How to measure propagation velocity in cardiac tissue: a simulation study

To estimate conduction velocities from activation times in myocardial tissue, the "average vector" method computes all the local activation directions and velocities from local activation times and estimates the fastest and slowest propagation speed from these local values. The "single vector" method uses areas of apparent uniform elliptical spread of activation and chooses a single vector for the estimated longitudinal velocity and one for the transversal. A simulation study was performed to estimate the influence of grid size, anisotropy, and vector angle bin size. The results indicate that the "average vector" method can best be used if the grid- or bin-size is large, although systematic errors occur. The "single vector" method performs better, but requires human intervention for the definition of fiber direction. The average vector method can be automate

Mapping and Surgical Ablation of Focal Epicardial Left Ventricular Tachycardia

We describe a technical challenge in a 17-year-old patient with incessant epicardial focal ventricular arrhythmia and diminished LV function. Failure of ablation at the earliest activated endocardial site during ectopy suggested an epicardial origin, which was supported by specific electrocardiographic criteria. Epicardial ablation was not possible due to the localization of the origin of the ventricular tachycardia adjacent to the phrenic nerve. Minimal invasive surgical multielectrode high-density epicardial mapping was performed to localize the arrhythmia focus. Epicardial surgical RF ablation resulted in the termination of ventricular ectopy. After 2 years, the patient is still free from arrhythmias

Dominant frequency of atrial fibrillation correlates poorly with atrial fibrillation cycle length

Localized sites of high frequency during atrial fibrillation (AF) are used as target sites to eliminate AF. Spectral analysis is used experimentally to determine these sites. The purpose of this study was to compare dominant frequencies (DF) with AF cycle length (AFCL) of unipolar and bipolar recordings. Left and right atrial endocardial electrograms were recorded during AF in 40 patients with lone AF, using two 20-polar catheters. Mean age was 53+/-9.9 years. Unipolar and bipolar electrograms were recorded simultaneously during 16 seconds at 2 right and 4 left atrial sites. AFCLs and DFs were determined. QRS subtraction was performed in unipolar signals. DFs were compared with mean, median, and mode of AFCLs; 4800 unipolar and 2400 bipolar electrograms were analyzed. Intraclass correlation was poor for all spectral analysis protocols. Best correlation was accomplished with DFs from unipolar electrograms compared with median AFCL (intraclass correlation coefficient, 0.67). A gradient in median AFCL of >25% was detected in 16 of 40 patients. In 13 of 16 patients (81%) with a frequency gradient of >25%, the site with highest frequency was located in the left atrium (posterior left atrium in 8 patients). The site with shortest median AFCL and highest DF corresponded in 25% if unipolar and in 31% if bipolar electrograms were analyzed. DFs from unipolar and bipolar electrograms recorded during AF correlated poorly with mean, median, and mode AFCL. If a frequency gradient >25% existed, the site with highest DF corresponded to the site of shortest median AFCL in only 25% of patients. Because spectral analysis is being used to identify ablation sites, these data may have important clinical implication

Thoracoscopic Video-Assisted Pulmonary Vein Antrum Isolation, Ganglionated Plexus Ablation and Periprocedural Confirmation of Ablation Lesions. First Results of a Hybrid Surgical-Electrophysiological Approach for Atrial Fibrillation

BACKGROUND: -Thoracoscopic pulmonary vein isolation (PVI) and ganglionated plexus (GP) ablation is a novel approach in the treatment of atrial fibrillation (AF). We hypothesize that meticulous electrophysiological confirmation of PVI results in fewer recurrences of AF during follow-up. METHODS AND RESULTS: -Surgery was performed through three ports bilaterally. GPs were localized and subsequently ablated. PVI was performed and entry and exit block was confirmed. Additional left atrial ablation lines (ALAL) were created, and conduction block verified, in patients with non-paroxysmal AF. The left atrial appendage was removed. Freedom of AF was assessed by ECGs and Holter monitoring every 3 months or during symptoms of arrhythmia. Anti-arrhythmic drugs (AAD) were discontinued after 3 months and oral anticoagulants were discontinued according to the guidelines. Thirty-one patients were treated (16 paroxysmal AF, 13 persistent AF, 2 long standing persistent (LSP) AF). Thirteen patients with non-paroxysmal received ALAL. After one year, 19/22 patients (86%) had no recurrences of AF, atrial flutter or atrial tachycardia and were not using AAD (11/12 paroxysmal, 7/9 persistent, 1/1 LSP). Three patients had a sternotomy because of uncontrolled bleeding during thoracoscopic surgery. Four adverse events were; 1 hemothorax, 1 pneumothorax and 2 pneumonia. No thromboembolic complications or mortality occurred. CONCLUSIONS: -Thoracoscopic surgery with PVI and GP ablation for AF is a safe and successful procedure with a single procedure success rate of 86% at one year. Electrophysiological guided thorough PVI and ALAL creation presumably contributes in achieving a high success rate in the surgical treatment of A

Slow and discontinuous conduction conspire in Brugada syndrome: a right ventricular mapping and stimulation study

BACKGROUND: Brugada syndrome (BrS) is associated with lethal arrhythmias, which are linked to specific ST-segment changes (type-1 BrS-ECG) and the right ventricle (RV). The pathophysiological basis of the arrhythmias and type-1 BrS-ECG is unresolved. We studied the electrophysiological characteristics of the RV endocardium in BrS. METHODS AND RESULTS: RV endocardial electroanatomical mapping and stimulation studies were performed in controls (n=12) and BrS patients with a type-1 (BrS-1, n=10) or type-2 BrS-ECG (BrS-2, n=12) during the studies. BrS-1 patients had prominent impairment of RV endocardial impulse propagation when compared with controls, as represented by: (1) prolonged activation-duration during sinus rhythm (86+/-4 versus 65+/-3 ms), (2) increased electrogram fractionation (1.36+/-0.04 versus 1.15+/-0.01 deflections per electrogram), (3) longer electrogram duration (83+/-3 versus 63+/-2 ms), (4) activation delays on premature stimulation (longitudinal: 160+/-26 versus 86+/-9 ms; transversal: 112+/-5 versus 58+/-6 ms), and (5) abnormal transversal conduction velocity restitution (42+/-8 versus 18+/-2 ms increase in delay at shortest coupling intervals). Wider and more fractionated electrograms were also found in BrS-2 patients. Repolarization was not different between groups. CONCLUSIONS: BrS-1 and BrS-2 patients are characterized by wide and fractionated electrograms at the RV endocardium. BrS-1 patients display additional conduction slowing during sinus rhythm and premature stimulation along with abnormal transversal conduction velocity restitution. These patients may thus exhibit a substrate for slow and discontinuous conduction caused by abnormal active membrane processes and electric coupling. Our findings support the emerging notion that BrS is not solely attributable to abnormal electrophysiological properties but requires the conspiring effects of conduction slowing and tissue discontinuitie

Local Depolarization Abnormalities Are the Dominant Pathophysiologic Mechanism for Type 1 Electrocardiogram in Brugada Syndrome A Study of Electrocardiograms, Vectorcardiograms, and Body Surface Potential Maps During Ajmaline Provocation

Objectives We sought to obtain new insights into the pathophysiologic basis of Brugada syndrome (BrS) by studying changes in various electrocardiographic depolarization and/ or repolarization variables that occurred with the development of the signature type 1 BrS electrocardiogram (ECG) during ajmaline provocation testing. Background BrS is associated with sudden cardiac death. Its pathophysiologic basis, although unresolved, is believed to reside in abnormal cardiac depolarization or abnormal repolarization. Methods Ajmaline provocation was performed in 269 patients suspected of having BrS with simultaneous recording of ECGs, vectorcardiograms, and 62-lead body surface potential maps. Results A type 1 ECG was elicited in 91 patients (BrS patients), 162 patients had a negative test result (controls), and 16 patients had an abnormal test result. Depolarization abnormalities were more prominent in BrS patients and were mapped to the right ventricle (RV) by longer right precordial filtered QRS complex durations (142 +/- 23 ms vs. 125 +/- 14 ms, p <0.01) and right terminal conduction delay (60 +/- 11 ms vs. 53 +/- 9 ms, p <0.01). Repolarization abnormalities remained concordant with depolarization abnormalities as indicated by steady low nondipolar content (12 +/- 8% vs. 8 +/- 4%, p = NS), lower spatial QRS-T integrals (33 +/- 12 mV . ms vs. 40 +/- 16 mV . ms, p <0.05), similar spatial QRS-T angles (92 +/- 39 degrees vs. 87 +/- 31 degrees, p = NS), similar T-peak-T-end interval (143 +/- 36 ms vs. 138 +/- 25 ms, p = NS), and similar Tpeak-Tend dispersion (47 +/- 37 ms vs. 45 +/- 27 ms, p = NS). Conclusions The type 1 BrS ECG is characterized predominantly by localized depolarization abnormalities, notably (terminal) conduction delay in the RV, as assessed with complementary noninvasive electrocardiographic techniques. We could not define a separate role for repolarization abnormalities but suggest that the typical signs of repolarization derangements seen on the ECG are secondary to these depolarization abnormalities. (J Am Coll Cardiol 2010; 55: 789-97) (C) 2010 by the American College of Cardiology Foundatio

Left atrial pressure reduction for mitral stenosis reverses left atrial direction-dependent conduction abnormalities

Left atrial (LA) stretch-associated electrophysiological changes in patients with mitral stenosis (MS) predispose to atrial fibrillation. We hypothesized that the normalization of the pressure gradient by percutaneous transvenous mitral balloon valvotomy (PTMV) affects LA but not right atrial (RA) conduction, depending on the site of stimulation. Because direction-dependent (asymmetric) changes of conduction may contribute to arrhythmogenesis, we assessed conduction symmetry in MS patients and tested whether it is restored by PTMV. In nine patients with MS, atrial effective refractory period and local activation times (ATs) were determined during stimulation before and after PTMV, with up to four decapolar catheters (LA and RA). Eight patients with ventricular pre-excitation served as controls. ATs at basic cycle length were similar before and after PTMV. With stimulation from either atrium, they were about 45 ms in the ipsilateral atrium and about 115 ms in the contralateral atrium. With premature stimulation, ATs increased dramatically. The shortest ATs were found in the RA with RA stimulation (78 +/- 9 and 80 +/- 6 ns, before and after PTMV). PTMV caused a shortening in LA-ATs (following LA stimulation) from 118 +/- 14 to 82 +/- 5 ms (before and after; P <0.05). Asymmetry in conduction properties was therefore normalized by PTMV. PTMV led to a decrease in RA-ATs (following LA stimulation) from 196 +/- 11 to 174 +/- 13 ms (P <0.02). In addition, following RA stimulation, the dispersion in ATs in the LA decreased significantly by PTMV (from 66 +/- 10 to 34 +/- 7 ms; P <0.02). MS is associated with LA conduction delay, increased LA dispersion of conduction, and conduction asymmetry. These changes are immediately reversible by PTMV

Mechanism of right precordial ST-segment elevation in structural heart disease: Excitation failure by current-to-load mismatch

BACKGROUND The Brugada sign has been associated with mutations in SCN5A and with right ventricular structural abnormalities. Their role in the Brugada sign and the associated ventricular arrhythmias is unknown. OBJECTIVE The purpose of this study was to delineate the role of structural abnormalities and sodium channel dysfunction in the Brugada sign. METHODS Activation and repolarization characteristics of the explanted heart of a patient with a loss-of-function mutation in SCN5A (G752R) and dilated cardiomyopathy were determined after induction of right-sided ST-segment elevation by ajmaline. In addition, right ventricular structural discontinuities and sodium channel dysfunction were simulated in a computer model encompassing the heart and thorax. RESULTS In the explanted heart, disappearance of local activation in unipolar electrograms at the basal right ventricular epicardium was followed by monophasic ST-segment elevation. The local origin of this phenomenon was confirmed by coaxial electrograms. Neither early repolarization nor late activation correlated with ST-segment elevation. At sites of local ST-segment elevation, the subepicardium was interspersed with adipose tissue and contained more fibrous tissue than either the left ventricle or control hearts. In computer simulations entailing right ventricular structural discontinuities, reduction of sodium channel conductance or size of the gaps between introduced barriers resulted in subepicardial excitation failure or delayed activation by current-to-load mismatch and in the Brugada sign on the ECG. CONCLUSION Right ventricular excitation failure and activation delay by current-to-load mismatch in the subepicardium can cause the Brugada sign. Therefore, current-to-load mismatch may underlie the ventricular arrhythmias in patients with the Brugada sig