The emerging role of cardiac contractility modulation in heart failure treatment.

PURPOSE OF REVIEW: Heart failure often progresses despite optimal medical and device therapies, and advanced mechanical circulatory support has limited availability and substantial associated morbidity. Cardiac contractility modulation (CCM) provides nonexcitatory stimulation to ventricular myocardium which increases cardiac contractility without increasing oxygen demand. This review describes the emerging role of CCM in heart failure treatment. RECENT FINDINGS: The FIX-HF-5C2 study demonstrated similar safety and efficacy profile of the two-lead Optimizer device in comparison with the prior three-lead system, thereby decreasing procedural complexity and minimizing endocardial hardware. The FIX-HF-5C trial underscored the benefit of CCM in patients with mild-moderate left ventricular dysfunction (ejection fraction, 25-45%) with New York Heart Association (NYHA) Class III symptoms. The summarized randomized trial data show consistent improvements in peak VO2, 6-min walk distance, and NYHA functional class with CCM. Future trials are planned to determine the role of CCM in heart failure patients with preserved ejection fraction, obligate ventricular pacing, and atrial arrhythmias. SUMMARY: Nonexcitatory extracellular electric potentials can facilitate inotropic improvements in the failing heart. The mechanism of CCM does not increase myocardial oxygen consumption and has been shown to mitigate heart failure symptoms, decrease hospitalizations, and work in synergy with guideline-directed therapy for heart failure.

Progression of infarct-mediated arrhythmogenesis in a rodent model of heart failure.

Heart failure (HF) post-myocardial infarction (MI) presents with increased vulnerability to monomorphic ventricular tachycardia (mmVT). To appropriately evaluate new therapies for infarct-mediated reentrant arrhythmia in the preclinical setting, chronologic characterization of the preclinical animal model pathophysiology is critical. This study aimed to evaluate the rigor and reproducibility of mmVT incidence in a rodent model of HF. We hypothesize a progressive increase in the incidence of mmVT as the duration of HF increases. Adult male Sprague-Dawley rats underwent permanent left coronary artery ligation or SHAM surgery and were maintained for either 6 or 10 wk. At end point, SHAM and HF rats underwent echocardiographic and invasive hemodynamic evaluation. Finally, rats underwent electrophysiologic (EP) assessment to assess susceptibility to mmVT and define ventricular effective refractory period (ERP). In 6-wk HF rats (n = 20), left ventricular (LV) ejection fraction (EF) decreased (P < 0.05) and LV end-diastolic pressure (EDP) increased (P < 0.05) compared with SHAM (n = 10). Ten-week HF (n = 12) revealed maintenance of LVEF and LVEDP (P > 0.05), (P > 0.05). Electrophysiology studies revealed an increase in incidence of mmVT between SHAM and 6-wk HF (P = 0.0016) and ERP prolongation (P = 0.0186). The incidence of mmVT and ventricular ERP did not differ between 6- and 10-wk HF (P = 1.0000), (P = 0.9831). Findings from this rodent model of HF suggest that once the ischemia-mediated infarct stabilizes, proarrhythmic deterioration ceases. Within the 6- and 10-wk period post-MI, no echocardiographic, invasive hemodynamic, or electrophysiologic changes were observed, suggesting stable HF. This is the necessary context for the evaluation of experimental therapies in rodent HF.NEW & NOTEWORTHY Rodent model of ischemic cardiomyopathy exhibits a plateau of inducible monomorphic ventricular tachycardia incidence between 6 and 10 wk postinfarction.

Non-Concordance between Patient and Clinician Estimates of Prognosis in Advanced Heart Failure.

IMPORTANCE: Despite efforts to enhance serious illness communication, patients with advanced heart failure (HF) lack prognostic understanding. OBJECTIVES: To determine rate of concordance between HF patients' estimation of their prognosis and their physician's estimate of the patient's prognosis, and to compare patient characteristics associated with concordance. DESIGN: Cross-sectional analysis of a cluster randomized controlled trial with 24-month follow-up and analysis completed on 09/01/2020. Patients were enrolled in inpatient and outpatient settings between September 2011 to February 2016 and data collection continued until the last quarter of 2017. SETTING: Six teaching hospitals in the U.S. PARTICIPANTS: Patients with advanced HF and implantable cardioverter defibrillators (ICDs) at high risk of death. Of 537 patients in the parent study, 407 had complete data for this analysis. INTERVENTION: A multi-component communication intervention on conversations between HF clinicians and their patients regarding ICD deactivation and advance care planning. MAIN OUTCOME(S) AND MEASURE(S): Patient self-report of prognosis and physician response to the "surprise question" of 12-month prognosis. Patient-physician prognostic concordance (PPPC) measured in percentage agreement and kappa. Bivariate analyses of characteristics of patients with and without PPPC. RESULTS: Among 407 patients (mean age 62.1 years, 29.5% female, 42.4% non-white), 300 (73.7%) dyads had non-PPPC; of which 252 (84.0%) reported a prognosis >1 year when their physician estimated <1 year. Only 107 (26.3%) had PPPC with prognosis of ≤ 1 year (n=20 patients) or > 1 year (n=87 patients); (Κ = -0.20, p = 1.0). Of those with physician estimated prognosis of < 1 year, non-PPPC was more likely among patients with lower symptom burden- number and severity (both p ≤.001), without completed advance directive (p=.001). Among those with physician prognosis estimate > 1 year, no patient characteristic was associated with PPPC or non-PPPC. CONCLUSIONS AND RELEVANCE: Non-PPPC between HF patients and their physicians is high. HF patients are more optimistic than clinicians in estimating life expectancy. These data demonstrate there are opportunities to improve the quality of prognosis disclosure between patients with advanced HF and their physicians. Interventions to improve PPPC might include serious illness communication training.

Percutaneous cryoablation for papillary muscle ventricular arrhythmias after failed radiofrequency catheter ablation.

BACKGROUND: Catheter ablation of ventricular arrhythmias (VA) from the papillary muscles (PM) is challenging due to limited catheter stability and contact on the PMs with their anatomic complexity and mobility. OBJECTIVE: This study aimed to evaluate the effectiveness of cryoablation as an adjunctive therapy for PM VAs when radiofrequency (RF) ablation has failed. METHODS: We evaluated a retrospective series of patients who underwent cryoablation for PM VAs when RF ablation had failed. The decision to switch to cryoablation was at the operator's discretion when intracardiac echocardiography (ICE) suggested that cryoablation might be more effective in achieving catheter stability and energy delivery. RESULTS: Sixteen patients underwent cryoablation of PM VAs between 2014 and 2016 after RF ablation was unsuccessful. VAs originated from the anterolateral left ventricle (LV) PM (six patients), posterolateral LV PM (six patients), and right ventricle PM (four patients). VAs were predominantly frequent premature ventricular complexes (PVCs); however, patients with sustained ventricular tachycardia and PVC-triggered VF were also represented. Fifteen of the 16 patients were treated with cryoablation; in one patient, a procedural complication with retrograde aortic access precluded treatment. In all patients treated with cryoablation, contact and stability was confirmed with ICE to be superior to the RF catheter, and there was acute and long-term elimination of VAs. CONCLUSION: Cryoablation is a useful adjunctive therapy in ablation of PM VAs, providing excellent procedural outcomes even when RF ablation has failed. Cryoablation catheters are less maneuverable than RF ablation catheters and care is required to avoid complications.

Long-term outcome of surgical cryoablation for refractory ventricular tachycardia in patients with non-ischemic cardiomyopathy.

Aims: Limited data exist on the long-term outcome of patients (pts) with non-ischemic cardiomyopathy (NICM) and ventricular tachycardia (VT) refractory to conventional therapies undergoing surgical ablation (SA). We aimed to investigate the long-term survival and VT recurrence in NICM pts with VT refractory to radiofrequency catheter ablation (RFCA) who underwent SA. Methods and results: Consecutive pts with NICM and VT refractory to RFCA who underwent SA were included. VT substrate was characterized in the electrophysiology lab and targeted by RFCA. During SA, previous RFCA lesions/scars were identified and targeted with cryoablation (CA; 3 min/lesion; target -150 °C). Follow-up comprised office visits, ICD interrogations and the social security death index. Twenty consecutive patients with NICM who underwent SA (age 53 ± 16 years, 18 males, LVEF 41 ± 20%; dilated CM = 9, arrhythmogenic right ventricular CM = 3, hypertrophic CM = 2, valvular CM = 4, and mixed CM = 2) were studied. Percutaneous mapping/ablation in the electrophysiology lab was performed in 18 and 2 pts had primary SA. During surgery, 4.9 ± 4.0 CA lesions/pt were delivered to the endocardium (2) and epicardium (11) or both (7). VT-free survival was 72.5% at 1 year and over 43 ± 31 months (mos) (range 1-83mos), there was only one arrhythmia-related death. There was a significant reduction in ICD shocks in the 3-mos preceding SA vs. the entire follow-up period (6.6 ± 4.9 vs. 2.3 ± 4.3 shocks/pt, P = 0.001). Conclusion: In select pts with NICM and VT refractory to RFCA, SA guided by pre-operative electrophysiological mapping and ablation may be a therapeutic option.

Diagnostic yield of asymptomatic arrhythmias detected by mobile cardiac outpatient telemetry and autotrigger looping event cardiac monitors.

INTRODUCTION: Asymptomatic arrhythmias can have important therapeutic implications in certain patient populations, for example, atrial fibrillation in patients with prior ischemic stroke. We sought to compare the diagnostic yield of two commercially available monitoring systems with automated arrhythmia detection algorithms. METHODS: We queried a large, proprietary database containing rhythm data for patients receiving ambulatory EKG monitoring (BioTelemetry, Malvern, PA, USA). We compared all patients prescribed mobile cardiac outpatient telemetry (MCOT™, Braemar Manufacturing, LLC, Eagan, MN, USA) versus autotrigger looping event recorder (AT-LER) devices over a consecutive 8-month period. Data from both device types were analyzed for diagnostic yields in detecting asymptomatic (device-triggered) arrhythmias consisting of atrial fibrillation (of any detected duration), bradycardia (ventricular rate ≤ 40 bpm), ventricular pause (≥ 3 seconds), supraventricular tachycardia (≥ 6 consecutive supraventricular beats), and ventricular tachycardia (≥ 4 consecutive premature ventricular contractions). The mean time to first diagnosis of each arrhythmia for each device was determined. Physician-designated diagnostic codes for patients prescribed each device were also determined from the database. RESULTS: The MCOT™ device had significantly higher diagnostic yields of all evaluated asymptomatic arrhythmias than the AT-LER. The MCOT™ device also produced an earlier mean time to diagnosis for all evaluated asymptomatic arrhythmias. These findings were noted despite a shorter average prescription length for MCOT™ monitored patients. CONCLUSIONS: In patients with conventional diagnostic monitoring indications, MCOT™ had significantly higher diagnostic yields for five asymptomatic arrhythmias compared to the AT-LER.

Outcomes of Catheter Ablation of Idiopathic Outflow Tract Ventricular Arrhythmias With an R Wave Pattern Break in Lead V2: A Distinct Clinical Entity.

INTRODUCTION: In outflow tract ventricular arrhythmias (OT-VAs), an abrupt loss of the R wave in lead V2 compared to V1 and V3 (pattern break in V2-PBV2) suggests an origin close to the anterior interventricular sulcus (anatomically opposite to lead V2) and adjacent to proximal coronaries. We studied the outcome of catheter ablation of OT-VAs with a PBV2. METHODS AND RESULTS: Of 130 consecutive patients with idiopathic left bundle block morphology OT-VAs and transition ≤V4, 12 (9%) had PBV2. Outcomes in this group were compared to the remaining 118 patients. Patients with PBV2 were more likely to be younger (41 ± 18 vs. 50 ± 14 years, P = 0.0384) and women (11 [92%] vs. 70 [59%], P = 0.0302). The earliest activation was at the RVOT in seven, left coronary cusp (LCC) in one, anterior interventricular vein (AIV) in two and the epicardium in two. In five (42%) cases (earliest activation in the AIV in two, epicardium in two, and RVOT below the valve level in one), ablation was aborted due to proximity to the left anterior descending (LAD) coronary artery. After 36 ± 17 months and 1.3 ± 0.5 procedures, VAs elimination was achieved in 58% of patients with PBV2 compared to 89% of the reference population (P = 0.0125) with effective site in five of seven at the most anterior and leftward RVOT adjacent to the pulmonic valve (PV). CONCLUSIONS: OT-VAs with PBV2 demonstrate a unique ECG pattern and challenging catheter ablation. Proximity to LAD precludes ablation in about half. Long-term VA suppression could be achieved in only 58% of cases most commonly when the earliest site is at the anterior and leftward RVOT just under the PV.

Predictors of finding occult atrial fibrillation after cryptogenic stroke.

BACKGROUND AND PURPOSE: Occult paroxysmal atrial fibrillation (AF) is found in a substantial minority of patients with cryptogenic stroke. Identifying reliable predictors of paroxysmal AF after cryptogenic stroke would allow clinicians to more effectively use outpatient cardiac monitoring and ultimately reduce secondary stroke burden. METHODS: We analyzed a retrospective cohort of consecutive patients who underwent 28-day mobile cardiac outpatient telemetry after cryptogenic stroke or transient ischemic stroke. Univariate and multivariable analyses were performed to identify clinical, echocardiographic, and radiographic features associated with the detection of paroxysmal AF. RESULTS: Of 227 patients with cryptogenic stroke (179) or transient ischemic stroke (48), 14% (95% confidence interval, 9%-18%) had AF detected on mobile cardiac outpatient telemetry, 58% of which was ≥30 seconds in duration. Age >60 years (odds ratio, 3.7; 95% confidence interval, 1.3-11) and prior cortical or cerebellar infarction seen on neuroimaging (odds ratio, 3.0; 95% confidence interval, 1.2-7.6) were independent predictors of AF. AF was detected in 33% of patients with both factors, but only 4% of patients with neither. No other clinical features (including demographics, CHA2DS2-VASc [combined stroke risk score: congestive heart failure, hypertension, age, diabetes, prior stroke/transient ischemic attack, vascular disease, sex] score, or stroke symptoms), echocardiographic findings (including left atrial size or ejection fraction), or radiographic characteristics of the acute infarction (including location, topology, or number) were associated with AF detection. CONCLUSIONS: Mobile cardiac outpatient telemetry detects AF in a substantial proportion of cryptogenic stroke patients. Age >60 years and radiographic evidence of prior cortical or cerebellar infarction are robust indicators of occult AF. Patients with neither had a low prevalence of AF.

Provocation of atrial fibrillation triggers during ablation: does the use of general anesthesia affect inducibility?

INTRODUCTION: The autonomic nervous system exerts important effects upon atrial fibrillation (AF) initiation. The strategy of anesthesia used during AF ablation may impact the provocation of AF triggers. We hypothesized that the use of general anesthesia (GA) would reduce the incidence of provokable AF triggers in patients undergoing AF ablation compared to patients studied while receiving only conscious sedation (CS). METHODS AND RESULTS: We performed a prospective, case control study comparing the incidence of provokable AF triggers in a consecutive series of patients undergoing AF ablation under GA using a standard trigger induction protocol. We compared the frequency and distribution of AF triggers to a second cohort of historical controls (matched for age, gender, left atrial dimension, and AF phenotype) who underwent ablation while receiving CS. We calculated that 44 total subjects (22 patients in each group) were required to detect a 50% reduction in the incidence of AF triggers in the GA cohort. There was no difference between the 2 groups in the rate of AF trigger inducibility (77% vs. 68%, P = 0.26) or the number of triggers provoked per patient (1.2 ± 0.8 vs. 1.3 ± 0.8, P = 0.38). Patients ablated under GA required higher doses of phenylephrine during the trigger induction protocol (408.3 mg [52-600] vs. 158.3 mg [0-75]; P = 0.003), and tended to require higher doses of isoproterenol to initiate triggers (92.8 mg [20-111] vs. 63.6 mg [6-103]; P = 0.25). CONCLUSION: AF trigger induction during GA is both safe and efficacious.

Electrophysiologic findings and long-term outcomes in patients undergoing third or more catheter ablation procedures for atrial fibrillation.

INTRODUCTION: Pulmonary vein (PV) status, arrhythmia sources, and outcomes with ≥3 ablation procedures have not been characterized. METHODS AND RESULTS: All patients with ≥3 procedures were included and underwent antral reisolation of reconnected PVs and ablation of non-PV triggers. Of 2,886 patients who underwent PVI, 181 (6%) had more than 2 ablation procedures (3 procedures in 146 and ≥4 procedures in 35). In 12 patients, the clinical arrhythmia was other than AF. Of the remaining 169 patients, 69 (41%) had 4 reconnected PVs, 27 (16%) had 3, 31 (18%) had 2, and 29 (17%) had 1. Only 13 (8%) had all PVs still isolated. Provocative techniques in 127 patients initiated PV triggers in 92 patients, including AF or PV atrial tachycardia in 64 (50%), and reproducible PV APDs in 28 (22%). Thirty-six (20%) had a new non-PV trigger targeted. At a mean of 36 months (12-119 months) after last procedure, 63 patients (47%) had no AF off antiarrhythmic drugs (AAD); 28 (21%) had no AF with AAD; and 18 (13%) had rare AF with good symptom control; 26 patients (19%) had recurrent AF. CONCLUSIONS: At time of third or greater AF ablation, PV reconnection is the rule (92%) and PV triggers initiating AF can be demonstrated. Following repeat PVI and targeting non-PV triggers, 81% of patients had clinical AF control. Our findings suggest that PV reisolation and attempts to identify and eliminate non-PV triggers are effective and support the role of multiple repeat procedures for AF recurrence.

Risk of stroke or transient ischemic attack after atrial fibrillation ablation with oral anticoagulant use guided by ECG monitoring and pulse assessment.

INTRODUCTION: We sought to gain insight into stroke risk after atrial fibrillation (AF) ablation. METHODS AND RESULTS: We followed 1,990 patients for >1 year (49 ± 29 months) who underwent AF ablation. Prior to stopping oral anticoagulants (OAC), we performed 3-week transtelephonic ECG monitoring (TTM) and taught patients heart rate and pulse assessment. Documented AF or inability to do monitoring or assess pulse precluded stopping OAC in CHADS2 ≥1 patients. OAC was stopped in 546/840 (65%) with CHADS2  = 0; 384/796 (48%) with CHADS2  = 1 and 101/354 (40%) with CHADS2 ≥ 2. Sixteen strokes or TIAs occurred (0.2%/patient-year); 5 in CHADS2  = 0 patients (all off OAC); 5 in CHADS2  = 1 (1 off and 4 on OAC); and 6 in CHADS2 ≥2 (2 off and 4 on OAC). Twelve of 16 patients (75%) with stroke or TIA had documented AF. In patients "off " OAC, stroke rate/year stratified by the CHADS2 score was similar (CHADS2  = 0: 0.28%; CHADS2  = 1: 0.07%; CHADS2 ≥2: 0.50%; P = NS). There was no difference in stroke risk "on" versus "off " OAC in CHADS2  = 1 (0.48% vs. 0.07%) or CHADS2 ≥2 (0.39% vs. 0.50%). Risk of major bleeding per patient year "on" OAC was > "off " OAC (13/1,138 (1.14%) versus 1/832 (0.1%); P<0.016). CONCLUSIONS: Post-AF ablation with OAC guided by TTM and pulse assessment: (1) Overall stroke or TIA rate risk is low and risk is due to recurrent AF and (2) OAC can be stopped in 40% of CHADS2 ≥2 patients with low stroke and hemorrhagic risk.

Unipolar voltage abnormality is associated with greater left ventricular dysfunction in ischemic cardiomyopathy.

INTRODUCTION: Following myocardial infarction (MI), left ventricular function is determined by cardiac remodeling occurring in both infarcted and noninfarcted myocardium (NIM). Unipolar voltage mapping may detect remodeling changes in NIM that are associated with the left ventricular ejection fraction (LVEF). We aimed to identify (1) unipolar voltage characteristics in patients with chronic MI, and (2) association of voltage abnormalities with degree of left ventricular dysfunction (LVD). METHODS AND RESULTS: Two groups of patients with ischemic cardiomyopathy (ICM) who underwent LV endocardial mapping during catheter ablation for ventricular tachycardia (VT) between January 2010 and December 2012 were studied. The first group (19 males) had mild to moderate LVD (M-LVD, LVEF >35%) and was matched for age, sex, infarction size, and infarction location with 10 males who had severe LVD (S-LVD, LVEF <35%). Both bipolar and unipolar endocardial abnormal voltage areas were measured and compared between groups. Abnormal bipolar area was comparable in both groups (30 ± 8% in the S-LVD group vs 28 ± 8% in the M-LVD group; P = 0.5). Total abnormal unipolar voltage area was significantly larger in the S-LVD group (57 ± 14% vs 43 ± 13%; P = 0.02). The abnormal unipolar voltage area within the normal bipolar voltage area was greater in the S-LVD group (26 ± 11% vs 15 ± 16%; P = 0.03). In receiver operating characteristic curve analysis, an 18.0% cut-off value for abnormal unipolar area within NIM identified severe LVD, with 90% sensitivity and 79% specificity (area under the curve 0.821). CONCLUSIONS: Patients with ICM and severe LVD have larger areas of unipolar voltage abnormality in the noninfarcted tissue than patients with M-LVD.

Cardiac blood vessels and irreversible electroporation: findings from pulsed field ablation.

The clinical use of irreversible electroporation in invasive cardiac laboratories, termed pulsed field ablation (PFA), is gaining early enthusiasm among electrophysiologists for the management of both atrial and ventricular arrhythmogenic substrates. Though electroporation is regularly employed in other branches of science and medicine, concerns regarding the acute and permanent vascular effects of PFA remain. This comprehensive review aims to summarize the preclinical and adult clinical data published to date on PFA's effects on pulmonary veins and coronary arteries. These data will be contrasted with the incidences of iatrogenic pulmonary vein stenosis and coronary artery injury secondary to thermal cardiac ablation modalities, namely radiofrequency energy, laser energy, and liquid nitrogen-based cryoablation.

An organized approach to the localization, mapping, and ablation of outflow tract ventricular arrhythmias.

The outflow tract (OT) regions of the right and left ventricles, common sites of origin for idiopathic ventricular arrhythmias (VA), have complex three-dimensional anatomical relationships. The understanding of in situ or "attitudinal" relationships not only informs the electrocardiographic interpretation of VA site of origin, but also facilitates their catheter-based mapping and ablation strategies. By viewing each patient as his or her own "control," the expected changes in ECG morphology (i.e., frontal plane QRS axis and precordial transition) between adjacent intracardiac structures (e.g., RVOT and aortic root) can be reliably predicted. Successful mapping of OT VAs involve a combination of activation and pacemapping guided by fluoroscopy, electroanatomical mapping, and intracardiac echocardiography. The purpose of this manuscript is to provide a simple, reliable strategy for catheter based mapping and ablation of OT VAs. We also discuss 2 specific challenges in OT VA mapping: (1) differentiating posterior RVOT from right coronary cusp VA origin; and (2) mapping VAs originating from the LV summit.

Inducibility of atrial fibrillation and flutter following pulmonary vein ablation.

INTRODUCTION: Prior reports demonstrate prognostic value in noninducibility of atrial arrhythmias after atrial fibrillation (AF) ablation and suggest their utility in guiding additional ablation lesion sets. The type and mechanism of induced atrial arrhythmias, their relationship to the underlying atrial substrate, and prognostic significance of induced organized atrial arrhythmias are unknown. METHODS AND RESULTS: One hundred forty-four patients (30 women; median age 60 years; 54% with paroxysmal AF) undergoing AF ablation (circumferential pulmonary vein isolation and focal ablation of nonvein triggers on isoproterenol) were evaluated prospectively. All underwent a standardized postablation induction protocol from the coronary sinus and right atrium: 15 beat burst pacing at 250 milliseconds and decrementing to 180 milliseconds. Sustained rhythms were defined as greater than 2 minutes Of 144 patients, 55 patients (38.2%) did not have sustained inducible arrhythmias. Fifty-two (36.1%) had inducible AF and 37 (25.7%) had inducible organized arrhythmias. A logistic regression analysis showed that age (OR 2.10 per decade; P = 0.003) and hypertension (OR 4.15; P = 0.009) were predictive of inducibility. However, inducibility of either AF or organized arrhythmias was not prognostic of clinical recurrence at 1 year postablation (P = 0.65). Furthermore, inducibility of organized arrhythmias did not predict clinical recurrence of an organized arrhythmia. Only LA size (OR 2.18; 95% CI 1.02-4.67; P = 0.04) and persistent AF (OR 2.43; 95% CI 1.09-5.40; P = 0.03) predicted atrial arrhythmia recurrence. CONCLUSIONS: Multisite atrial burst pacing post-AF ablation induced organized rhythms in 25.7% and AF in 36.1% of patients after AF ablation. Hypertension and age predict inducibility of arrhythmias, but inducibility did not predict clinical recurrence in follow-up. Distinguishing organized atrial arrhythmias from AF did not yield any further prognostic information. The utility of aggressive stimulation protocols after AF ablation for prognosis and to guide therapy appears limited.

Assessing arrhythmia burden after catheter ablation of atrial fibrillation using an implantable loop recorder: the ABACUS study.

INTRODUCTION: Arrhythmia monitoring in patients undergoing atrial fibrillation (AF) ablation is challenging. Transtelephonic monitors (TTMs) are cumbersome to use and provide limited temporal assessment. Implantable loop recorders (ILRs) may overcome these limitations. We sought to evaluate the utility of ILRs versus conventional monitoring (CM) in patients undergoing AF ablation. METHODS AND RESULTS: Forty-four patients undergoing AF ablation received ILRs and CM (30-day TTM at discharge and months 5 and 11 postablation). Over the initial 6 months, clinical decisions were made based on CM. Subjects were then randomized for the remaining 6 months to arrhythmia assessment and management by ILR versus CM. The primary endpoint was arrhythmia recurrence. The secondary endpoint was actionable clinical events (change of antiarrhythmic drugs [AADs], anticoagulation, non-AF arrhythmia events, etc.) due to either monitoring strategy. Over the study period, 6 patients withdrew. In the first 6 months, AF recurred in 18 patients (7 noted by CM, 18 by ILR; P = 0.002). Five patients in the CM (28%) and 5 in the ILR arm (25%; P = NS) had AF recurrence during the latter 6 months. AF was falsely diagnosed frequently by ILR (730 of 1,421 episodes; 51%). In more patients in the ILR compared with the CM arm, rate control agents (60% vs 39%, P = 0.02) and AADs (71% vs 44%, P = 0.04) were discontinued. CONCLUSION: In AF ablation patients, ILR can detect more arrhythmias than CM. However, false detection remains a challenge. With adequate oversight, ILRs may be useful in monitoring these patients after ablation.