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Background Cardiac positron emission tomography (PET) is routinely utilized to diagnose cardiac sarcoidosis, but may be positive in other cardiac conditions that result in myocardial inflammation. ATTR cardiac amyloidosis, an infiltrative disease that causes atrial arrhythmias and heart failure, is not typically thought to present with an inflammatory process. However, we observed four cases in which 18F-flurodeoxyglycose (FDG) PET scan findings were suspicious for cardiac sarcoidosis, but right ventricular endomyocardial biopsy (RV EMB) pathology specimens revealed ATTR wild-type (ATTRwt) cardiac amyloidosis. Methods Retrospective chart review was performed on patients with a positive cardiac FDG PET scan who also had a concomitant diagnosis of ATTR cardiac amyloidosis at Mayo Clinic Rochester between January 1, 2000 and March 24, 2019. Results Four patients with clinical presentation suggestive of cardiac sarcoidosis had positive FDG PET scans but were found to have biopsy-proven ATTRwt cardiac amyloidosis. All four patients were male with an average age of 71 years (62, 75). Two patients presented with ventricular arrhythmias and had transthoracic echocardiograms that were not suggestive of cardiac amyloidosis. FDG PET scans of these two patients revealed myocardial FDG uptake, similar to what can be seen in cardiac sarcoidosis. Both patients underwent RV EMB, with pathology specimens and mass spectrometry revealing ATTRwt cardiac amyloidosis. One of these two patients had a positive nuclear 99mTechnetium-pyrophosphate (PYP) scan (H/Cl ratio 1.9) and the other had a negative PYP scan (H/CL 1.2). The third patient, with a history of biopsy proven pulmonary sarcoidosis, presented with atrial fibrillation and conduction abnormalities. FDG PET scan revealed myocardial perfusion defects and patchy FDG uptake, but RV EMB revealed ATTRwt cardiac amyloidosis. Nuclear PYP was positive (H/Cl ratio of 1.8). The fourth patient presented with intermittent high grade AV block and underwent pacemaker implantation. He later developed frequent monomorphic premature ventricular contractions. Cardiac FDG PET scan illustrated FDG uptake, but the concurrent CT trunk did not illustrate any FDG uptake suspicious for extra-cardiac sarcoidosis. RV EMB was consistent with ATTRwt cardiac amyloidosis, but PYP was negative. Discussion These findings suggest that inflammation could play a role in ATTR cardiac amyloidosis. We have previously seen inflammatory changes of lymphohistiocytic infiltration around areas of amyloid protein deposition on biopsy specimens in ATTR cardiac amyloidosis. The role of therapy targeted at stabilizing transthyretin versus immunosuppressive agents in this subgroup remains unclear.

Current Heart Rhythm Society (HRS) guidelines regarding the diagnosis of cardiac sarcoidosis (CS) require histologic evidence of sarcoidosis. Due to limitations of endomyocardial biopsy (EMB) and variable extra-cardiac involvement, CS may be under-diagnosed. Patients evaluated for CS (n=277) were

Although most commonly diagnosed via endomyocardial biopsy, a diagnosis of definite cardiac sarcoidosis (CS) can be achieved through pathologic evaluation of apical cores at LVAD placement or on explanted hearts at cardiac transplantation. However, patients diagnosed at the time of advanced heart

One doesn't discover new lands without consenting to lose sight, for a very long time, of the shore. —Andre Gide, Les faux-monnayeurs [(1)][1] It is certainly difficult to be a patient with atrial fibrillation (AF) or an electrophysiologist caring for this patient. We live with the frustration

Background— Identification of intramural basal-septal ventricular tachycardia (VT) substrate is challenging in nonischemic cardiomyopathy. We sought to (1) characterize normal/abnormal trans-septal right ventricular (RV) to left ventricular activation; (2) assess the effect of opposite RV pacing on left ventricular septal bipolar electrograms (EGMs); and (3) establish criteria for the identification of intramural septal VT substrate. Methods and Results— Endocardial activation mapping and local EGM assessment of the left interventricular septum was performed during RV basal septal pacing in 40 patients undergoing VT ablation with no evidence of septal scar (group 1, n=14) and with septal scar (group 2, n=26) defined by low septal unipolar voltage (P =0.003). In 6 group 2 patients, left ventricular septal breakthrough was displaced to the scar border. During RV pacing, group 2 had fractionated (8.8%), late (2.8%), and split (5.7%) EGMs not seen in group 1. Trans-septal activation >40 ms (sensitivity 60%, specificity 100%; P 95 ms during pacing (sensitivity 22%, specificity 91%; P Conclusions— In patients with nonischemic cardiomyopathy, VT and septal scar, delayed transmural conduction time (>40 ms) and fractionated, late, split, and wide (>95 ms) bipolar EGMs during RV basal pacing identify intramural VT substrate. In select cases, the basal septum appears compartmentalized as the stimulated wavefront is rerouted to the scar border.

The diagnostic yield of remote monitoring for atrial fibrillation (AF) improves with longer periods of monitoring, being greatest with monitored telemetry and least with short-term (24–48 hour) Holters. The burden of AF required to incur an increased risk of thromboembolic complications may range from 5 minutes to 24 hours. There is poor symptom-rhythm correlation in AF, and identifying episodes of AF is better with the use of monitoring rather than patient-reported symptoms alone. Monitoring to manage patients after prior AF ablation is useful to identify clinically significant arrhythmia recurrence, and implantable loop recorders (ILRs) may prove more useful than external monitoring strategies, such as transtelephonic monitors (TTMs) or monitored telemetry.

Clinical use of remote monitoring is trending toward greater use of wireless transmission, which is less dependent on the patient transmitting their own data. Advances in wireless transmission, smaller technologies, and applications on smartphones may allow for the easier monitoring of patients in the ambulatory setting. Advances in physiologic sensors for heart failure, blood pressure, and other biological parameters may improve management of patients in the long-term but still requires research as to clinical validity and efficacy. Future technologies will require extensive validation, especially in terms of data management and evaluation of cost-effectiveness.

Assessing Arrhythmia Burden After AblationIntroduction 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.

Steven R. Bailey, MD, FACC, FSCAI, FAHA, Moderator Andrea M. Russo, MD, FACC, FHRS, Writing Group Liaison [⁎][1] Suraj Kapa, MD, Writing Group Liaison Michael B. Alexander, MD, FACC[§][2] Steven R. Bailey, MD, FACC, FSCAI, FAHA[∥][3] Ulrika Birgersdotter-Green, MD, FHRS[∥][3] Alan S.

Denervation of the extrinsic cardiac sympathetic nervous system is a method of altering the autonomic tone experienced by the heart and vasculature. It has been studied and employed as a therapy for cardiac disease for decades. Currently, there is a high level of interest in using cardiac denervation for treatment of arrhythmias. This review describes the anatomy and physiology of the cardiac autonomic nervous system followed by a discussion of the mechanistic studies which provide a basis for the therapeutic use of sympathetic denervation. The clinical research supporting its use in human arrhythmias is then appraised, covering the standard indications, such as long QT syndrome, as well as future possibilities. Last, a detailed account of the methods for performing surgical cardiac denervation and percutaneous stellate ganglion anesthetic block is provided, including the complications of each procedure. An understanding of the anatomy and physiology of the cardiac autonomic nervous system along with the techniques of surgical denervation and percutaneous anesthetic block will allow the clinician to effectively discuss and implement these therapies.

Efficient and robust control of cardiac pacemaker is essential for providing life-saving control action to regulate Heart Rate (HR) in a dynamic environment. Several controller designs involving proportional-integral-derivative (PID) and fuzzy logic controllers (FLC) have been reported but each have their limitations to face the dynamic challenge of regulating HR. Fractional-order control (FOC) systems provide controllers that are described by fractional-order differential equations that offers fine tuning of the control parameters to provide robust and efficient performance. In this work a robust fractional-order PID (FOPID) controller is designed based on Ziegler-Nichols tuning method. The stable FOPID controller outperformed PID controllers with different tuning methods and also the FLC in terms of rise time, settling time and % overshoot. The FOPID controller also demonstrated feasibility for rate-adaptive pacing. However, the FOPID controller designed in this work is not optimal and is limited by the tuning procedure. More efficient design using optimization techniques such as particle swarm intelligence or genetic algorithm tuning can offer optimal control of the cardiac pacemaker.

An 89-year-old man with a 12-year history of atrial fibrillation and atrial flutter was referred for pacemaker implantation and atrioventricular node ablation 19 months after discontinuing amiodarone due to side effects. He had no prior cardiac surgery or catheter ablation. …

Papillary muscle is an endocavitary structure that can give rise to ventricular arrhythmias in a structurally normal heart. Its manifestation is generally benign. The papillary muscle's complex anatomy and the presence of intermixed Purkinje fibers can create a substrate for idiopathic ventricular fibrillation. Although differentiating ventricular arrhythmias originating from the papillary muscle and the fascicles is challenging and not always possible, the distinction may be helpful for planning ablation. The propensity for difficulty with ablation of papillary arrhythmias results in a variable success rate. Improvement in techniques to stabilize the catheter, use of imaging, and methods of energy delivery are required to improve ablation outcomes.

Although electrolyte disturbances may affect cardiac action potential, little is known about the association between serum magnesium and corrected QT (QTc) interval as well as clinical outcomes.A consecutive 8498 patients admitted to the Mayo Clinic Hospital-Rochester cardiac care unit (CCU) from January 1, 2004 through December 31, 2013 with 2 or more documented serum magnesium levels, were studied to test the hypothesis that serum magnesium levels are associated with in-hospital mortality, sudden cardiac death, and QTc interval.Patients were 67 ± 15 years; 62.2% were male. The primary diagnoses for CCU admissions were acute myocardial infarction (50.7%) and acute decompensated heart failure (42.5%), respectively. Patients with higher magnesium levels were older, more likely male, and had lower glomerular filtration rates. After multivariate analyses adjusted for clinical characteristics including kidney disease and serum potassium, admission serum magnesium levels were not associated with QTc interval or sudden cardiac death. However, the admission magnesium levels ≥2.4 mg/dL were independently associated with an increase in mortality when compared with the reference level (2.0 to2.2 mg/dL), having an adjusted odds ratio of 1.80 and a 95% confidence interval of 1.25-2.59. The sensitivity analysis examining the association between postadmission magnesium and analysis that excluded patients with kidney failure and those with abnormal serum potassium yielded similar results.This retrospective study unexpectedly observed no association between serum magnesium levels and QTc interval or sudden cardiac death. However, serum magnesium ≥2.4 mg/dL was an independent predictor of increased hospital morality among CCU patients.

Epicardial access (EpiAcc) has become an important adjunct for ventricular tachycardia (VT) or premature ventricular complex (PVC) ablation. We hypothesized that post-procedural pericarditis may lead to an increased risk of atrial fibrillation (AF), and therefore assessed the incidence and clinical impact of post-procedural AF in patients undergoing EpiAcc. We reviewed the records of all patients who underwent EpiAcc as part of an ablation procedure between January 1, 2004 and July 31, 2014 at Mayo Clinic Rochester. AF occurrence was determined by clinical documentation or electrocardiographic recordings post procedure. Epicardial access was obtained in 170 pts (indication 110 VT and 60 PVC). The mean age was 53 ± 16 years and 122 (72%) were male. Seven (4.1%) patients developed AF within 7 days of the procedure, at a mean of 49 ± 18 h post procedure; it was paroxysmal in all patients with an average duration 6.0 ± 5.5 h (range 2–18). All patients spontaneously converted to sinus rhythm; but 3 needed rate control with AV nodal blockade (calcium channel blockers [n = 2] or beta blockers [n = 1]). One patient out of 60 who received intrapericardial steroids developed AF (2%), while of the 110 who did not receive steroids, 6 developed AF (5%) (p = 0.42). During average follow-up 2.3 years, there were no documented recurrences of atrial fibrillation in these patients. Atrial fibrillation following epicardial access is infrequent. When it occurs, it tends to be paroxysmal in nature and without severe symptoms. Administration of intrapericardial steroids did not affect the rate of AF post procedure; further studies however are needed to define their role.

Patients with advanced heart failure (HF) are predisposed to ventricular arrhythmias (VAs), particularly following implantation of a left ventricular assist device (LVAD). There is minimal evidence for appropriate management strategies.This study aimed to compare the burden of VA and response to ablation performed either before or following LVAD implantation.We created a retrospective cohort of patients who underwent both VA ablation and Heart Mate II (Thoratec, Pleasanton, CA, USA) LVAD implantation at Mayo Clinic (Rochester, MN, USA). Patients were stratified based on whether they underwent VA ablation before (pre-LVAD) or after LVAD (post-LVAD) implantation. Descriptive analyses assessed 6-month arrhythmia burden in relation to LVAD implantation and VA ablation.A total of 9 patients underwent both LVAD implantation and VA ablation. There were 3 and 6 patients, respectively, in the pre-LVAD and post-LVAD cohorts. Among patients in the pre-LVAD cohort, the median number of VAs tended to increase after ablation (9 vs. 72) and decreased after LVAD implantation (72 vs. 63). Similarly among patients in the post-LVAD cohort, the median burden of VAs increased after LVAD implantation (1 vs. 22) and the median burden decreased after ablation (22 vs. 13). Two of 6 patients had substrate related to the LVAD inflow cannula site, while other substrate was not related directly to the cannula.In patients with progressive HF and LVAD implantation, ablation is associated with reduced VA rates. In LVAD patients, most VAs arise from substrate unrelated to the inflow cannula site.

Background— Although the vast majority of mitral valve prolapse (MVP) is benign, a small subset of patients, predominantly women, with bileaflet prolapse, complex ventricular ectopy (VE), and abnormal T waves comprise the recently described bileaflet MVP syndrome. We compared findings on electrophysiological study in bileaflet MVP syndrome patients with and without cardiac arrest to identify factors that may predispose to malignant ventricular arrhythmia. Methods and Results— Fourteen consecutive bileaflet MVP syndrome patients (n=13 women; median [limits], age at index ablation, 33.8 [21.0–58.7] years; ejection fraction, 60% [45%–67%]; all ≤ moderate mitral regurgitation; n=6 with previous cardiac arrest and implantable cardioverter defibrillator shocks for ventricular fibrillation; and n=8 without implantable cardioverter defibrillator although with symptomatic complex VE) were included. The 2 groups had similar baseline echocardiographic and electrocardiographic characteristics. All patients had at least 1 left ventricular papillary or fascicular VE focus. Purkinje origin VE was identified as the ventricular fibrillation trigger in 6 of 6 cardiac arrest patients (4 from papillary muscle) and Purkinje origin of dominant VE was seen in 5 of 8 (3 from papillary muscle) nonarrest patients. Acute success was seen in 17 of 19 procedures, and a ventricular fibrillation storm occurred within 24 hours of ablation in a single patient. Repeat ablation for recurrent symptomatic arrhythmia was performed in 6 patients. At 478 (39–2099) days of follow-up, 2 cardiac arrest patients received appropriate shocks. Symptoms from VE were reduced in 12 of 14. Conclusions— Bileaflet MVP syndrome is characterized by fascicular and papillary muscle VE that triggers ventricular fibrillation. Ablation of clinically dominant VE foci improves symptoms and reduces appropriate implantable cardioverter defibrillator shocks.

Adenosine infusion during atrial fibrillation ablation is often used to evaluate for dormant pulmonary vein (PV) conduction. Several physiologic effects of adenosine may be seen during infusion, including atrioventricular (AV) block, hypotension, sinus tachycardia (as a reflex mechanism), and sinus bradycardia. However, hypotension and sinus tachycardia may be seen in the absence of AV block. Whether the dose required to achieve AV block versus any physiologic effect (e.g., hypotension) is relevant when evaluating for PV reconnection is unclear. In consecutive patients undergoing first-time atrial fibrillation radiofrequency ablation for persistent or paroxysmal atrial fibrillation, adenosine testing was performed 30 min after successful PV isolation. When testing each PV after isolation, a circular mapping catheter was placed at the ostium and a 12-mg bolus of adenosine was given via peripheral line. The presence of some physiologic effect (e.g., sinus tachycardia or hypotension) versus AV block was recorded as was PV reconnection. If no AV block and no PV reconnection were seen, the dose was escalated by 6-mg increments to assess for PV reconnection until AV block or PV reconnection was achieved. Among 50 patients, there were 3 to 5 PVs isolated (median 4; mean 4.4). In 35 patients, a 12-mg bolus resulted in AV block and 16/155 (10 %) veins exhibited reconnection requiring additional ablation. In all other patients, sinus tachycardia and hypotension were seen in response to 12-mg infusion but no AV block and no PV reconnection was seen. No sinus bradycardia was seen in any patients. In 10/15 patients without AV block with 12 mg, 18 mg of adenosine was sufficient to achieve AV block and 5/43 (12 %) PVs exhibited reconnection. Among the remaining 5 patients, 3 patients required a dose of 24 mg to achieve AV block, and PV reconnection was seen in 1/14 (7 %) PVs. The remaining two patients required a dose of 30 mg to achieve AV block, but no PV reconnection was seen. There was no difference in symptomatic recurrence rate between those who exhibited adenosine-induced reconnection and those who did not after 1-year follow-up. A fixed dose of adenosine may be insufficient to assess for PV reconnection. Furthermore, the presence of a physiologic effect (e.g., sinus tachycardia or hypotension) in the absence of AV block may reflect an insufficient dose. The dose needed may vary between patients, and AV block may reflect a minimal requirement when administering adenosine to assess for PV reconnection.

We have previously shown that sympathetic ganglia stimulation via the renal vein rapidly increases blood pressure. This study further investigated the optimal target sites and effective energy levels for stimulation of the renal vasculatures and nearby sympathetic ganglia for rapid increase in blood pressure.The pre-study protocol for endovascular stimulations included 2 minutes of stimulation (1-150 V and 10 pulses per second) and at least 2 minutes of rest during poststimulation. If blood pressure and/or heart rate were changed during the stimulation, time to return to baseline was allowed prior to the next stimulation.In 11 acute canine studies, we performed 85 renal artery, 30 renal vein, and 8 hepatic vasculature stimulations. The mean arterial pressure (MAP) rapidly increased during stimulation of renal artery (95 ± 18 mmHg vs. 103 ± 15 mmHg; P0.0001), renal vein (90 ± 16 mmHg vs. 102 ± 20 mmHg; P = 0.001), and hepatic vasculatures (74 ± 8 mmHg vs. 82 ± 11 mmHg; P = 0.04). Predictors of a significant increase in MAP were energy10 V focused on the left renal artery, bilateral renal arteries, and bilateral renal veins (especially the mid segment). Overall, heart rate was unchanged, but muscle fasciculation was observed in 22.0% with an output10 V (range 15-150 V). Analysis after excluding the stimulations that resulted in fasciculation yielded similar results to the main findings.Stimulation of intra-abdominal vasculatures promptly increased the MAP and thus may be a potential treatment option for hypotension in autonomic disorders. Predictors of optimal stimulation include energy delivery and the site of stimulation (for the renal vasculatures), which informs the design of subsequent research.

Ventricular arrhythmias involving the fascicular system may be seen in both structurally normal and abnormal hearts. Idiopathic fascicular ventricular tachycardia represents almost 10% to 15% of idiopathic ventricular tachycardia related to the left ventricle.1,2 Cohen et al3 and subsequently Zipes et al4 first described these arrhythmias in the 1970s as relatively narrow right bundle left axis arrhythmias that arose close to the posterior fascicle and could be induced with atrial pacing. Belhassen et al5 later described the responsiveness of these arrhythmias to verapamil. Although initial studies focused on arrhythmias related to the left posterior fascicle, it is possible for arrhythmias to arise from any portion of the fascicular system and in both structurally normal and abnormal hearts. Furthermore, when approaching the patient presenting with arrhythmias arising from the His-Purkinje system, it is important to consider the unique complexities related to mapping and ablation. In this review, we will focus on the mechanisms of such arrhythmias, relevant embryology, anatomy and physiology, and approaches to management in both the presence and absence of other structural heart disease. Broadly, fascicular ventricular tachycardia in the absence of other structural heart disease will be termed idiopathic fascicular ventricular tachycardia (IFVT), whereas that related to structural disease will be discussed in the context of the relevant disease state. Generally, IFVT is separated into 3 types—left posterior fascicular with a right bundle branch block pattern and left axis deviation, left anterior with a right bundle branch block and right axis deviation pattern, and left upper septal fascicular with a narrow QRS and normal axis but often with a right bundle branch block morphology. There are rare reported cases of left bundle branch block pattern, V3–V4 transition IFVT with a normal axis arising from the right bundle branch. In …

> It’s always seemed like a big mystery how nature, seemingly so effortlessly, manages to produce so much that seems to us so complex. Well, I think we found its secret. It’s just sampling what’s out there in the computational universe. > > –Stephen Wolfram, 2010 Pathogenesis of nearly all arrhythmia relies on a fundamental premise—that there exists within the cellular milieu regions of unexpected or unwanted heterogeneous conduction that may allow for initiation and propagation of wave fronts along a nonstandard pattern. The simplest paradigm for this may be atrioventricular reentrant tachycardias wherein 2 paths exist, both capable of propagating signals in either the antegrade or retrograde direction, but with fundamentally different conductive properties that ultimately allow for development of reentry with an appropriately timed stimulus. This appropriately timed stimulus, or trigger, has for the past 3 decades been the focus of electrophysiologists in the treatment of more complex arrhythmias that exist outside the ability of our modern day understanding and technology to map and ablate. Where a single circuit exists, mapping and ablation is straightforward, and we must prove it exists and that it participates in the tachycardia, identify its location, and then determine the best means by which to ablate it. However, in the case of atrial fibrillation, understanding, identifying, and determining an ideal ablative solution for the substrate is eminently more difficult. This is because the propagation and continuation of atrial fibrillation is fundamentally dependent on the continuous activity of many sites simultaneously. Thus, we have often referred to atrial fibrillation almost as chaos, throwing up arms at the seemingly inexplicable and indescribable complexity and focused instead on the elimination of triggers, whether by pulmonary vein isolation or targeting other sites, rather than the myocardial substrate responsible for arrhythmia maintenance as we would with any other simpler arrhythmia, such …

Most patients referred for ventricular tachycardia (VT) ablation have already suffered multiple therapies for recurrent VT, typically in the form of implantable cardioverter defibrillator (ICD) shocks. Recent landmark trials have looked at these populations and suggest potential usefulness of early, preventive ablation of VT in patients with ischemic cardiomyopathy. In this review the potential role of early VT ablation in patients with ischemic cardiomyopathy, current controversies regarding VT ablation in this population, and ongoing and future research that may further inform clinical decision making regarding optimal timing of ablation in these patients are discussed.

Background Studies suggest that 18%–50% of the patients develop atrial fibrillation (AF) after typical atrial flutter (AFL) ablation. However, little data exist about the incidence of and risk factors for stroke and AF after successful ablation of typical AFL. Objectives To determine the risk of stroke and AF after radiofrequency ablation of typical AFL. Methods A retrospective review of patients undergoing AFL ablation between 2002 and 2010 was performed to determine the incidence of and risk factors for stroke and AF after successful ablation of typical AFL. Results The study cohort consisted of 126 patients (age 66 ± 10 years) with a mean follow-up of 40 ± 30 months after ablation. Following successful AFL ablation, AF occurred in 46 patients (37%), with an incidence of 104 cases of documented AF per 1000 person-years after AFL ablation. Twenty patients (16%) developed new AF after AFL ablation. Stroke occurred in 8 patients (6%) during follow-up, with an incidence of 21 strokes per 1000 person-years. Six of the 8 patients (75%) with strokes had documented AF occurrences after AFL ablation. The presence of AF after AFL ablation was the only risk factor associated with the risk for future stroke. Conclusions Patients with typical AFL undergoing successful ablation are at an elevated risk for AF and stroke following the procedure. Because postprocedure AF is the only identifiable risk factor for stroke, rigorous monitoring of patients after typical AFL may help identify those patients who are at an increased risk for stroke.

While for decades right ventricular (RV) apical pacing has been the standard of care for patients requiring pacemaker or defibrillator lead placement, investigators have sought alternatives to achieve more physiologic electrical activation of the heart and reduce long-term pathologic effects of nonphysiologic apical pacing. These investigations have included attempts at identifying superior pacing sites within the right atrium and RV and development of new leads to enhance specificity of sensing and capture. This review focuses on recent advances in alternative sites for pacing and developments in novel pacing technology ranging from intramyocardial electrodes to leadless pacemakers. First, there have been several studies demonstrating potential benefits of site-specific pacing, including His bundle pacing and RV outflow tract pacing in potentially attenuating electromechanical dyssynchrony and long-term functional decline seen with RV apical pacing. Available options for lead placement have been enhanced by development of intramyocardial electrodes that may significantly reduce far-field oversensing and nonchamber specific capture. With development of intramyocardial electrodes, the potential for atrioventricular septal pacing has recently been described, making synchronous activation of both ventricles with a one-lead system possible without crossing the tricuspid valve and offering an alternative to modern cardiac resynchronization therapy (CRT). Finally, recent advances in leadless pacemaker systems using ultrasound or magnetic fields are briefly discussed. The results of these studies suggest that there may be options to the RV apex, made possible by novel lead and pacemaker technology. These advances can potentially aid in reducing long-term negative effects of chronic pacemaker therapy.

There is an increasing need for invasive electrophysiologists to appreciate the exact anatomy of the epicardial space and the coronary veins. The location of the epicardial fat, the complementary relationship with the main cardiac veins, and the location of sensitive structures (arteries, phrenic nerve, esophagus) have become required knowledge for electrophysiologists, and accessing the epicardial space with this thorough knowledge of the pericardial sinuses and recesses is essential to allow radiographic correlation during catheter manipulation. In this review, we briefly describe the anatomy of the pericardial space and then discuss the specific correlation for the invasive electrophysiologist, highlighting epicardial access, catheter navigation, and avoidance of collateral injury with specific attention to the important recesses of the pericardial space, their regional anatomy, and radiographic correlation when navigating catheters to these locations. We also discuss the anatomy of the main cardiac veins in the context of catheter mapping and ablation of the epicardial substrate through the venous system and without subxiphoid pericardial access. In Part I of this two-part series, we discuss the regional anatomy of the pericardial space, oblique sinus, and transverse sinus.

During magnetic resonance imaging (MRI), pacemaker and defibrillator leads can focus energy onto the myocardium causing heating and arrhythmias in animal models. Direct exposure of the devices to the magnetic field in thoracic MRI could potentially augment this risk. However no data is currently

Left ventricular noncompaction (LVNC) is an inherited cardiomyopathy with an underlying arrhythmogenic substrate. Limited information is available on prevalence and risk factors of atrial arrhythmias in LVNC. Imaging databases were queried from 2000-16 to identify a cohort of patients with LVNC

Recurrent SVT due to the presence of an inappropriately positioned intra-atrial CVC is an under-recognized complication. A 60-year-old female presented with a 10-year history of palpitations in the setting of iatrogenic short bowel syndrome requiring total parenteral nutrition via long-term

Rotational vertebrobasilar insufficiency (RVBI) is a rare syndrome presenting with vertigo, dizziness or syncope when the patient rotates their head. A 65-year-old man presented to medicine with presyncope while he was backing up his truck to put his boat in the water. This only occurred when he

Despite the primary trigger for atrial fibrillation (AF) being within the pulmonary vein, current treatments avoid direct ablation of this substrate because of the prohibitive incidence of pulmonary vein (PV) stenosis. Given the suboptimal results with contemporary thermal AF ablation, we previously

Asymptomatic left ventricular dysfunction (ALVD) is present in 2-9% of the population, is associated with reduced longevity and is treatable when found. Inexpensive, reliable, in office screening is not available. The area under the curve (AUC) for a BNP screening blood test is 0.79 to 0.89. We

Complications of atrial fibrillation (AF) ablation include thromboembolism, tamponade, pulmonary vein stenosis, acute lung injury and phrenic nerve injury (PNI), all of which can present with shortness of breath (SOB). A 55-year-old obese female underwent radiofrequency AF ablation. Shortly after

Endocavitary Structures and Ventricular Tachycardia Ablation. Background: Radiofrequency (RF) ablation for ventricular tachycardia (VT) has high failure rates. Whether endocavitary structures (ECS) such as the papillary muscles (PMs), moderator bands (MBs), or false tendons (FTs) impact VT ablation is unknown. Methods and Results: We retrospectively reviewed records of 190 consecutive patients presenting for VT ablation and identified 46 (24%) where ECS affected ablation. In 31 of 46 patients (67%), the ECS created difficulty with catheter manipulation (n = 20), interpretation of pace map data (n = 7), or with accurately defining a scar (n = 4). In 15 of 46 (33%), specific mapping and RF energy delivery targeting the ECS itself was necessary to eliminate the arrhythmia. Detailed electroanatomic mapping was performed in 11 of 15 (73%), noncontact mapping in 3 of 15 (20%), multielectrode catheter mapping in 1 of 15 (7%), and intracardiac ultrasound in 14 of 15 (93%) patients. The ablated ECS was a PM in 5 of 15, the MB in 7 of 15, and an FT in 3 of 15. The arrhythmogenic substrate on the ECS was a focus of automatic tachycardia in 9 of 15 and the slow zone responsible for reentrant arrhythmia in the remaining 6 of 15. Successful elimination of tachycardia without recurrence was obtained in all 15 cases. There was no evidence of valvular damage or disruption of the valvular apparatus. Conclusion: During VT ablation procedures, ECS should be considered for specific mapping and targeted ablation. Once recognized, these structures can be successfully targeted for ablation without valve damage. (J Cardiovasc Electrophysiol, Vol. 21, pp. 245–254, March 2010)

Ablation procedures for atrial fibrillation (AF) have become an established and increasingly used option for managing patients with symptomatic arrhythmia. The anatomic structures relevant to the pathogenesis of AF and ablation procedures are varied and include the pulmonary veins (PVs), other thoracic veins, the left atrial myocardium, and autonomic ganglia. Exact regional anatomic knowledge of these structures is essential to allow correlation with fluoroscopy and electrograms, and, importantly, to avoid complications from damage of adjacent structures within the chest. We have presented this information in a 2-part series. In the present article, we examine the general anatomic characteristics of the PVs, superior vena cava, and vein of Marshall. Features of particular relevance for the invasive electrophysiologist are pointed out. In a subsequent article, we discuss the regional anatomy of the left and right atria and anatomic considerations in preventing complications during AF ablation.

Background Device implantation is sometimes required in congenitally corrected transposition of the great arteries (ccTGA) because of morphologic right ventricular (RV) dysfunction and complete heart block. The anatomical course of the veins remains unknown, despite well-described coronary arterial anatomy. Knowledge of the venous anatomy may facilitate planning of percutaneous cardiac procedures in these patients. Objective This study sought to characterize the venous anatomy in ccTGA. Methods Pathologic cardiac specimens from patients with ccTGA were identified from the Mayo Clinic pathology database. Coronary sinus (CS) anatomy and distances from the CS ostium to the major cardiac veins were evaluated. Thebesian veins with ostial openings >1 mm, epicardial veins, and venous collaterals were also quantified. Results There were 56 hearts with a diagnosis of ccTGA identified. The CS was unidentifiable in 5 hearts due to slicing, and assessment of the Thebesian veins was not possible in 16. Seven hearts had an abnormal CS, 2 of which had atretic ostia and the other 5 of which either had an abnormal ostial location or multiple ostia. There were 28 hearts with at least 1 Thebesian vein with an ostial opening >1 mm. All 12 hearts with unidentifiable Thebesian veins had venous collaterals from the right ventricle (RV) to the major cardiac veins. Epicardial veins extended to the proximal, middle, and distal thirds of the RV in 71%, 23%, and 6%, respectively. Conclusion In ccTGA, the ventricular venous anatomy is abnormal and follows the morphologic RV. However, large interventricular and Thebesian veins may offer options for percutaneous lead or catheter placement when approaching the systemic RV.

Ablation for atrial fibrillation (AF) is a genuinely viable and increasingly used option for improving quality of life in patients with symptomatic drug-refractory AF. What is remarkable about the limited success achieved with these procedures is that progress has occurred despite a near complete lack of knowledge about what causes or maintains AF. Focal origins for AF were first demonstrated decades ago1–4 with topical application of acetylcholine to junctional tissues and atrial sites triggering AF. More recently, there has been convincing documentation of rapid tachycardia arising from the pulmonary veins inciting AF, thus supporting the concept of “trigger elimination” contributing to the success of pulmonary vein isolation. However, studies also support the presence of multiple reentrant circuits maintaining and possibly initiating AF.5, 6 The ablation era has taught us7–9 that in persistent and chronic AF, trigger elimination alone is not enough and that substrate modification is probably necessary to decrease the likelihood of reentrant wavelet continuance and thereby increase success rates. Even the most ardent supporter of either hypothesis recognizes the limitations of each. How can a focal source exist in this milieu indefinitely, producing and maintaining chronic AF, and how do multiple reentrant wavelets arise spontaneously? Article see p 384 In this issue of Circulation: Arrhythmia and Electrophysiology , Niu et al10 provide important, interesting, and novel insights into solving this age-old riddle using a previously unexplored angle-autonomic manipulation. Acetylcholine was used to induce AF in 31 canines. In 12 of the animal studies, propafenone was administered. They then ablated the ganglionated plexi (GP). Before ablation, AF could still be induced despite administration of propafenone. After ablation, there was a consistent pattern of electrogram organization and atrial synchronization. In addition, subsequent administration of propafenone resulted in the inability to induce atrial tachyarrhythmia. There are several …

Introduction: Defining whether retrograde ventriculoatrial (V-A) conduction is via the AV node (AVN) or an accessory pathway (AP) is important during ablation procedures for supraventricular tachycardia (SVT). With the introduction of ventricular extrastimuli (VEST), retrograde right bundle branch block (RBBB) may occur, prolonging the V-H interval, but only when AV node conduction is present. We hypothesized that when AP conduction was present, the V-A interval would increase less than the V-H interval, whereas with retrograde nodal conduction, the V-A interval would increase at least as much as the V-H interval. Methods and Results: We retrospectively reviewed the electrophysiological studies of patients undergoing ablation for AVN reentrant tachycardia (AVNRT) (55) or AVRT (50), for induction of retrograde RBBB during the introduction of VEST, and the change in the measured V-H and V-A intervals. Results were found to be reproducible between independent observers. Out of 105 patients, 84 had evidence of induced retrograde RBBB. The average V-H interval increase with induction of RBBB was 53.7 ms for patients with AVRT and 54.4 ms for patients with AVNRT (P = NS). The average V-A interval increase with induction of RBBB was 13.6 ms with AVRT and 70.1 ms with AVNRT (P < 0.001). All patients with a greater V-H than V-A interval change had AVRT, and those with a smaller had AVNRT. Conclusions: Induction of retrograde RBBB during VEST is common during an electrophysiological study for SVT. The relative change in the intervals during induction of RBBB accurately differentiates between retrograde AVN and AP conduction.

The SVC may require ablation to treat atrial fibrillation. Phrenic nerve proximity identified with pacing maneuvers may preclude ablation.We tested a new method using "cryo-mapping" to ablate despite nerve proximity.Of 833 patients undergoing ablation, 110 (12%) had arrhythmogenic substrate at the SVC/RA junction. Of these 110 patients, 66 (60%) had consistent diaphragmatic stimulation when pacing at 10 mA at the prospective site of ablation. Of these 66 patients, 7 had continued arrhythmogenicity despite attempts to modify this substrate. For these 7 patients, we paced 4 cm into the SVC where consistent phrenic nerve stimulation was obtained, and cryoablation at -30 degrees C was performed at sites requiring ablation. In 6 of 7 patients (86%), with continued diaphragmatic capture, cryoablation at -70/-80 degrees C was then performed. In 1 of 7 patients (14%), diaphragmatic stimulation ceased at -30 degrees C, and energy delivery stopped. In the 6 patients in whom cryoablation was completed, the arrhythmogenic substrate was successfully ablated without phrenic nerve injury.A novel "cryo-mapping" technique during phrenic nerve pacing can be used to successfully ablate arrhythmogenic substrate at the SVC/RA junction despite phrenic nerve proximity.

There is a relationship between arrhythmias and sleep apnea, most notably during sleep. A common rhythm disturbance is nocturnal bradyarrhythmias that occur in association with apneic episodes; however, because of long-term autonomic, functional, and structural cardiac changes, in addition to decreased ischemic threshold, patients with sleep apnea may potentially be at higher risk for developing atrial fibrillation and ventricular arrhythmias. These complications of untreated sleep apnea may conceivably be implicated in nocturnal sudden cardiac death.

Background:Recent advisories and recalls of pacemakers and implantable cardioverter-defibrillators (ICDs) have highlighted the need for evidence-based recommendations regarding management of patients with advisory devices. In order to better facilitate decision-making when weighing the relative risks and benefits of performing generator changes in these patients, we conducted a review to assess operative complication rates. Methods:We reviewed generator changes performed between 2000 and 2005 at the Mayo Clinic-Rochester, including a total of 732 change-outs consisting of 570 done for elective replacement indicators (ERI) and 162 for manufacturer advisories or recalls. Complications included all those requiring reoperation, occurring within a 60-day period postoperatively and directly attributable to the generator change. These included infection requiring device excision, hematoma requiring evacuation, and incisional dehiscence requiring reclosure. Results:Operation-associated complications requiring intervention were noted in 9 patients, or 1.24% of our population. Of these nine complications, eight occurred among patients receiving pulse generator replacement for ERI (1.40%) and one occurred in a patient receiving replacement for a manufacturer advisory or recall (0.62%). Complications included 5 infections, 3 hematomas, and 1 incisional dehiscence. Conclusions:Generator replacement is not a benign procedure and associated risks must be weighed in the context of other variables when making management choices in patients with advisory or recall devices.

Background Repaired congenital heart disease (rCHD) is strongly associated with ventricular tachycardia (VT) as an important late cause of morbidity and mortality. Ventricular reentry most commonly includes anatomic isthmuses created during the repair procedures. Objective The purpose of this study was to analyze the long-term outcomes of catheter ablation, a commonly used standalone or adjunctive therapy, in a cohort of rCHD patients. Methods A retrospective analysis of 21 consecutive patients with rCHD (45.0 ± 3.0 years, 71.4% male) undergoing ablation for VT was performed. The primary composite outcome was defined as in-hospital arrhythmic death, out-of-hospital sudden cardiac death, or appropriate implantable cardioverter-defibrillator therapy. Results At initial electrophysiologic study, 14 patients (66.7%) had reentrant VT through an electroanatomic isthmus; the remaining 7 patients (33.3%) demonstrated focal VT. Isthmus-dependent reentry was identified as the mechanism for VT in 14 patients (66.7%), and conduction block was confirmed in 8 of these patients (57.1%). No patients with confirmed block developed VT recurrence. During long-term follow-up (33 ± 7 months), 20 of 21 patients (95.2%) had not reached the primary composite outcome. Three patients died of nonarrhythmic causes. Conclusion Catheter-based VT ablation in patients with rCHD is associated with a low rate of VT recurrence. Focal VT was not uncommon in this cohort. If a reentrant mechanism is present, confirmation of conduction block across the isthmus is vital to prevent recurrence.

Magnetic resonance imaging (MRI) has been safely performed in many patients with cardiac implantable electronic devices (CIEDs) using institution-specific protocols. A potential risk of MRI is myocardial heating and cardiac injury, which might be detectable with cardiac Troponin (cTn). We evaluated this in patients with CIEDs undergoing MRI.Prospective data were collected from 2008 to the present in patients with CIEDs undergoing clinically indicated MRI performed under institutional protocol. Cardiac Troponin T (cTnT) levels were drawn both before and 24–36 h after the procedure. The collective data were retrospectively analyzed.MRI exams (n=512) were performed in 398 patients. Of these, there were 348 unique scans with cTnT recorded before and after MRI (median age 68, IQ 56–78; 62%men). cTnT did not significantly change for the group as a whole (0.00±0.056). There were 22 (6.3 %) exams with cTnT change ≥0.002 ng/mL following MRI (range 0.01–0.09 ng/mL). There were no clinically significant events in these patients directly attributable to MR. There were no significant changes in pacing threshold or impedance in the group with elevated cardiac biomarkers.There are very few situations where myocardial injury as detected by cTnT in patients undergoing MRI with CIEDs could be detected. No adverse clinical events or functional changes of the device were noted, even in those with increases in cTnT. Our experience supports that MRI can be performed safely for appropriately selected patients under close clinical observation. Proactive monitoring with the present iteration of cardiac biomarkers appears to be of limited utility, but prospective monitoring with high sensitivity assays may be able to detect subclinical myocardial damage.

Background: It is known that hypokalemia, hypocalcemia and hypomagnesemia cause a prolonged QTc interval and are associated with an increased risk of ventricular arrhythmias. However, there are limited data on optimal serum electrolytes for patients admitted to the coronary care unit (CCU). Objective: Here, we aimed to evaluate the relationship between serum potassium, ionized calcium and magnesium levels and in-hospital mortality in the CCU setting. Methods: This retrospective cohort study included 8,498 consecutive patients admitted to the CCU at an academic tertiary medical center from 2004 through 2013. The mean of serum electrolytes was categorized as Results: Of the 8,498 patients, 599 (7%) died during hospitalization. Relationship between mean serum potassium (U-shaped), ionized calcium (inverted J-shape) and magnesium (J-shaped) and in-hospital mortality was present in Figure. Serum potassium levels Conclusions: In the CCU setting, serum potassium 3.5