John M. Miller

Subendocardial resection for ventricular tachycardia: predictors of surgical success.

We retrospectively evaluated the first 100 patients who underwent mapping-guided subendocardial resection (SER) at our hospital for drug-refractory sustained ventricular tachycardia caused by coronary artery disease. There were 91 survivors of surgery with 200 morphologically distinct types of ventricular tachycardia. Eighty-three patients (91%) were cured of ventricular tachycardia by SER alone (60 patients or 66%) or by SER in combination with antiarrhythmic drug therapy (23 patients or 25%) (mean follow-up, 28 +/- 19 months). There were four late sudden deaths and four patients continued to have rare episodes of spontaneous ventricular tachycardia after surgery despite receiving antiarrhythmic drugs. Factors associated with failure of SER alone to cure ventricular tachycardia were presence of disparate sites of ventricular tachycardia origin (greater than 5 cm between mapped sites of origin; 64% vs 30% failure rate) and presence of multiple morphologically distinct spontaneous tachycardias (47% vs 25% failure rate). A log-linear model of multivariate analysis identified disparate sites of origin of ventricular tachycardia and the absence of a discrete left ventricular aneurysm as the only independent variables associated with failure of surgery alone. Inferior wall site of origin (41% vs 12% failure) and right bundle branch block morphology of ventricular tachycardia (20% vs 7% failure) were also significantly associated with failure of surgery to cure ventricular tachycardia. Mapping-guided SER is a highly effective mode of treatment for drug-refractory ventricular tachycardia, despite the existence of subgroups of patients with higher-than-average surgical failure rates.

Endocardial catheter mapping in patients in sinus rhythm: relationship to underlying heart disease and ventricular arrhythmias.

Catheter mapping during sinus rhythm was performed in 132 patients with coronary artery disease and 26 patients with congestive noncoronary cardiomyopathy. Each of the patients had a clinical history of one of the following: no ventricular arrhythmia, nonsustained ventricular tachycardia, cardiac arrest, or sustained ventricular tachycardia. The characteristics of the endocardial electrogram and other measured indexes of slow endocardial conduction were compared between patients with different types of disease and in different arrhythmia groups to determine if differences existed. The cardiomyopathic group had a higher percent of normal endocardial electrograms than the coronary artery disease group, with no evidence of slow endocardial conduction. The sustained ventricular tachycardia group exhibited a greater percent of abnormal endocardial electrograms and more evidence of slow endocardial conduction, distinguishing this group from the three other arrhythmia groups. We conclude the following: The underlying electrophysiologic substrate varies in patients with different ventricular arrhythmias. It is therefore inappropriate to analyze all patients with ventricular arrhythmias as a single group. Patients with congestive noncoronary cardiomyopathy, regardless of the type of their arrhythmia, have a relatively normal endocardium. Those patients with serious ventricular arrhythmias should not be considered candidates for surgery directed at removing abnormal endocardium.

Left ventricular endocardial activation during right ventricular pacing: effect of underlying heart disease.

Endocardial catheter mapping of the left ventricle was performed in 40 patients during right ventricular pacing to determine the effect of underlying myocardial infarction on endocardial activation. Group I comprised 18 patients without infarction, Group II 12 patients with inferior infarction and Group III 10 patients with anteroseptal infarction. Thirty-nine of the 40 patients had only a single left ventricular breakthrough site located on the midseptum in 33 cases, apical septum in 4 cases and basal septum in 2 cases. The earliest left ventricular local activation time during right ventricular pacing was earlier in Group III (40 +/- 11 ms) than in Group I (55 +/- 17 ms) and Group II (60 +/- 15 ms) (p less than 0.01). Total endocardial activation time was significantly longer in Group III (118 +/- 30 ms) than in Group I (76 +/- 14 ms) and Group II (72 +/- 20 ms) (p less than 0.001). The latest left ventricular site of activation during right ventricular pacing was the inferoposterior base in 14 (77%) of the 18 Group I patients, and 10 (83%) of the 12 Group II patients. The latest site of activation in Group III patients was variable. It is concluded that: left ventricular endocardial activation patterns and conduction times are influenced by the site of previous infarction. Longer total endocardial activation in Group III suggests that specialized conducting tissue in the septal and anterior walls may play an important role in left ventricular activation during right ventricular pacing.(ABSTRACT TRUNCATED AT 250 WORDS)

Relationship between the 12-lead electrocardiogram during ventricular tachycardia and endocardial site of origin in patients with coronary artery disease.

Previous studies in patients with sustained ventricular tachycardia (VT) have demonstrated the efficacy of surgical and catheter-mediated ablative procedures based on activation mapping during VT. Since extensive preoperative or intraoperative mapping may be impractical due to time constraints or patient intolerance, we sought to define characteristics of the 12-lead electrocardiogram (ECG) during VT that could suggest a particular endocardial region of origin and thus facilitate mapping studies. Endocardial mapping was performed during 182 VTs in 108 patients with prior myocardial infarction of either the anterior or inferior wall. Endocardial sites of origin (sites from which greater than or equal to 40 msec of presystolic electrical activity was consistently recorded) were identified with use of catheter (154 VTs) or intraoperative (85 VTs) activation mapping (both methods used in 57 Vts). Twelve-lead ECGs obtained during these VTs were characterized by four features: location of infarction, bundle branch block type configuration, quadrant of QRS axis, and precordial R wave progression pattern. A specific combination of these four features was associated with a particular endocardial region containing the mapped site of origin in 87 VTs (48% of total). An association (greater than or equal to 70% positive predictive accuracy) was more likely to be found in the presence of left, as opposed to right, bundle branch block type patterns (53/73 [73%] vs 34/109 [31%]; p less than .001) and in the presence of VT related to inferior, as opposed to anterior, infarction (40/54 [74%] vs 47/128 [37%]; p less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)

Relation of the intraoperative defibrillation threshold to successful postoperative defibrillation with an automatic implantable cardioverter defibrillator

To determine the relation between the intraoperative defibrillation threshold and successful postoperative termination of induced ventricular fibrillation (VF) with the automatic implantable cardioverter defibrillator (AICD), 33 patients who underwent AICD implantation were studied. The defibrillation threshold, determined after at least 10 seconds of VF, was 5 J in 2, 10 J in 6, 15 J in 10, 20 J in 10 and 25 J in 5 patients. The AICD energy rating on the first discharge was 28 +/- 1.8 J. Defibrillation of induced VF was demonstrated postoperatively in 29 of 33 (88%) patients. The AICD terminated VF postoperatively in all 18 patients with a defibrillation threshold less than or equal to 15 J. Only 11 of the 15 (73%) patients with a defibrillation threshold greater than or equal to 20 J (p less than 0.04) had VF terminated postoperatively. In all 4 patients in whom the AICD failed to terminate induced VF, the energy difference between the AICD rating and the defibrillation threshold was less than or equal to 10 J. Among the 14 patients with a difference of less than or equal to 10 J between the AICD energy rating and the defibrillation threshold, there were no significant differences between the 4 patients with and the 10 without successful VF termination with respect to the duration of VF induced postoperatively or the AICD lead system. In summary, failure to terminate VF with the AICD is not uncommon (27%) when the defibrillation threshold approaches the energy delivering capacity of the AICD.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrioventricular nodal reentrant tachycardia: studies on upper and lower 'common pathways'.

Electrophysiologic studies were performed in 28 patients with documented atrioventricular (AV) nodal reentrant supraventricular tachycardia (SVT) to investigate the presence of AV nodal tissue situated between the tachycardia circuit and both the atrium (upper common pathway, UCP) and the His bundle (lower common pathway, LCP). All patients demonstrated a 1:1 AV relationship during SVT. The study protocol consisted of atrial then ventricular pacing at the SVT cycle length. UCPs were manifested in eight of 28 (29%) patients by either antegrade AV Wenckebach (six patients) or a paced atrium-His (AH) interval exceeding the AH in SVT (two patients, differences 5 and 9 msec). LCPs were manifested in 21 of 28 (75%) patients by either retrograde Wenckebach periodicity (two patients) or a paced HA interval exceeding the HA in SVT (19 patients, mean difference 25 +/- 20 msec). By these criteria, eight patients (29%) had evidence for both UCPs and LCPs. UCPs were more likely than LCPs to be manifested by Wenckebach criteria (p less than .05). Thus the AV nodal reentrant SVT circuit appears to be intranodal and is frequently surrounded by AV nodal tissue (UCP and LCP), antegrade and retrograde conduction properties of these common pathways are discordant in some cases, and conduction properties of UCP tissue differ from those of LCP tissue. These findings may have relevance in that the UCP or LCP may limit the ability of premature extrastimuli to penetrate the circuit to initiate or terminate AV nodal SVT.

Intraoperative endocardial mapping during sinus rhythm: relationship to site of origin of ventricular tachycardia.

Mapping-guided endocardial resection has proved to be an effective therapy for recurrent sustained ventricular tachycardia. However, some patients cannot be mapped during ventricular tachycardia, so that guidance from findings during normal sinus rhythm would be highly desirable. We examined the frequency, timing, and duration of several abnormal types of electrograms recorded endocardially during sinus rhythm and related these findings to activation mapping during sustained ventricular tachycardia. Thirteen patients with extensive myocardial infarction complicated by recurrent sustained ventricular tachycardia were studied intraoperatively during sinus rhythm and induced ventricular tachycardia with a standardized mapping scheme involving the entire endocardial surface. Fractionated electrograms (multicomponent with amplitude less than 1 mV and duration greater than 50 msec) were recorded in all patients. This type of electrogram could be recorded at up to 36% of mapped sites. Split electrograms (two components separated by isoelectric period) were also frequently seen but involved only a mean of 5.8% of mapped sites. Late electrograms (inscribed entirely after the QRS complex) were only recorded in four of 13 patients at a mean of 5% of mapped sites. The location of these electrograms was related to an arbitrary 8 cm2 zone around the earliest site of endocardial activation recorded during ventricular tachycardia. The longest fractionated electrogram was closely related to nine of 22 morphologies of induced ventricular tachycardia, split electrograms were related to seven of 16 morphologies, and late electrograms to two of four morphologies. We have concluded that extremely abnormal electrograms recorded endocardially during sinus rhythm are widespread in patients with extensive myocardial infarction complicated by ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Pattern of endocardial activation during sustained ventricular tachycardia

Fifty-five patients with sustained ventricular tachycardia due to prior myocardial infarction underwent intraoperative endocardial activation mapping during ventricular tachycardia to guide subendocardial resection. The mapping data were analyzed to determine the pattern of endocardial activation during tachycardia. Of a total of 122 tachycardias, 101 had a pattern of activation assigned: in 90 (90%), endocardial activation spread centrifugally from a tachycardia site of origin, and 11 (10%) had a continuous loop of electrical activity around an aneurysm. All patients had at least one tachycardia having the centrifugal spread pattern. Tachycardias with a continuous loop pattern had a shorter mean cycle length than those with a centrifugal spread pattern (260 +/- 33 versus 338 +/- 81 ms, p less than 0.002) and a longer duration of endocardial activation relative to the tachycardia cycle length (100 +/- 0 versus 58 +/- 19%, p less than 0.001). There was no difference in preoperative patient characteristics, operative survival or cure of tachycardia between patients having any tachycardias of the continuous loop pattern and those having only centrifugal spread tachycardias. Thus, the vast majority of ventricular tachycardias in this group of patients are characterized by a centrifugal spread of endocardial activation from a site of origin less than 6 cm2 in size. Mapping-guided ablative surgery may remove the entire tachycardia circuit in these patients and a critical portion of the circuit in the minority of patients with continuous loop tachycardias.

Usefulness of the ΔHA interval to accurately distinguish atrioventricular nodal reentry from orthodromic septal bypass tract tachycardias

Surface electrocardiographic criteria may be inadequate to distinguish some cases of atrioventricular (AV) nodal reentrant supraventricular tachycardia (SVT) from those with orthodromic SVT incorporating a posterior septal bypass tract (orthodromic SVT) because of similarities in P-wave morphology and timing during SVT. Invasive electrophysiologic studies may occasionally leave uncertainty in the correct diagnosis, using currently accepted criteria. A new criterion for distinguishing these 2 forms of SVT was therefore devised and tested based on differences in the sequence of activation of the His bundle and atrium during SVT and ventricular pacing. Eighty-four patients underwent invasive electrophysiologic studies (60 with proved AV nodal SVT, 24 with proved orthodromic SVT), during which His to atrial (HA) intervals were measured during SVT as well as ventricular pacing at the same rate. The newly devised criterion, the delta HA interval (HApace-HAsvt) was found to accurately distinguish AV nodal SVT (delta HA greater than 0 ms) from orthodromic SVT (delta HA less than -27 ms). An intermediate value of delta HA = -10 ms was chosen which had a 100% sensitivity, specificity and predictive accuracy in differentiating the 2 forms of SVT. A clear retrograde His potential during ventricular pacing, which is essential for application of this criterion, was present in 78 of 84 (93%) cases. In summary, patients with delta HA intervals greater than -10 ms separate AV nodal reentry from orthodromic SVT incorporating a septal bypass tract, and no overlap exists between the 2 groups. This criterion may be useful in differentiating the mechanism of SVT in cases in which distinction is not possible by other methods.

Effect of Subendocardial Resection on Sinus Rhythm Endocardial Electrogram Abnormalities

BACKGROUND Patients with sustained ventricular tachycardia after acute myocardial infarction frequently have characteristic abnormalities of left ventricular endocardial electrical activity, including fractionated (prolonged, multicomponent, low-amplitude), split (having discrete widely separated deflections), and late (extending after the end of the QRS complex) electrograms. The exact cause and source of these electrograms are not clear. METHODS AND RESULTS In this study, endocardial electrograms from 18 patients were recorded with a 20-electrode array from the same area immediately before and immediately after resection of subendocardial tissue at the time of surgery for ventricular tachycardia. Electrograms could be compared before and after resection from 298 of 360 (83%) of the electrodes. Before resection, split electrograms were present in 130 (44%) and late components in 81 (27%) of the recordings. Recordings made after resection showed fewer abnormalities, including complete absence of split electrograms as well as all previously recorded late components (P < .02). Mean electrogram amplitude increased from 0.5 +/- 0.8 to 1.0 +/- 1.6 mV (P < .0001) because of removal of the attenuating effect of endocardial scar; mean duration decreased from 112 +/- 38 to 65 +/- 27 ms (P < .0001) mainly because of loss of late and split components. Overall electrogram contour was very similar aside from these changes. CONCLUSIONS These data show that (1) some of the signal recorded on the endocardial surface is derived from deeper tissue layers and (2) split and late electrogram components appear to be generated by cells in the superficial endocardial layers, since they are eradicated by removal of this tissue. These findings correspond well with previous histological studies of resection specimens that show bundles of surviving muscle cells separated by layers of dense scar that act as an insulator.