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Catheter ablation is an established treatment option for atrial fibrillation (AF), and pulmonary vein isolation (PVI) has become the gold standard in AF ablation. AF recurrence after PVI remains an important clinical problem. Recovery of conduction from the pulmonary veins (PVs) is considered the dominant mechanism for AF recurrence in paroxysmal AF. However, the underlying mechanism of AF recurrence after PVI is more complex in patients with persistent and longstanding persistent AF. Different ablation technologies and energy sources have been developed aimed at improving lesion quality and durability with an acceptable safety profile. Novel technologies are under evaluation which have a great potential to produce permanent PVI after a single ablation procedure. However, clinical value of these novel devices needs to be tested in adequately powered randomized controlled trials. In this article, we review the history of catheter ablation for AF and discuss the present and future ablation technologies.

[Figure][1] Cardiology in the 1960s had yet to embrace the importance of clinical cardiac electrophysiology (CCE). Supraventricular tachycardias (SVT) were usually lumped into a single undifferentiated group, most clinicians could not distinguish type I from type II second-degree AV block

Focal atrial tachycardia (AT) is characterized by atrial activation starting at a small area (focus), from which it spreads out centrifugally. “Focal” implies that the site of origin cannot be mapped spatially beyond a single point or a few adjacent points with the resolution of a standard 4-mm-tip catheter. In contrast, macroreentrant AT is defined by activation that can be recorded over the entire tachycardia cycle length around a large central obstacle, which is generally several centimeters in diameter. Relatively small reentry circuits can resemble focal AT, especially if limited numbers of endocardial recordings are collected. Available data suggest that a focal activation pattern can be caused by automaticity, triggered activity, or microreentry. Delineating the mechanism of focal AT, however, can be difficult, and the means of distinguishing focal AT mechanisms through pharmacological testing or electrophysiological (EP) study have limited sensitivity and specificity. In addition, there is a significant overlap in the EP characteristics of tachycardias with differing mechanisms. When paroxysmal, AT frequently manifests with episodes of palpitations and heart racing that start and terminate abruptly. Incessant AT can precipitate cardiomyopathy in approximately one-third of patients. Pharmacological therapy is associated with limited efficacy in the treatment of focal AT. Catheter ablation is recommended in patients with recurrent symptomatic AT, especially when pharmacological therapy is unsuccessful, not tolerated, or not preferred.

Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common form of paroxysmal supraventricular tachycardia. The exact electroanatomic circuit responsible for AVNRT remains elusive. Current evidence suggests that dual atrioventricular nodal (AVN) pathway physiology constitutes the substrate for AVN reentry. The different atrial inputs to the AVN, rather than functional longitudinal dissociation within the compact AVN, represent the fast and slow pathways involved in the reentrant circuit. AVNRT can manifest in different forms depending on the anatomic substrate forming the anterograde and retrograde pathways incorporated in the reentry circuit. Traditionally, AVNRT has been classified into “typical” or “atypical” forms. Typical AVNRT (anterograde slow-retrograde fast) accounts for 90% of AVNRTs. Atypical AVNRT variants are traditionally subclassified as either fast-slow or slow-slow types. Maintenance of AVNRT is dependent on AVN conduction; hence, maneuvers or drugs that slow AVN conduction and prolong AVN refractoriness are used to terminate the tachycardia. For chronic management of AVNRT, pharmacological therapy and catheter ablation can be considered. Long-term pharmacological therapy (including beta blockers and calcium channel blockers) can be effective in 30% to 60% of patients. On the other hand, catheter ablation is associated with higher efficacy (>95%) and low incidence of complications and therefore has become the preferred initial therapeutic approach. The slow pathway is the target of ablation for all variants of AVNRT. Initially, the rightward inferior AVN extension is targeted. Then, the leftward inferior AVN extension is targeted if needed.

Arrhythmogenic right ventricular cardiomyopathy (ARVC), also referred to as “arrhythmogenic cardiomyopathy,” is an inherited desmosomal cardiomyopathy with incomplete penetrance and variable expressivity. ARVC is char­acterized by ventricular arrhythmias and structural abnormalities of the right ventricle. The hallmark pathological findings are progressive myocyte loss and fibrofatty (fibrous and adipose) tis­sue replacement, with a predilection for the right ventricle, but the left ventricle also can be affected. Fibrofatty replacement of the myocardium produces “islands” of scar that can lead to reentrant ventricular tachycardias (VTs) and increased risk of sudden cardiac death. The clinical presentation varies widely because ARVC includes a spectrum of different conditions rather than a single entity. Four clinicopathological stages of ARVC can be considered: (1) “concealed” phase, (2) “overt electrical disorder,” (3) phase of “right ventricular failure,” and (4) phase of “biventricular failure.” ARVC is one of the most arrhythmogenic human heart diseases known. Electrical instability is present at the very early stages of ARVC; ventricular arrhythmias and sudden death often are presenting symptoms before the development of any overt myocardial dysfunction. Ventricular arrhythmias range from isolated ectopy to sus­tained VT or ventricular fibrillation, and characteris­tically they occur during exercise. At present, catheter ablation of VT is considered palliative rather than curative and is recommended mainly for patients with recurrent VT causing frequent defibrillator shocks and those with VT storm or incessant VT refractory to antiarrhythmic drug therapy.

A “supraventricular” origin of a tachycardia implies the obligatory involvement of one or more cardiac structures above the bifurcation of the His bundle (HB), including atrial myocardium, atrioventricular node (AVN), proximal HB, coronary sinus, pulmonary veins, venae cavae, or abnormal atrioventricular (AV) connections other than the HB (i.e., bypass tracts). Narrow complex supraventricular tachycardias (SVTs) include sinus tachycardia, inappropriate sinus tachycardia, sinoatrial nodal reentrant tachycardia, focal atrial tachycardia (AT), multifocal AT, atrial fibrillation (AF), atrial flutter (AFL), junctional tachycardia, AVN reentrant tachycardia (AVNRT), and AV reentrant tachycardia (AVRT). Paroxysmal SVT is the term generally applied to intermittent SVT other than AF, AFL, and multifocal AT, and describes a clinical syndrome characterized by the presence of a regular and rapid tachycardia of abrupt onset and termination. The major causes are AVNRT (approximately 50% to 60% of cases), AVRT (approximately 30% of cases), and focal AT (approximately 10% of cases). Most paroxysmal SVTs are generally benign and do not influence survival; therefore the primary indication for treatment is to alleviate symptoms and improve quality of life. The threshold for initiation of therapy and the decision to treat SVT with oral pharmacological therapy or catheter ablation depends on the frequency and duration of the arrhythmia, severity of symptoms, presence of concomitant structural heart disease, and patient preference. Given the high success rates and the low complication rate, catheter ablation is the treatment of choice in patients who desire to avoid or are unresponsive or intolerant to drug therapy.

Bypass tracts (BTs) are remnants of the atrioventricular (AV) concaused by incomplete embryological development of the AV annuli and failure of the fibrous separation between the atria and ventricles. There are several types of BTs, according to the structures they connect, including atrioventricular, atrionodal, atrio-Hisian, atriofascicular, fasciculoventricular, and nodofascicular BTs. In the Wolff-Parkinson-White (WPW) syndrome, AV conduction occurs, partially or entirely, through an AV BT, which results in earlier activation (preexcitation) of the ventricles than if the impulse had traveled through the AVN. Concealed AV BTs refer to AV BTs that conduct only in the retrograde direction and therefore do not result in ventricular preexcitation. AV reentrant tachycardia (AVRT) is a macroreentrant tachycardia with an anatomically defined circuit that consists of two distinct pathways, the normal AV conduction system and an AV BT, linked by common proximal (atrial) and distal (ventricular) tissues. Atrial tachycardia, atrial fibrillation, and AV nodal reentrant tachycardia can all coexist with a BT, whereby the BT serves as a bystander route for venor atrial activation. The prevalence of WPW pattern on the surface ECG is 0.1% to 0.3% in the general population. The prevalence of the WPW syndrome (i.e., the combination of ventricular preexcitation and either a documented tachyarrhythmia or symptoms of a tachyarrhythmia) is substantially lower than that of the WPW ECG pattern. Catheter ablation is considered the treatment of choice for patients with the WPW syndrome. Catheter ablation is curative in more than 95% of patients with a relatively low complication rate.

The autonomic nervous system regulates all aspects of normal cardiac function, and is recognized to play a critical role in the pathophysiology of many cardiovascular diseases. As such, the value of neuroscience-based cardiovascular therapeutics is increasingly evident. This White Paper reviews the current state of understanding of human cardiac neuroanatomy, neurophysiology, pathophysiology in specific disease conditions, autonomic testing, risk stratification, and neuromodulatory strategies to mitigate the progression of cardiovascular diseases.

Objectives The primary objective of the study was a change in left ventricular end-systolic volume index (LVESVi) from baseline to 6 months of spinal cord stimulation (SCS) therapy in the treatment arm compared to the control arm as measured by echocardiography. Secondary objectives were changes in peak oxygen uptake and N-terminal pro–B-type natriuretic peptide (NT-proBNP) between the treatment arm and control arm from baseline through 6 months. Background Abnormal neurohormonal activation is often responsible for progression of heart failure (HF). Treatment has often included drug therapy to modulate the neurohormonal axis. The purpose of the DEFEAT-HF (Determining the Feasibility of Spinal Cord Neuromodulation for the Treatment of Chronic Heart Failure) clinical study was to evaluate whether direct modulation of the nervous system through SCS improved HF metrics, including heart size, biomarkers, functional capacity, and symptoms. Methods The DEFEAT-HF study was a prospective, multicenter randomized (3:2), parallel, single-blind, controlled study to investigate whether SCS was a feasible therapy for the treatment of systolic HF for patients with New York Heart Association functional class III HF, left ventricular ejection fraction (LVEF) ≤35%, QRS duration Results In total, 81 patients were enrolled, with 66 successfully randomized and implanted with the SCS device system. Seventy-six percent (50 of 66) had an implantable cardioverter-defibrillator at the baseline visit. Among randomized patients, the mean age was 61 years, 79% were male, mean LVEF was 27%, and mean QRS duration was 105 ms. The change in LVESVi over 6 months was not significantly different between randomization arms (SCS OFF: –2.2 [95% confidence interval: –9.1 to 4.6] vs. SCS ON: 2.1 [95% confidence interval: –2.7 to 6.9]; p = 0.30). Analyses of secondary endpoints for the study were also not significantly different. Conclusions The present study does not provide evidence to support a meaningful change in clinical outcomes for HF patients receiving SCS. (Determining the Feasibility of Spinal Cord Neuromodulation for the Treatment of Chronic Heart Failure [DEFEAT-HF]; NCT01112579 )

Eric S. Williams, MD, MACC, Chair Jonathan L. Halperin, MD, FACC, Co-Chair James A. Arrighi, MD, FACC Eric H. Awtry, MD, FACC Eric R. Bates, MD, FACC John E. Brush, Jr, MD, FACC Salvatore Costa, MD, FACC Lori Daniels, MD, MAS, FACC Akshay Desai, MD, FACC[‡][1] Douglas E. Drachman, MD

Background—The risks of sports participation for implantable cardioverter-defibrillator (ICD) patients are unknown. Methods and Results—Athletes with ICDs (age, 10–60 years) participating in organized (n=328) or high-risk (n=44) sports were recruited. Sports-related and clinical data were obtained by phone interview and medical records. Follow-up occurred every 6 months. ICD shock data and clinical outcomes were adjudicated by 2 electrophysiologists. Median age was 33 years (89 subjects

The US Department of Justice (DOJ) conducted an investigation into implantable cardioverter-defibrillators (ICDs) not meeting the Centers for MedicareMedicaid Services National Coverage Determination (NCD) criteria.To examine changes in the proportion of initial primary prevention ICDs that did not meet NCD criteria following the announcement of the DOJ investigation at hospitals that reached settlements (settlement hospitals) and those that did not (nonsettlement hospitals).Multicenter, longitudinal, serial cross-sectional analysis of 300 151 initial primary prevention ICDs among Medicare beneficiaries from January 1, 2007, through December 31, 2015, at 1809 US hospitals in the National Cardiovascular Data Registry (NCDR) ICD Registry, of which 452 hospitals (with 99 591 primary prevention ICDs) reached settlements with the DOJ.The DOJ investigation announcement in 2010.Proportion of initial primary prevention ICDs not meeting NCD criteria.In January 2007, the proportion of initial ICDs not meeting NCD criteria was 25.8% (95% CI, 24.7% to 26.8%) at settlement hospitals and 22.8% (95% CI, 22.1% to 23.5%) at nonsettlement hospitals (P .001). Over the study period, there was a 62.7% (95% CI, 59.2% to 66.1%) relative decrease and 16.1% (95% CI, 14.8% to 17.5%) absolute decrease in the proportion of ICDs not meeting NCD criteria at settlement hospitals compared with a 53.2% (95% CI, 50.4% to 56.0%) relative decrease and 12.1% (95% CI, 11.2% to 13.0%) absolute decrease in proportion at nonsettlement hospitals (P .001 for both; P for interaction .001). Trends significantly differed between hospital groups only in the period following the announcement of the DOJ investigation (January 2010-June 2011) [corrected], with larger and more rapid decreases at settlement hospitals (P for interaction = .01). Over the study period, there was a 32.8% (95% CI, 29.9% to 35.7%) relative decrease and a 1703 ICDs (95% CI, 1520 to 1886) absolute decrease in the volume of primary prevention ICDs implanted at settlement hospitals compared with a 17.4% (95% CI, 14.8% to 20.0%) relative decrease and a 1495 ICDs (95% CI, 1249 to 1741) absolute decrease in volume at nonsettlement hospitals (P .001 for both; P for interaction .001), with more modest decreases or slight increases in secondary prevention ICD volume. These patterns were similar when examining ICD utilization among non-Medicare beneficiaries.From 2007 through 2015, the volume of primary prevention implantable cardioverter-defibrillators and the proportion of devices not meeting the Centers for MedicareMedicaid Services National Coverage Determination criteria decreased at all hospitals with substantially larger decreases at hospitals that reached settlements in the US Department of Justice investigation. These patterns extended to implantable cardioverter-defibrillators placed in non-Medicare beneficiaries, which were not the focus of the US Department of Justice investigation.

Professional society recommendations to decrease sudden cardiac death in athletes, including eligibility requirements with disqualification for athletes with diagnosed disease as well as preparticipation screening and emergency preparedness, were updated in 2015. The update includes new sections on aortic disease, channelopathies, and sickle cell trait, as well as a change in format from the previous binary yes/no format to the more nuanced and contemporary “class and level of evidence” format. Eighty-four of the 246 recommendations now carry Class II designation—“reasonable,” or “may be considered.” New language in the document emphasizes counseling as part of the decision process. New data on athletes with implantable cardioverter-defibrillators, and on those with long QT syndrome, have led to a change from blanket restriction of competitive sports participation to a Class IIB “may be considered” recommendation.