Earliest Epicardial Activation Research Articles

Electrophysiological properties and involvement of anatomical factors for the prediction of intramural origin in patients with ventricular tachyarrhythmia arising from the left ventricular outflow tract.

To elucidate the electrophysiological predictors of the intramural origins of left ventricular outflow tract-ventricular tachyarrhythmias (LVOT-VAs), and to clarify the involvement of anatomical factors. Twenty-nine successfully ablated LVOT-VAs patients with origins in the aortomitral continuity (AMC) (n = 8), aortic sinus of valsalva (ASV) (n = 9), great cardiac vein (GCV) (n = 5), and intramural myocardium (n = 7) were enrolled. Intramural origins were defined as when effective ablation from AMC and epicardium (ASV and/or GCV) was needed. The local activation time difference (LATD) was calculated as follows: (earliest AMC activation) - (earliest epicardial activation), and was presented as an absolute value. Electrophysiological parameters and anatomical factors predisposing the intramural origins were investigated. LATD of intramural origins was significantly shorter than that of AMC and GCV (4.5 ± 2.6 vs. 12.1 ± 7.4 vs. 17.4 ± 4.7, P < 0.05), respectively. In multivariate logistic regression analysis, LATD was associated with intramural origins (odds ratio: 0.711, confidence interval: 0.514-0.985, P = 0.040). ROC analysis revealed LATD of 7 ms as cut-off value. In computed tomography analysis, some patients who had thick fat tissue below the GCV, and an unusual GCV running pattern might be misdiagnosed as intramural origins. LATD ≤ 7 ms was associated with intramural origins, but with some anatomical limitations.

PP-271 EXERCISE-INDUCED TACHYCARDIA BOTH WIDE AND NARROW QRS COMPLEX

Figure 1. Idiopathic epicardial ventricular tachycardia originating from the great cardiac vein. (A) ECG revealed VPCs with LBBB QRS morphology and a inferior axis. (B) In cardiovascular stress test frequency of VPCs increased and the test terminated because of a sustained VT in stage 3. (C) Holter monitorisation showed frequent monomorphic VPCs, and several times of sustained-nonsustained VTs. (D) In the course of mapping of the coronary sinus in EPS, during VPCs, the earliest epicardial activation preceding the onset of the QRS complex by 32ms. (E) The distance from the catheter tip to coronary arteries was acceptable. (F) After the procedure ECG showed neither PVCs nor VTs.

Spectral analysis of electrograms during ventricular tachycardia in a canine model: Relation with epicardial isochronal maps

The purpose of this study was to assess the capability of magnitude-squared coherence and bicoherence to differentiate monomorphic ventricular tachycardia (MVT) and polymorphic ventricular tachycardia (PVT) in a canine model and to relate these results to the epicardial isochronal maps on a beat-to-beat basis. Unipolar electrograms were simultaneously recorded from the surface of both ventricles with a 127-lead sock electrode array in 12 open-chest anesthetized dogs. The sampling frequency was 500 Hz. Atrioventricular block was induced by formaldehyde injection into the atrioventricular node. The left anterior descending coronary artery was occluded for 60 minutes under ventricular pacing (140 beats/min). During reperfusion, 12 MVT episodes lasting more than 42 seconds were recorded. Left stellate ganglion stimulation induced five PVT episodes lasting more than 42 seconds. Each of these recordings was divided into seven segments of 3,072 points (6.144 seconds). After visual selection, 104 segments were extracted and classified as 73 MVT and 31 PVT segments. Magnitude-squared coherence was estimated as the cross-spectrum from two epicardial signals (on the right and left ventricles, respectively), normalized with the respective autopower spectrum. Bicoherence was estimated as the bispectrum normalized with the autopower spectrum. Magnitude-squared coherence correctly identified 96% of MVT. and 81% of PVT segments for a total accuracy of 91%. Bicoherence estimated with the left ventricular lead correctly identified 100% of MVT and 77% of PVT segments with an accuracy of 93%. Beat-to-beat epicardial maps of MVT displayed a cluster of sites of origin close to the reperfusion area, while the sites of origin from beats during PVT were much more dispersed over both ventricles. A strong and significant correlation was found between the number of electrodes with the earliest epicardial activation and coherence ( r = .76, P < .0001) and bicoherence ( r = .68, P < .0001), respectively. A high and significant correlation was also found between both spectral estimators ( r = .74, P < .0001). Coherence and bicoherence discriminated accurately between MVT and PVT. Coherence achieved better results compared with bicoherence. Coherence and bicoherence measurements showed a quantitative relation with the spatial dispersion of the sites of origin. Both spectral techniques seemed powerful enough to be used in the development of implantable devices.

On-line epicardial mapping of intraoperative ventricular arrhythmias: Initial clinical experience

An on-line automatic mapping system was developed for beat by beat display of epicardial activation during ventricular tachycardia induced at the time of cardiac surgery. A sock array of 110 button electrodes was used to record and display local activation on a video monitor at 8.3 ms intervals. On instant replay in slow motion, epicardial pacing sites were accurately localized to the nearest electrode. Local unipolar electrograms were also recorded, first from the sock array, then from an array of 16 transmural needle electrodes. The epicardial display was verified by retrospective manually derived maps using the recorded epicardial electrograms. In four patients with coronary artery disease and recurrent inducible ventricular tachycardia, earliest epicardial activation was located on slow motion replay within 1 minute. Subendocardial sites of early activation were located within 10 minutes by replay of electrograms from the needle array before ventriculotomy. Transmural and endocardial resection of these sites prevented inducibility of the tachycardia on postoperative electrophysiologic study in three of the four patients. There has been no clinical recurrence of ventricular tachycardia after 3 to 14 months of follow-up despite cessation of antiarrhythmic therapy in three of the patients. This technique has unique advantages over existing mapping methods. It provides beat by beat display of activation sequences so that clinical tachycardias that are short in duration or pleomorphic in configuration now become amenable to mapping. In addition, it markedly shortens total time on cardiopulmonary bypass.

Epicardial and endocardial activation during sustained ventricular tachycardia in man.

Ventricular activation during ventricular tachycardia was studied by intraoperative epicardial and endocardial mapping in 21 patients with coronary artery disease and previous myocardial infarction who underwent operation for recurrent ventricular tachycardia. Twenty-nine morphologically distinct tachycardias were mapped; 18 tachycardias had a right bundle branch block morphology and 11 had a left bundle branch block morphology. After cannulation for bypass, the tachycardias were induced and electrograms were recorded at 55-75 epicardial sites. After starting cardiopulmonary bypass, the infarction was incised and electrograms were recorded at 28-55 left ventricular endocardial sites during ventricular tachycardia. All mapping data were analyzed with three simultaneously recorded ECG lead and two reference electrograms. Earliest activation in all tachycardias occured on the endocardial surface of the infarction. In each tachycardia, endocardial electrical activity was recorded before the onset of the QRS complex. Earliest epicardial activation in the 29 tachycardias occurred 10 msec after the onset of QRS complex. Epicardial breakthrough occurred on the right (19 tachycardias) as well as the left ventricle (10 tachycardias). We conclude that ventricular tachycardia associated with ischemic heart disease originates near the endocardial surface of the left ventricle along the border of the infarction and that epicardial mapping alone is insufficient to identify the site of origin of these tachycardias.

Comparison of SA nodal and subsidiary atrial pacemaker function and location in the dog

A 3-4 cm length of sulcus terminalis tissue including the sinoatrial node (SAN) was excised from 14 dogs. After an initial junctional rhythm with SAN excision a P wave emerged within days to weeks in 12 animals. Maximum heart rates of the SAN (preoperative) in response to exercise (276 +/- 15 beats/min), isoproterenol infusion in conscious animals (272 +/- 11 beats/min), and stellate stimulation during anesthesia (273 +/- 9 beats/min) were significantly greater than subsidiary pacemakers (postoperatively) for exercise (219 +/- 9 beats/min), isoproterenol (226 +/- 8 beats/min), and stellate stimulation (197 +/- 9 beats/min). During a final experiment, electrophysiological mapping of the area of earliest epicardial activation (pacemaker location) was carried out. By use of a suction electrode in reference to plunge electrodes located in the anterior interatrial band (AIB), eustachian ridge of the coronary sinus, and limbus of the fossa ovalis, the pacemaker was located at the inferior vena cava-inferior right atrial junction in 80% of the animals mapped. During isoproterenol infusion the foci shifted to regions of the AIB in 70% of the animals mapped. The concept of pacemaker hierarchy is discussed.

Spread of the epicardial excitation in right bundle branch block pattern.

Electrophysiologic mapping was performed on 29 dogs and 35 patients to investigate the ventricular excitation sequence of normal hearts and various cardiac lesions exhibiting the electrocardiographic pattern of right bundle branch block (RBBB). The activation times of epicardial surface were referenced to the onset of left ventricular cavity potential or QRS wave of lead II ECG. Epicardial activation sequence was represented by isochrones. 1. In normal hearts, the earliest epicardial breakthrough occurred at the mid-anterior paraseptal area in the right ventricle and the activation spread in a circular fashion. In the left ventricle, the epicardial activation occurred at three areas and then spread to the posterobasal area. The epicardial activation sequence was a good representation of the ventricular excitation. 2. In RBBB due to trauma to the main right bundle branch, the right ventricular activation showed marked delay and the characteristic V-shaped pattern. 3. Following vertical ventriculotomy, the right ventricular epicardial activation showed marked delay at sites distal to the incision but no significant delay proximal to it. Regarding postoperative RBBB, central right bundle branch injury was able to be differentiated from distal Purkinje injury due to right ventriculotomy by means of epicardial mapping. 4. In left ventricular pacing, the activation spread in a circular fashion with the prolonged right ventricular activation. 5. In ostium secundum defect, the right ventricular epicardial activation sequence showed various patterns of activation delay resulting from right ventricular hypertrophy. In ostium primum defect, the earliest epicardial activation was found in the left posterior paraseptal area, and the right ventricular activation showed a normal pattern with some delay. Epicardial mapping has been the precise representation of ventricular excitation by direct measurement of cardiac potentials. Cardiac lesions exhibiting the electrocardiographic RBBB pattern provided various patterns of the right ventricular activation delay according to the geneses of RBBB.