Intravascular extraction of chronic pacemaker leads: efficacy and follow-up.

Extraction of chronic pacemaker leads has been recommended for infections, prevention of venous thrombosis, migration, and possible perforation. Success with constant traction techniques has been variable, and the cost and morbidity of open chest surgical procedures are prohibitive. Efficacy of a new system for lead extraction using intravascular techniques was analyzed. The system (Cook Pacemaker) uses a locking stylet, which is secured at the distal electrode by counterclockwise rotation to reinforce the lead and facilitate traction, and dilator sheaths that are used to free the lead from adhesions in the venous system. In a series of 56 patients (ages 19-88) who presented for lead extraction because of erosion (5), infection (14), lead replacement (35), or other (2), 86 leads were extracted. Thirty-two were atrial leads and 54 ventricular; 23 had active fixation and 63 passive. Average duration of implant was 58 +/- 42 months (range 1-264). Eighty-four leads were totally removed and two partially removed. For these two leads, the distal tip was not removed; in both cases the locking stylet was not secured at the distal electrode due to obstruction within the lead. Two patients developed arm edema following the procedure, which resolved with elevation. One patient developed a subclavian thrombosis, which resolved with warfarin anticoagulation. Four patients have expired due to unrelated causes. In conclusion, this intravascular approach for extraction of chronic leads is effective, and the procedure is safe when performed by experienced personnel.

Laser photoablation of ventricular tachycardia: correlation of diastolic activation times and photoablation effects on cycle length and termination--observations supporting a macroreentrant mechanism.

Neodymium:yttrium-aluminum-garnet (YAG) photocoagulation during ventricular tachycardia allows the electrophysiologic effects of the temporal and spatial sequence of energy delivery to be correlated with local activation times. A retrospective analysis was performed of the termination of 19 episodes of ventricular tachycardia for which the local diastolic activation time was known for all successful ablation sites and for 95% of all ablation sites. The mode of termination was compared with that of 26 episodes of spontaneously terminating ventricular tachycardias. Spontaneous terminations occurred without a change in cycle length (54%) or with a 7 +/- 15% change in cycle length over one to three terminal beats (46%). In contrast, laser ablation-induced terminations resulted in a 39 +/- 55% increase in cycle length over nine or more cycles. The effect of attempted laser ablation was compared with the local presystolic activation time and the local activation time expressed as a percent of the diastolic interval (end of QRS complex = 0%, onset of next QRS complex = 100%). With one exception, no tachycardia terminated at ablation sites activating less than -50 ms before the QRS complex. All 8 successful first ablation attempts and 13 of all 19 successful ablations occurred in the 35% to 50% interval of diastolic activation. All successful ablations at sites activating at greater than 50% of the diastolic interval required multiple ablation attempts. Successful ablation was performed from the epicardium in 6 and from the endocardium in 13 episodes of ventricular tachycardia. These results are most consistent with a macroreentrant mechanism with a region of high vulnerability represented by the 35% to 50% interval of diastolic activation.(ABSTRACT TRUNCATED AT 250 WORDS)

Surgical division of posterior septal accessory pathways in the Wolff-Parkinson-White syndrome: a new modified approach.

A new modified surgical approach for the division of posterior septal accessory pathways is described. This method incorporates some of the desirable components of previously reported techniques, while eliminating difficult and unreliable aspects of those same techniques. Interestingly this procedure was initially illustrated by Sealy and Mikat in 1983, although it has not been used clinically until now. The recognized intent of this dissection is to totally separate atrial and ventricular structures within the posterior septal space so that all accessory pathways encountered are permanently interrupted.

Functional role of the epicardium in postinfarction ventricular tachycardia. Observations derived from computerized epicardial activation mapping, entrainment, and epicardial laser photoablation.

BACKGROUND: Conventionally, monomorphic sustained ventricular tachycardia in patients with remote myocardial infarction is believed to originate from the subendocardium. In a previous study, we demonstrated that electrical activation patterns during ventricular tachycardia occasionally suggest a subepicardial rather than subendocardial reentry. METHODS AND RESULTS: This study prospectively evaluated the functional role of the epicardium in postinfarction ventricular tachycardia with complex intraoperative techniques including computerized electrical activation mapping, entrainment, observation of changes in activation pattern during successful epicardial laser photoblation, and histological study. Five of 10 consecutive patients undergoing intraoperative computerized activation mapping had 10 ventricular tachycardia morphologies displaying epicardial diastolic activation These 10 "epicardial" ventricular tachycardias revealed the following global activation patterns: monoregional spread (two), figure-eight activation (five), and circular macroreentry (three). Entrainment of ventricular tachycardia using epicardial stimulation was successfully performed from an area of slow diastolic conduction in four tachycardia morphologies. During entrainment, global activation remained undisturbed with recordings showing a long stimulus to QRS interval, unchanged QRS morphology, and pacing capture of all components of the reentry circuit. Neodymium:yttrium aluminum garnet laser photocoagulation was delivered during ventricular tachycardia to epicardial sites of presumed reentry. Epicardial photoablation terminated five of five figure-eight tachycardias, two of three circular macroreentry tachycardias but not the monoregional tachycardias. Electrophysiological recordings during epicardial laser photocoagulation demonstrated progressive prolongation of ventricular tachycardia cycle length and apparent interruption of the presumed reentrant circuit. Histological evaluation of the reentrant region (three patients) showed a rim of surviving myocardium under the epicardial surface. CONCLUSIONS: This study suggests that 1) chronic postinfarction ventricular tachycardia may result from subepicardial macroreentry, 2) slow conduction within the reentry circuit can be localized by computerized mapping and epicardial entrainment, and 3) ventricular tachycardia interruption by laser photocoagulation results from conduction delay and block within critical elements of the reentrant pathway. Viable subepicardial muscle fibers may constitute the underlying pathology.

Termination of ventricular tachycardia with epicardial laser photocoagulation: a clinical comparison with patients undergoing successful endocardial photocoagulation alone.

Electrical activation-guided laser photocoagulation was used intraoperatively to terminate ventricular tachycardia in patients with ischemic heart disease. During ventricular tachycardia, laser irradiation was delivered to mapped sites with local diastolic activation. In 30 long-term survivors, 85 ventricular tachycardia configurations were terminated by ablation; 72 (84.7%) were terminated by endocardial photocoagulation. Thirteen (15.3%) required epicardial photocoagulation; however, these 13 ventricular tachycardias occurred in 10 (33%) of the 30 patients. An aneurysm was present in 70% of patients with successful endocardial photocoagulation, but in only 10% of patients requiring epicardial photocoagulation for at least one ventricular tachycardia configuration; 90% of all patients requiring epicardial laser photocoagulation had no aneurysm and had either a right or a left circumflex coronary artery-related infarction. In this group, epicardial activation data were similar to those described for ventricular tachycardia with an "endocardial" origin and included 1) delayed potentials during sinus rhythm, 2) presystolic or pandiastolic activation sequences during ventricular tachycardia, and 3) regions of block near the presumed region of reentry during ventricular tachycardia. This study suggests that the critical anatomic substrates supporting reentry in postinfarction ventricular tachycardia may occur at intramural or epicardial sites, particularly in patients with right or circumflex coronary artery-related infarction and no aneurysm.

Utility of introducing ventricular premature complexes during reciprocating tachycardia in specifying the location of left free wall accessory pathways.

The usefulness of the response to single and double ventricular premature complexes (VPCs) introduced during reciprocating tachycardia (RT) in predicting the location of a left free wall accessory pathway was studied in 55 patients with the Wolff-Parkinson-White syndrome. One VPC introduced from the right ventricle into narrow QRS RT when the His bundle was refractory resulted in retrograde atrial preexcitation in 25 of 55 (45%) patients, while 30 (55%) showed no preexcitation. Double VPCs produced retrograde atrial preexcitation in 9 of 26 patients not responding to a single VPC. No difference in RT cycle length, AH, HV or ventriculoatrial intervals was found between those patients who did or did not show retrograde atrial preexcitation. The response to single and double VPCs during RT was related to the location of the AP. The average distance of the AP from the crux determined by intraoperative epicardial mapping in the 41 patients who underwent surgery was 2.7 +/- 0.7 mapping units (left posterolateral region) in patients showing retrograde atrial preexcitation with a single VPC, 3.6 +/- 0.7 units (at the lateral left ventricular margin) in those responding to double VPCs and 4.3 +/- 0.8 units (beyond the LV margin) in those showing no response. Left bundle--branch block (LBBB) aberrancy during RT resulted in an average 60 +/- 14 ms prolongation of the ventriculoatrial interval in 40 patients, including 5 in whom LBBB was seen only after procainamide infusion. VPCs introduced into LBBB RT resulted in significant retrograde atrial preexcitation in 6 additional patients in whom no response during normal QRS RT was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Frequency, diagnosis and clinical characteristics of patients with multiple accessory atrioventricular pathways.

Multiple accessory atrioventricular (AV) pathways were documented in 52 of 388 patients (13%) who underwent detailed electrophysiologic evaluation. Multiple AV pathways were identified during intraoperative mapping or electrophysiologic study by different patterns of ventricular preexcitation during atrial fibrillation, flutter or atrial pacing with different delta-wave morphologic and ventricular activation patterns; different sites of atrial activation during right ventricular pacing or orthodromic reciprocating tachycardia; or preexcited reciprocating tachycardia using a second pathway as the retrograde limb of the tachycardia. A logistic model was used to determine which clinical, electrocardiographic and electrophysiologic variables were associated with multiple AV pathways. Right free-wall and posteroseptal accessory AV pathways were more common in patients with multiple AV pathways and were frequently associated. Multivariate logistic regression identified Ebstein's anomaly, and a history of preexcited reciprocating tachycardia as significant variables (p less than 0.0001). Pathway location was not subjected to statistical analysis because of confounding variables.

The spectrum of pathology associated with percutaneous transluminal coronary angioplasty during acute myocardial infarction.

The purpose of this study was to determine at necropsy the morphologic consequences of percutaneous transluminal coronary angioplasty performed during acute myocardial infarction. The heart was examined in four patients who died between 6 hours and 4 days after coronary angioplasty. The patients had angioplasty of the left main coronary artery (one patient), left anterior descending coronary artery (two patients) and left circumflex coronary artery (one patient). Necropsy revealed residual stenosis, intimal hemorrhage and plaque disruption in all four patients. Also noted were distal embolization of plaque elements (two patients) and thrombotic occlusion of the coronary artery (one patient). In conclusion, the morphologic changes after angioplasty are varied. These changes illustrate the mechanisms of angioplasty and some of the complications that can be expected in a small number of cases. The morphologic changes associated with coronary angioplasty are similar in patients undergoing elective or emergency angioplasty although medial dissection was not observed in these patients with an evolving myocardial infarction.

Determination of effects of internal countershock by direct cardiac recordings during normal rhythm.

Recording cardiac electrical activity after a countershock has been limited by amplifier saturation. Modifications to our computer-assisted mapping system allowed us to record electrical activity from 56 epicardial electrodes within 5 ms of the end of a countershock. Modifications included the use of solid-state switches to disconnect the filter section of the amplifiers during the shock and changing the low-frequency response of the amplifiers from 0.1 to 10 Hz to filter out large, low-frequency potentials after the shock. Six-millisecond truncated exponential shocks were delivered between the superior vena cava and right ventricular apex through a quadripolar catheter during normal rhythm in seven dogs. As shocks of increasing voltage were delivered during the T-Q interval, progressively more of the epicardium was directly depolarized. A shock of 109 +/- 17 (SD) V directly depolarized the entire epicardium. Shocks of constant voltage were then delivered with increasing prematurity during diastole. As the ventricles became more refractory with increasing shock prematurity, the amount of epicardium depolarized became progressively less. Thus computer-assisted mapping techniques are capable of measuring the area depolarized by a shock during normal rhythm and may be useful during arrhythmias to improve our understanding of defibrillation and cardioversion.

Characterization of retrograde conduction by direct endocardial recording from an accessory atrioventricular pathway.

Accessory pathway electrograms are rarely recorded in patients with Wolff-Parkinson-White syndrome. In one patient, during electrophysiologic study, simultaneous local ventricular (V) accessory pathway (AP) and atrial (A) deflections were recorded during bipolar catheter endocardial mapping over the pathway. Analysis of changes in electrographic intervals during performance of the ventricular extrastimulus technique allowed characterization of the retrograde conduction properties of the pathway. As coupling intervals were decreased, an initial increase was seen in the AP2A2 interval with subsequent ventriculoatrial block between the accessory pathway and atrium. When coupling intervals were further decreased, the V2AP2 interval lengthened with ultimate block between the ventricle and accessory pathway. These findings support the concept of impedance mismatch as the cause of conduction block in accessory pathways with the distal junction of the accessory pathway being the most vulnerable.

Cardiac function in patients on chronic amiodarone therapy.

Antiarrhythmic agents may depress cardiac contractility and worsen heart failure. Few data are available describing the chronic effects of amiodarone on myocardial function. To assess the effects of amiodarone on cardiac function, we studied 41 consecutive patients with first-pass or equilibrium radionuclide angiography prior to and 3 months after drug therapy was initiated. The mean heart rate, systolic blood pressure (BP), and diastolic BP were not significantly altered by treatment. The mean ejection fraction was 36% +/- 19 (mean +/- 1 SD) at the time of drug initiation and 36% +/- 17 3 months later (p less than 0.05). Nineteen patients had an ejection fraction greater than 30% and 16 had an ejection fraction less than 30%. The mean change in ejection fraction for these two subgroups showed no statistically significant difference, although a decrease in EF greater than 10% was seen in three patients (symptomatic in two), necessitating an increase in diuretic dose. No correlation between amiodarone dose and change in ejection fraction (r = -0.12, p greater than 0.05) was noted. There was no correlation between baseline ejection fraction and change in ejection fraction over this 3-month period (r = -0.36, p greater than 0.05). In summary, amiodarone does not depress left ventricular function and as a result can be used safely in patients with mild to moderate impairment of left ventricular function. In patients with stable left ventricular function, serial tests of left ventricular function may not be necessary.

Frequency-dependent effects of verapamil on atrioventricular nodal conduction in man.

We sought to determine if verapamil induces frequency-dependent prolongation of atrioventricular nodal conduction in 10 consecutive patients studied in the electrophysiology laboratory. We used a maintenance infusion of verapamil designed to produce plasma concentrations of verapamil in the "therapeutic" range and that did not alter heart rate or blood pressure significantly. Frequency-dependent prolongation of atrioventricular nodal conduction (AH interval) was demonstrated in all 10 patients (p less than .001), and no change in HV conduction time with decreasing cycle length was noted in any patients while receiving verapamil. Two patterns of use-dependent response were seen. In four patients frequency-dependent prolongation of the delta(AH) interval [delta(AH) = AHverapamil - AHcontrol at a given cycle length] was seen with each decrement in pacing cycle length. In six patients frequency-dependent prolongation of the delta(AH) interval was not manifest until the fifth to eighth pacing cycle length tested. There was no association between the pattern observed and the initial heart rate or AH interval. After an abrupt change in pacing cycle length, the kinetics of delta (AH) interval prolongation were rapid; equilibrium was achieved by five to eight pulses in all patients. There was no correlation between the magnitude of prolongation of the AH interval noted at a particular cycle length and the concentration of verapamil during the maintenance infusion. These results indicate that verapamil causes use-dependent prolongation of atrioventricular nodal conduction in man.

Development of an endocardial-epicardial gradient of activation rate during electrically induced, sustained ventricular fibrillation in dogs.

Electrograms recorded with currently available electrodes become indistinct soon after the onset of ventricular fibrillation (VF), thus, little is known about transmural myocardial depolarization during VF. A plunge electrode system (plunge) was developed that registers discrete deflections during VF. These plunges were used to record for 20 minutes after inducing VF with a single premature shock in 20 open-chest dogs. In the first 6 dogs the epicardium was exposed to room temperature and in 14 dogs transmural temperature was maintained at 38 degrees C. Electrograms recorded with the transmural plunges contained sharp, discrete deflections during early VF in all dogs. Over the next 20 minutes of VF, the rate, regularity of cycle length and discreteness of the deflections in the electrograms decreased with time, first at the epicardial level, then deeper toward the endocardium. In all dogs, however, discrete, regular, rapid deflections persisted in the most subendocardial electrogram throughout the recording period. In 8 dogs, transmural myocardial biopsy samples were taken before fibrillation, and at intervals after the onset of fibrillation. The high-energy phosphate content of the myocardium decreased during VF, with comparable decreases in the epicardial and endocardial halves. Coronary perfusion was maintained during the first 20 minutes of VF in 6 additional dogs by cardiopulmonary bypass. A gradient of activation rates did not develop on bypass, but did develop within 1 minute of halting bypass. Thus, the endocardial-epicardial gradient of activation rates during VF is caused by ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)