vulnerable window corresponding to the pulmonary vein region.

Background: Tachycardia-induced cardiomyopathy caused by ventricular tachycardia is a well-defined clinical entity. Less well appreciated is whether simple ventricular ectopy can result in cardiomyopathy. We sought to examine a potential causal relationship between repetitive monomorphic ventricular ectopy originating from the right ventricular outflow tract and cardiomyopathy and the role of ablation in reversing this process., Methods and Results: The study consisted of 27 patients (11 men; age, 47+/-15 years) with repetitive monomorphic ventricular ectopy, including 8 patients (30%) with depressed ventricular function (ejection fraction < or =45%). All patients underwent assessment of cardiac structure and function. The burden of ectopy was quantified through 24-hour Holter monitoring. Patients then underwent ablation guided by 3D mapping. After ablation, patients underwent repeated Holter monitoring and reassessment of cardiac function. Patients with depressed ventricular function were more likely to be older than patients with normal function (58+/-14 versus 42+/-18 years; P=0.013). However, the burden of ventricular ectopy was similar in patients with (17,859+/-13,488 ectopic beats per 24 hours) and without (17,541+/-11,479 ectopic beats per 24 hours; P=0.800) preserved ventricular function. Successful ablation was performed in 23 patients (85%), including 7 of 8 patients with depressed ventricular function. In this latter group, ventricular function improved in all patients (from 39+/-6% to 62+/-6%; P=0.017)., Conclusions: Repetitive monomorphic ventricular ectopy (in the absence of sustained ventricular tachycardia) originating from the right ventricular outflow tract is an underappreciated cause of unexplained cardiomyopathy. Successful ablation of the focal source of ventricular ectopy results in normalization of left ventricular function. Patients with ectopy-induced cardiomyopathy are significantly older than patients with preserved ventricular function, which suggests either that older patients are more susceptible to the development of a cardiomyopathy or that the cardiomyopathy has had a longer period of time in which to evolve.