Ryan Cooley

Computed Tomography‐Fluoroscopy Image Integration‐Guided Catheter Ablation of Atrial Fibrillation

Introduction: This study examines the feasibility of atrial fibrillation (AF) ablation using registered three‐dimensional computed tomography (CT) images of the left atrium with fluoroscopy.

Electroanatomically Guided Catheter Ablation of Ventricular Tachycardias Causing Multiple Defibrillator Shocks

SRA, J., et al.: Electroanatomically Guided Catheter Ablation of Ventricular Tachycardias Causing Multiple Defibrillator Shocks. With conventional techniques, RF catheter ablation is difficult in patients with unstable VT or with multiple VTs. The feasibility of RF catheter ablation guided by three‐dimensional electroanatomic mapping technique in patients whose implanted ICD continued to deliver multiple shocks due to VT despite use of antiarrhythmic medications was assessed in 19 patients (15 men, 4 women; mean age [± SD] 70 ± 7 years). All had a prior history of MI and subsequently had received an ICD due to VT. During the 12‐week preablation period, these patients received 31 ± 15 shocks (range 4–62 shocks) due to refractory monomorphic VTs. An electroanatomic mapping technique using the CARTO system was performed to delineate scar tissue. RF catheter ablation was then performed at appropriate sites identified by pacemapping and by substrate mapping. Seventeen patients were on amiodarone at the time of ablation. Twenty‐seven VTs were documented clinically, and 45 were induced during electrophysiological evaluation. Of the 45 tachycardias induced, 38 VTs were targeted for ablation. Catheter ablation was performed during sinus rhythm in 31 episodes and during VT in 7 episodes. During a mean follow‐up of 26 ± 8 weeks (range 18–48 weeks), 13 (66%) patients had no recurrence of VT (P < 0.0001) and antiarrhythmic drugs were discontinued or the number of medications reduced in 17 patients (P < 0.0001). Electroanatomic mapping is helpful in identifying sites for catheter ablation in highly symptomatic patients with refractory VT associated with myocardial scarring.

Catheter location, tracking, cardiac chamber geometry creation, and ablation using cutaneous patches.

Objective: The ability to construct a three-dimensional (3-D) surface model of the endocardium and track the location of catheters within a cardiac chamber, using only cutaneous patches, would be a useful advancement in treating arrhythmias. We tested the feasibility of such a system, Ensite NavX (Endocardial Solutions, Inc., St. Paul, MN, USA), in patients undergoing catheter ablation for SVTs.Methods: Sixteen patients with 20 arrhythmias undergoing ablation were selected. Skin electrode patches were placed on the chest to create a 3-D coordinate system. A low-amplitude, 5.7 kHz signal emitted from the patches was received by conventional catheters positioned in the heart.Catheter location was determined by measuring the field strength received by the catheters. Location points were successively acquired while catheters were moved throughout the chamber. This information was collected and processed by a workstation to create a detailed 3-D model of the endocardial surface. Anatomic landmarks were labeled on the model as the mapping catheter was navigated. 3-D cardiac chamber geometry reconstruction, landmark labeling, and real time catheter tracking were performed successfully in all patients. Up to six catheters, with a total of up to 26 intracardiac electrodes, were tracked simultaneously.Results: Constructed geometries, including major vessels and valves, correlated closely with traditional anatomic models as well as intracardiac recordings and fluoroscopic images.Conclusions: Real-time catheter tracking and 3-D cardiac chamber model construction is feasible using cutaneous patches and conventional catheters. This approach may be useful in the treatment of patients with cardiac arrhythmias where ablation therapy is primarily anatomically based.

Atrial fibrillation: Epidemiology, mechanisms, and management

The incidence of AF, the most common sustained arrhythmia in clinical practice, increases with age and coronary artery disease, hypertension and valvular heart disease are common underlying substrates; however, occasionally, AF may occur without any underlying heart disease. The most widely accepted theory of its mechanism is Moes multiple wavelet hypothesis, although recent studies are helping to shed light on other mechanisms, including the focal origin of AF in some patients. Most patients experience palpitations, but fatigue, dyspnoea, and dizziness may also occur. Therapy includes prevention of thromboembolism, control of rate, and restoration and maintenance of sinus rhythm. The risks and benefits of each treatment modality need to be assessed according to each patients circumstances. Unlike other arrhythmias, there is still no highly successful therapy for treating AF. However, significant advances are being made using non-pharmacological approaches to either prevent or cure this troublesome arrhythmia.

Periprocedural anticoagulation for atrial fibrillation ablation.

Background: Catheter ablation for atrial fibrillation (AF) can increase risk of left atrial (LA) thrombi and stroke. Optimal periprocedural anticoagulation has not been determined.

Sudden cardiac death.

Abstract SCD continues to be an important cause of death and morbidity. Despite expanding insight into the mechanisms causing SCD, the population at high risk is not being effectively identified. Although there is still much to do in the management phase of SCD (predicting the efficacy of various therapies), recent clinical trials have helped define the relative risks and benefits of therapies in preventing SCD. Trials are underway to determine whether treating other patient populations, including asymptomatic patients after MI, will improve survival rate. The approach to reducing mortality rate will always be multifaceted; primary prevention of coronary artery disease and prompt salvage of jeopardized myocardium are 2 important aspects of this approach. In addition to interventions for MI, such as myocardial revascularization when indicated, simple and easily administered therapies that are likely to remain the most effective prophylactic interventions are aspirin, ACE inhibitors, β-blockers, and cholesterol-lowering agents. However, the MADIT and AVID data clearly demonstrate a role for ICD therapy in a subgroup of patients who have VT/VF and are at risk of cardiac arrest. Even though the absolute magnitude of benefit associated with ICDs is still to be determined, the AVID study and other recent reports provide convincing evidence that patients who have VT/VF fare better with ICDs than with antiarrhythmic drug therapy. For the high-risk population described in this article, in addition to aggressive antiischemic and heart failure therapy, ICDs are now a mainstay of life-saving treatment. Still to be surmounted is the challenge of identifying patients who have nonischemic substrates and of providing them with the appropriate therapy. Guided by genetic studies and new insight into the mechanisms of such problems as congenital long QT syndrome, life-saving and life-enhancing therapies may soon be available for the management of SCD.

Electroanatomic Mapping to Identify Breakthrough Sites in Recurrent Typical Human Flutter

SRA, J., et al.: Electroanatomic Mapping to Identify Breakthrough Sites in Recurrent Typical Human Flutter. The accuracy of conventional techniques in localizing previous radiofrequency (RF) ablation sites and thus breakthrough sites of recurrent atrial flutter is somewhat limited. We investigated the role of electroanatomic mapping for identifying breakthrough sites or “gaps” at the tricuspid annulus and inferior vena cava (IVC)/eustachian ridge isthmus to help RF ablation in patients with recurrent typical flutter. Twelve patients (8 men, 4 women, age 63 ± 10 years) with recurrent typical atrial flutter were included in the study. An electroanatomic mapping system (CARTO) was used to create a voltage map and activation and propagation patterns in the right atrium. Detailed voltage, activation, and propagation mapping of the tricuspid annulus and IVC/eustachian ridge isthmus allowed precise identification of gaps in all 12 patients at the tricuspid annulus (eight sites), IVC ridges (two sites), mid‐isthmus region (one site), and tricuspid annulus and IVC ridges (one site). Radiofrequency energy directed at these sites eliminated atrial flutter in all 12 patients, confirmed by noninducibility of atrial flutter and demonstration of conduction block during atrial pacing on either side of the lesion lines. During a mean follow‐up of 14.8 ± 3.5 months (range 8–19 months), paroxysmal atrial flutter recurred in only one patient and was subsequently treated with amiodarone, although this had been ineffective prior to ablation. Electroanatomic mapping can precisely identify gaps in the lesion line responsible for breakthrough of recurrent typical atrial flutter at the tricuspid annulus and at the IVC/eustachian ridge isthmus. These sites can be targeted with RF ablation with a high degree of success.

Anterolateral papillary muscle ventricular tachycardia

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Acute angiographic and clinical outcome of high speed percutaneous rotational atherectomy (rotablator

-see front matter B 2014 Heart Rhythm Society. All rights reserved. on nuclear myocardial perfusion imaging. Twenty-four-hour Holter monitoring revealed 58,612 monomorphic ectopic ventricular beats (50.8% of all beats), with series of ventricular tachycardia up to 91 beats in duration. Betablockers, calcium-channel blockers, and flecainide were unsuccessful in treating PVCs and symptoms. Echocardiography revealed a left ventricular ejection fraction (during sinus beats) of 32%. An earlier catheter ablation attempt to target the site of earliest ventricular activation preceding the PVCs was unsuccessful. Intracardiac electrode contact and mapping via both the retrograde aortic approach and a transseptal puncture had proved difficult. The earliest site of activation covered a large area of myocardium and preceded the surface ventricular activation only by 10– 15 ms. The PVC morphology (Figure 1A) suggested an