Idiopathic ventricular tachycardia originating from the left ventricle near the His bundle.

A 62-year-old man with idiopathic ventricular tachycardia (VT) exhibiting left bundle branch block and left inferior axis QRS morphology with a Qr in lead III underwent electrophysiological testing. Successful ablation was achieved in the left ventricle (LV) at a site with an excellent pace map, adjacent to the His bundle electrogram recording site. At that site, the sequence of the ventricular electrogram and late potential recorded during sinus rhythm reversed during spontaneous premature ventricular contractions with the same QRS morphology as the VT. This case shows that VT can arise from the LV ostium adjacent to the membranous septum.

Atrial tachycardia originating from the cavo-tricuspid isthmus may exhibit narrow P waves.

An 83-year-old man underwent electrophysiological testing for focal atrial tachycardia (AT) exhibiting narrow P waves with negative deflections in the inferior leads. Catheter ablation at the cavo-tricuspid isthmus (CTI) successfully eliminated the AT. The propagation map during AT and pacing study from the successful ablation site demonstrated that the atrial activation throughout the CTI did not produce significant P wave deflections. Consequently, during AT, the left atrial activation time determined the P wave duration. This case demonstrates that AT originating from the CTI may exhibit narrow P waves which can be misinterpreted as AT originating from the inter-atrial septum.

Idiopathic focal ventricular arrhythmias originating from the anterior papillary muscle in the left ventricle.

INTRODUCTION: Focal ventricular arrhythmias (VAs) have been reported to arise from the posterior papillary muscle in the left ventricle (LV). We report a distinct subgroup of idiopathic VAs arising from the anterior papillary muscle (APM) in the LV. METHODS AND RESULTS: We studied 432 consecutive patients undergoing catheter ablation for VAs based on a focal mechanism. Six patients were identified with ventricular tachycardia (VT, n = 1) or premature ventricular contractions (PVCs, n = 5) with the earliest site of ventricular activation localized to the base (n = 3) or middle portion (n = 3) of the LV APM. No Purkinje potentials were recorded at the ablation site during sinus rhythm or the VAs. All patients had a normal baseline electrocardiogram and normal LV systolic function. The VAs exhibited a right bundle branch block (RBBB) and right inferior axis (RIA) QRS morphology in all patients. Oral verapamil and/or Na(+) channel blockers failed to control the VAs in 4 patients. VT was not inducible by programmed electrical stimulation in any of the patients. In 4 patients, radiofrequency current with an irrigated or conventional 8-mm-tip ablation catheter was required to achieve a lasting success. Two patients had recurrent PVCs after a conventional radiofrequency ablation with a 4-mm-tip ablation catheter had initially suppressed the arrhythmia. CONCLUSIONS: VAs may arise from the base or middle portion of the APM and are characterized by an RBBB and RIA QRS morphology and focal mechanism. Catheter ablation of APM VAs is typically challenging, and creation of a deep radiofrequency lesion may be necessary for long-term success.

Ventricular fibrillation induced by a radiofrequency energy delivery for idiopathic premature ventricular contractions arising from the left ventricular anterior papillary muscle.

A 73-year-old man with idiopathic premature ventricular contractions (PVCs) underwent electrophysiological testing. Left ventricular activation mapping revealed a focal mechanism of the PVCs with the earliest activation on the anterior papillary muscle (APM). Irrigated radiofrequency (RF) current delivered at that site induced a cluster of non-sustained ventricular tachycardia episodes with the same QRS morphology as the PVCs, followed by ventricular fibrillation (VF). The APM might have served as an abnormal automatic trigger and driver for the VF occurrence. Ventricular fibrillation may occur as a complication during RF catheter ablation of papillary muscle ventricular arrhythmias even if the clinical arrhythmia is limited to PVCs.

Biventricular ICD implantation using the iliofemoral approach: providing CRT to patients with occluded superior venous access.

A 32-year-old woman with a history of nonischemic dilated cardiomyopathy, left bundle branch block, left ventricular ejection fraction of 0.15, and New York Heart Association Class III congestive heart failure, despite optimal medical treatment, was referred for cardiac resynchronization therapy with implantation of an implantable cardioverter defibrillator. The patient had prior chemotherapy for non-Hodgkin's lymphoma and was shown to have chronic total occlusion of the superior vena cava (SVC) by magnetic resonance imaging. Cardiac resynchronization was accomplished with an iliofemoral approach without complications resulting in marked clinical improvement. We conclude that the iliofemoral approach allows transvenous implantation of cardiac resynchronization therapy in patients with superior vena cava occlusion.

The transmural activation sequence in porcine and canine left ventricle is markedly different during long-duration ventricular fibrillation.

BACKGROUND: Humans are more similar in transmural Purkinje and cardiac ion channel distributions to dogs than pigs. The Purkinje network in pigs is transmural but confined to the endocardium in dogs. Little is known about intramural activation during long-duration ventricular fibrillation (LDVF) given these differences. We tested the hypothesis that the transmural activation sequence is similar in sinus rhythm (SR) and LDVF in dogs as well as pigs, but different between species. METHODS AND RESULTS: In six pigs and seven dogs, 50-60 plunge needles (six electrodes, 2-mm spacing) were placed throughout the left ventricle. Unipolar recordings were made for >10 minutes of LDVF. SR and LDVF activation times were grouped into waves by linking activations along each needle. Origin (earliest activation) and propagation direction were determined for each wave. The mean wave origin was significantly more endocardial in dogs than pigs for SR and 1 through 10 minutes of LDVF. Predominant propagation direction in LDVF and SR was endocardial to epicardial in dogs, but the opposite or equal in both directions in pigs. Fastest activation rate was epicardial in pigs, but endocardial in dogs with an increasing endocardial-to-epicardial activation rate gradient as LDVF progressed in dogs but not pigs. CONCLUSIONS: The transmural activation sequence in SR and LDVF is markedly different between pigs and dogs. These differences may be related to differences in Purkinje fiber and ion channel distributions and suggest that dogs are a better model for investigating activation sequences during LDVF, given the similarities with humans.

Transmural and endocardial Purkinje activation in pigs before local myocardial activation after defibrillation shocks.

BACKGROUND: Earliest recorded postshock myocardial activations in pigs originate in the subepicardium of the apex and lateral free wall of the left ventricle (LV) 30-90 ms after the shock. OBJECTIVE: The purpose of this study was to determine whether the Purkinje system is a candidate for the source of postshock activations by performing endocardial and transmural postshock activation mapping. METHODS: In five pigs, 32 plunge needles with 12 electrodes (1-mm spacing) were inserted into the LV apex and lateral free wall. Up to 70 plunge needles with six electrodes (2-mm spacing) were spread throughout the remainder of the LV, while 9-12 plunge needles with four electrodes (2-mm spacing) were inserted into the right ventricle. A basket catheter with 32 bipolar recording sites was inserted into the LV. Defibrillation-threshold (DFT)-level shocks were delivered during 10 episodes of electrically induced ventricular fibrillation. Electrograms of postshock activation cycles were analyzed for Purkinje and myocardial activations. RESULTS: Purkinje activations were recorded before local myocardial activation in 9% of basket electrograms and in 15% of plunge needles during the first postshock activation cycle. Purkinje activations were identified during the first and subsequent several postshock activation cycles in at least one basket and one needle electrogram in 96% and 98% of defibrillation episodes, respectively. CONCLUSIONS: The Purkinje system is active during the early postshock activation cycles after DFT-level shocks. Further studies are required to determine whether activation initiates in the Purkinje system or whether it is activated by the myocardium or by Purkinje-myocardial junctional cells.

Transmural recording of shock potential gradient fields, early postshock activations, and refibrillation episodes associated with external defibrillation of long-duration ventricular fibrillation in swine.

BACKGROUND: Knowledge of the shock potential gradient (nablaV) and postshock activation is limited to internal defibrillation of short-duration ventricular fibrillation (SDVF). OBJECTIVE: The purpose of this study was to determine these variables after external defibrillation of long-duration VF (LDVF). METHODS: In six pigs, 115-20 plunge needles with three to six electrodes each were inserted to record throughout both ventricles. After the chest was closed, the biphasic defibrillation threshold (DFT) was determined after 20 seconds of SDVF with external defibrillation pads. After 7 minutes of LDVF, defibrillation shocks that were less than or equal to the SDVF DFT strength were given. RESULTS: For DFT shocks (1632 +/- 429 V), the maximum minus minimum ventricular voltage (160 +/- 100 V) was 9.8% of the shock voltage. Maximum cardiac nablaV (28.7 +/- 17 V/cm) was 4.7 +/- 2.0 times the minimum nablaV (6.2 +/- 3.5 V/cm). Although LDVF did not increase the DFT in five of the six pigs, it significantly lengthened the time to earliest postshock activation following defibrillation (1.6 +/- 2.2 seconds for SDVF and 4.9 +/- 4.3 seconds for LDVF). After LDVF, 1.3 +/- 0.8 episodes of spontaneous refibrillation occurred per animal, but there was no refibrillation after SDVF. CONCLUSION: Compared with previous studies of internal defibrillation, during external defibrillation much less of the shock voltage appears across the heart and the shock field is much more even; however, the minimum nablaV is similar. Compared with external defibrillation of SDVF, the biphasic external DFT for LDVF is not increased; however, time to earliest postshock activation triples. Refibrillation is common after LDVF but not after SDVF in these normal hearts, indicating that LDVF by itself can cause refibrillation without requiring preexisting heart disease.

Printed circuit board electrodes for transmural cardiac mapping.

Plunge needle recording techniques have provided valuable insights into transmural activation in cardiac tissue. Construction of plunge needles has been a costly and time intensive endeavor. Plunge needles constructed with standard printed circuit board (PCB) technology and methods are outlined. PCB plunge needles are less expensive in terms of raw materials and time required for construction than hypodermic stock or epoxy plunge needles. Tested PCB plunge needles recorded signals comparable to signals recorded by other plunge needles. PCB plunge needles provide an economical and rapid alternative to previously published techniques for plunge needle design.

Guidelines for plunge needle recording for effective detection of purkinje activation.

Direct recording of Purkinje fiber activity may lead to a better understanding of the role of the specialized conduction system in pathological cardiac conditions. Two studies were conducted in pigs to determine guidelines for effective plunge needle recording techniques. In the first experiment, Purkinje fiber activations were recorded at 16 KHz with 3 bipolar electrodes (2 mm spacing) on epoxy plunge needles, and were later lowpass filtered and downsampled to determine the rate required for effective identification of Purkinje activation. Purkinje spikes were identifiable at sampling rates of 4 KHz and greater, but were not easily distinguished at sampling rates of 2 KHz or less. In the second experiment, 4 plunge needles with 15 electrodes (1 mm spacing) were inserted 8 times into different locations around the left ventricle. Unipolar (15 per needle) and bipolar (14 per needle) signals were recorded simultaneously at a sampling rate of 8 KHz. Purkinje activations were identified in 13/32 plunge needle sites. Of the 13 sites with identified Purkinje activations, 10 were within 2 mm of the endocardium. Bipolar recordings demonstrated Purkinje potentials that were 13% of the amplitude of the following myocardial activation, while unipolar recordings from the same electrodes recorded Purkinje potentials that were only 5% of the amplitude of the following myocardial activations. Three guidelines were developed for effective Purkinje fiber recording: 1) use a minimum sampling rate of 4 KHz., 2) record near the endocardium, and 3) use bipolar rather than unipolar recording electrodes.