Thomas Deneke

Utility of Esophageal Temperature Monitoring During Pulmonary Vein Isolation for Atrial Fibrillation Using Duty-Cycled Phased Radiofrequency Ablation

Esophageal Temperature Monitoring During PVAC Ablation. Introduction: A novel ablation system has been introduced for rapid treatment of atrial fibrillation (AF). This system delivers duty‐cycled phased radiofrequency (RF) energy via an over‐the‐wire catheter (PVAC®, Medtronic) to achieve pulmonary vein (PV) isolation. Lower power and depth control suggests that collateral damage might be minimized. However, no studies have investigated the potential for thermal effect and damage to the esophagus.

Acute Safety and Efficacy of a Novel Multipolar Irrigated Radiofrequency Ablation Catheter for Pulmonary Vein Isolation

“Single shot” ablation devices to treat symptomatic atrial fibrillation have been engineered over the last years. Safety and efficacy also includes subclinical complications only detected with esophageal endoscopy or cerebral MRI in asymptomatic patients.

Silent Cerebral Events/Lesions Related to Atrial Fibrillation Ablation: A Clinical Review

Brain magnetic resonance imaging (MRI) has identified a high incidence of cerebral ischemia in asymptomatic patients after atrial fibrillation (AF) ablation (silent). Detection of cerebral ischemic events on MRI is based on acute hyperintense lesions on diffusion‐weighted imaging. In the literature, the incidence is related to specifications of MRI and depends on the definition applied. In comparative studies, silent cerebral events (SCE, diffusion‐weighted MRI [DWI] positive only) appear to be approximately 3 times more common compared to using a definition of silent cerebral lesions (SCL; without fluid attenuated inverse recovery sequence [FLAIR] positivity). Whereas the FLAIR sequence may turn positive within days after the ischemic event, SCE definition is highly sensitive for early phases of ischemic brain damage. SCE/SCL appear to represent cerebral ischemic infarcts and determine the “embolic fingerprint” of a specific ablation technology and strategy used. The optimum time point for detecting SCE is early after AF ablation (24–72 hours), whereas detection of SCL can only be performed within the first 2–7 days (due to delay of FLAIR positivity). Different technology‐, procedure‐, and patient‐related parameters have been identified to play a role in the multifactorial genesis of SCE/SCL. In recent years, evidence has been gathered that there may be differences of SCE/SCL rates depending upon the ablation technology used, but small patient numbers and a large number of potential confounders hamper all studies. As major findings of recent studies, mode of periprocedural and intraprocedural anticoagulation has been identified as a major predictor for incidences of SCE/SCL. Whereas procedural characteristics related to higher SCE/SCL‐rates may be modified, unchangeable patient‐related factors should be taken into account for future individualized risk assessment. Novel ablation devices introduced into the market should be tested for their potential embolic fingerprint and refinements of ablation procedures to reduce their embolic potential should be prompted. The knowledge of “best practice” in terms of low SCE/SCL rates has prompted changes in work‐flow, which have been implemented into ablation procedures using novel ablation devices. So far, no study has linked SCE/SCL to neuropsychological decline and the low number of AF‐ablation‐associated events needs to be weighted against the multitude of preexisting asymptomatic MRI‐detected brain lesions related to the course of AF itself. Future studies are needed to evaluate if more white matter hyperintensities due to AF may be prevented by AF ablation (producing only a small number of SCE/SCL).

Human histopathology of electroanatomic mapping after cooled-tip radiofrequency ablation to treat ventricular tachycardia in remote myocardial infarction.

Introduction: Catheter ablation of ventricular tachycardia (VT) in remote myocardial infarction (MI) often requires excessive mapping procedures. Documentation of the electrical substrate via electrogram amplitude may help to identify regions of altered myocardium resembling exit areas of reentrant VTs.

Esophago‐pericardial Fistula Complicating Atrial Fibrillation Ablation Using a Novel Irrigated Radiofrequency Multipolar Ablation Catheter

Atrioesophageal fistula is a rare but devastating complication of atrial fibrillation ablation and has been identified with different ablation strategies and technologies. We report the case of esophagopericardial fistula with fatal outcome after an uneventful ablation of atrial fibrillation using a novel multipolar irrigated RF ablation catheter (nMARQTM, Biosense Webster, Diamond Bar, USA). During ablation, the maximum esophageal temperature rose to 40.4 ◦C and ablation was immediately stopped. In our case, ablations were performed with high-energy output (preset maximum 25 Watts energy and a maximum temperature of 45 ◦C, ablation duration 60 seconds),

Correlation between total atrial conduction time estimated via tissue Doppler imaging (PA-TDI Interval), structural atrial remodeling and new-onset of atrial fibrillation after cardiac surgery.

Recent studies identified total atrial conduction time (TACT) as an independent and powerful predictor of new‐onset atrial fibrillation (AF). The purpose of this study was to assess the association between the degree of atrial fibrosis, TACT, and frequency of postoperative atrial fibrillation (POAF) among patients undergoing cardiac surgery.

Largest amplitude ablation is the optimal approach for typical atrial flutter ablation: a subanalysis from the AURUM 8 study.

Voltage‐Guided Cavotricuspid Isthmus Ablation.

Catheter Ablation of Regular Atrial Arrhythmia Following Surgical Treatment of Permanent Atrial Fibrillation

Introduction: Surgical treatment of atrial fibrillation (AF) is gaining widespread acceptance. However, therapeutic modalities for secondary regular atrial tachycardia are still empiric.

Increased Preoperative Serum Apoptosis Marker Fas Ligand Correlates With Histopathology and New-Onset of Atrial Fibrillation in Patients After Cardiac Surgery

We evaluated if preoperative serum apoptosis markers correlate with atrial histological remodeling and postoperative atrial fibrillation (POAF) after cardiac surgery.

ARBs, ACE‐Is, or Statins After Catheter Ablation of Atrial Fibrillation?

Interventional therapy of atrial fibrillation (AF) has become more engaged in everyday practice of electrophysiologic centers with around 53,000 worldwide cases of AFablation in the year 2006 (25,000 within the United States). A wide variety of different catheter ablation techniques are performed and have been established as second-line therapy of symptomatic AF. Interestingly enough, no recommendations regarding postinterventional medication are available. The pathogenesis of AF is a multicomponent complex process involving not only electrical, but also structural changes of atrial myocardium. The term “AF begets AF” very well describes the complex nature of atrial electrophysiological and structural changes involved in the persistence of AF.1 Inflammation and oxidative stress have been documented to be part of the early remodeling process during the occurrence of AF. Alterations of the atrial tissue architecture involve fibrosis and are part of the structural remodeling process leading to persistent AF. Effects of the healing process of inflammation may be the connecting part between early inflammation and later structural changes in the remodeling process of AF.2-5 In the last years, growing evidence has emerged that the renin-angiotensin system (RAS) is involved in the process of electrophysiological and structural substrate formation perpetuating AF. Angiotensin-mediated pathways induce cellular differentiation processes and activation of fibroblast that play an important role in the induction of atrial fibrosis during AF. In experimental studies, blockade of angiotensin-II prevented early electrical remodeling and attenuated the arrhythmogenic substrate. Inhibition of the angiotensin-converting enzyme (ACE) may prove less effective than blocking the angiotensin receptor itself because the main angiotensin forming enzyme in the human atrium is chymase, not ACE. In addition, even under the conditions of renin-angiotensin system blockade, local activation of aldosterone may occur and participate in the enhancement of atrial fibrosis (so-called “aldosterone escape”).2,3 These experimental analyses gave rise to mostly retrospective clinical studies evaluating the effect of ACE-inhibitors (ACE-Is) and angiotensin receptor blockers (ARBs) on the