Oliver R. Segal

Mechanisms that initiate ventricular tachycardia in the infarcted human heart

Background Precise mechanisms that initiate ventricular tachycardia (VT) in the intact infarcted human heart have not been defined. Objective The purpose of this study was to investigate the mechanisms that underlie human postinfarct VT initiation. Methods Noncontact mapping of the left ventricle was performed in 9 patients (age 67.1 ± 7.8 years, ejection fraction 34.4% ± 5%) with previous myocardial infarction and sustained monomorphic VT. Results Circuits in which ≥30% of the diastolic pathway (DP) could be defined were identified in 12 VTs (cycle length 357 ± 60 ms). Eighteen VT episodes were initiated with pacing, and one occurred spontaneously. Ten complete and two partial circuits were mapped (89% ± 25% of the DP). In all complete circuits, pacing led to the development of unidirectional conduction block at the location of the subsequent VT exit site and the formation of functional block creating a border(s) for subsequent DP. Wavefront velocity in the DP region slowed from 1.22 ± 0.2 m/s during sinus rhythm to 0.59 ± 0.14 m/s during VT (P <.005). In 11 initiation episodes, lines of functional block and areas of slow conduction developed progressively over one to six reentrant cycles before a stable DP was established and sustained monomorphic VT ensued. The formation of unidirectional or functional lines of block was not identified during identical pacing protocols that failed to initiate VT (n = 14). Conclusion Initiation of sustained monomorphic VT requires the development of unidirectional block and formation of lines of functional block creating borders for a DP in areas of slow conduction. A transitional stage often exists during the initiation process before a stable VT circuit is established.

A novel algorithm for determining endocardial VT exit site from 12-lead surface ECG characteristics in human, infarct-related ventricular tachycardia.

Introduction: Characteristics of the 12‐lead ECG during VT are used to guide initial placement of mapping catheters in endocardial ventricular tachycardia (VT) ablation. Previously constructed algorithms for guidance in human infarct‐related VT are limited to patients known to have anterior or inferior infarcts only. We hypothesized that 12‐lead ECG characteristics could be used to determine VT exit site in patients with all types of infarction of unknown location.

Mechanism of Pacing-Induced Ventricular Fibrillation in the Infarcted Human Heart

Background—The mechanisms by which ventricular fibrillation (VF) is initiated in the infarcted human heart have not been defined. Methods and Results—Left ventricular noncontact mapping of 8 episodes of pacing-induced VF in 6 patients (age 64.8±7.9 years, with previous myocardial infraction and left ventricular ejection fraction of 36±4%) undergoing ventricular tachycardia (VT) ablation revealed a consistent mechanism of VF induction. Whether during VT or sinus rhythm, the first of a train of paced extrastimuli to capture the LV produced an arc or arcs of functional block at regions bordering scar. With subsequent extrastimuli, the arcs elongated to circumscribe an enlarging area of increasingly late activation, with reentry through part of this functional (unidirectional) block leading to wavefront fragmentation and VF. These regions had longer fibrillation intervals (263±63 ms) than remote LV regions (209±23.4 ms; P<0.0001), implying longer refractory periods, and in 6 of the 8 VF episodes, these regions correlated with VT exit sites. In each of the 2 patients with 2 episodes of VF, both episodes formed arcs of functional block in the same location, despite pacing from different sites. Conclusions—Pacing-induced VF in the infarcted human heart is initiated by the development of functional lines of block dictated by the properties of a particular region of myocardium characterized by longer refractory periods, at or near VT circuit exit sites. Identification of these characteristic properties may help stratify risk of arrhythmic death and explain the potential for VT ablation to modify risk of VF in the infarcted heart.

Intra-coronary guidewire mapping–A novel technique to guide ablation of human ventricular tachycardia

HypothesisEndocardial catheter ablation of ventricular tachycardia (VT) may fail if originating from epicardial or intramural locations. We hypothesized that mapping could be achieved using an angioplasty guidewire in the coronary circulation, to guide trans-coronary ablation.Methods and resultsSix patients (2 male), 64u2009±u200914xa0years and previously unsuccessful endocardial VT ablation were studied. Using ECG and existing endocardial mapping data, a coronary artery supplying the predicted VT origin was selected. A 0.014-in angioplasty guidewire was advanced into branches of the artery and connected to an amplifier to record unipolar signals against an indifferent electrode within the inferior vena cava. An uninflated angioplasty balloon was advanced over the wire such that only the distal 5xa0mm was used for mapping. One VT per patient was mapped (CL 348u2009±u2009102.1xa0ms). Diastolic potentials were recorded from all (77.7u2009±u200943.8xa0ms pre-QRS onset) and concealed entrainment demonstrated in 3. Pacemapping during sinus rhythm was used in the remainder due to failure of entrainment (nu2009=u20092) or degeneration to VF (nu2009=u20091). Following branch identification, cold saline injection causing VT termination was used for further confirmation. Five VTs were ablated using intra-coronary ethanol injection via the central lumen of the inflated over the wire balloon. The other was ablated using radiofrequency energy in a coronary vein adjacent to the target artery, which was too small for an angioplasty balloon. No complications or recurrence of ablated VT was seen over 19u2009±u200917xa0months of follow up.ConclusionsIntracoronary guidewire mapping is a novel method of electrophysiological epicardial mapping to help guide trans-coronary VT ablation.

Chapter 93 – Mapping

Cardiac mapping is the process of identification, characterization, and localization of an arrhythmia. With few exceptions, such as the anatomical approach sometimes adopted for the ablation of some arrhythmias (e.g., typical atrial flutter), mapping forms the basis for guiding therapeutic intervention, usually in the form of percutaneous ablation. The principles and techniques used for mapping vary considerably, depending on the likely arrhythmic substrate. A careful evaluation of the patients history, echocardiographic and other imaging data, and the 12-lead electrocardiogram (ECG) during sinus rhythm and clinical arrhythmia before the procedure can greatly facilitate the selection of initial strategy for mapping.

Multiple distinct right atrial endocardial origins in a patient with atrial tachycardia: mapping and ablation using noncontact mapping.

Noncontact mapping identified the endocardial origins of four distinct atrial tachycardias in a young patient with drug refractory palpitations and effected successful ablation with no recurrence of symptoms in 5 months of follow‐up. (PACE 2004; 27:541–544)

Too focused?: the perils of a fashionable diagnosis.

A 33-year-old-man presented with a 1-year history of frequent irregular palpitation. A typical example of his tachycardia recorded by Holter monitoring (Fig. 1A) was interpreted as high-frequency atrial ectopy degenerating at times to atrial x8e brillation, so-called focal atrial x8e brillation (FAF). His symptoms did not improve despite various antiarrhythmic therapies, including amiodarone, atenolol, digoxin, verapamil, and x8f ecainide. He was referred and accepted specix8e cally for FAF ablation. Upon arrival, the patient was in almost incessant irregular tachycardia (Fig. 2). What is the arrhythmia?

The effects of the gap junction uncoupler carbenoxolone on human myocardial conduction and arrhythmogenicity

Background: Conventional antiarrhythmic drugs modify action potential and are potentially pro-arrhythmic. Carbenoxolone (CARB), an anti-ulcer drug, has been shown to reduce gap junctional coupling without affecting cellular ion channels. Hypothesis: CARB decreases endocardial conduction velocity (CV) without altering refractoriness (AERP). Methods: Right atrial (RA) and ventricular (RV) mapping during sinus rhythm was performed using the CARTO system. AERP was measured at the coronary sinus, RA and RV apex. Ventricular tachycardia (VT) stimulation was performed. 100mg of CARB was given orally and the protocol repeated after 1 hour. CV, specifically in the direction of propagation, was determined from the activation maps using a triangulation method. Sinus rhythm cycle length, PR, QT intervals, QRS amplitude and duration were measured. Results: 11 patients with VT, aged 60.8 15.1 years completed the protoccol. 6 patients had ischemic heart disease (IHD) and impaired LV function and the other patients had structurally normal hearts. CV was reduced from 79.6 13.5 cm/s to 57.2 9.2 cm/s (27.1%, p 0.01) in the right atrium and from 98.7 19.8 cm/s to 76.5 21.7 cm/s (22.7%, p 0.01) in the right ventricle. Slowing of conduction was more marked in the 6 patients with IHD (RV 33.8% vs. 9.3%, p 0.01; RA by 35.1% vs. 17.5%, p 0.02) than the patients with normal hearts. There were no significant changes to AERP or ECG parameters following CARB. In a patient with IHD, VT with a CL of 290 ms was induced which was not pace terminable. Following CARB, the same VT was initiated at a CL of 320ms and was readily terminated with 2 extrastimuli. Conclusion: CARB causes a 27.1% reduction in CV in the human RA and 22.7% in the RV without affecting AERP. A greater reduction in CV in IHD patients may be due to more profound uncoupling of initially poorly coupled cells. The ability to terminate VT with pacing was effected by CARB in 1 patient due to slowing of conduction and apparent enlargement of the excitable gap. CARB, already licensed for human use, provides a tool for investigating the effects of specific gap junction uncoupling in human arrhythmogenesis.