PubMed Health⌕ Search

Biomedical subjects

A R Easley

Publications and source records attributed to A R Easley.

10 recordsLinked to original sources
PubMed1995

Defibrillator patch electrode constriction: an underrecognized entity.

Pericardial constriction associated with the placement of intrapericardial defibrillator patches is a rare occurrence that is reported only one tenth as often in defibrillator patients as in patients undergoing other types of cardiac operations. Although this discrepancy may be attributable to a lower incidence of constriction with the defibrillator patch electrode procedure, it may also indicate a failure to recognize that progressive right heart failure and signs of low cardiac output that could be due to pericardial constriction and not progressive systolic dysfunction. Because surgical removal of the patches and decortication of the epicardial surface is the only effective therapy, it is important to recognize this uncommon, but profoundly debilitating entity.

Adult↗
PubMed1994

Options in managing the patient with high defibrillation thresholds.

The desired defibrillation threshold (DFT) obtained during intraoperative testing of an implantable cardioverter defibrillator (ICD) should be 10 J lower than the maximal energy delivered by the ICD generator. Of the 206 patients undergoing ICD implantation since December 1986, 8 (3.9%) have had initial DFTs with less than the 10-J safety margin using the standard large patch-large patch configuration. Patches were implanted by left thoracotomy in 6 and sternotomy in 1, and 1 had implantation of a transvenous defibrillation lead and subcutaneous patch. Of note, 6 (75%) of the 8 patients with high DFTs had prior open heart operations, half were on a regimen of long-term amiodarone therapy, and the mean left ventricular mass index was quite large but not significantly greater than that of patients with low DFTs. Multiple techniques was tried to improve the DFTs in this group. Satisfactory DFTs were eventually obtained in 7 (88%); the threshold was lowered from a mean of 41.4 +/- 3.8 J to 26.9 +/- 8.8 J (p = 0.002). The most effective techniques were addition of a superior vena cava lead attached by a Y connector to one of the large patch leads in some patients and conversion to a biphasic-waveform generator in 2 others. Adding a third epicardial lead did not lower the DFTs. There were no major postoperative complications or deaths attributable to these supplemental procedures. Using these techniques, satisfactory DFTs were obtained in almost all patients with an ICD.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Scatter diagram analysis: a new technique for discriminating ventricular tachyarrhythmias.

With the increasing flexibility allowed by implantable cardioverter defibrillators that use tiered therapy, it is important to match the therapy with the arrhythmia. In this article we present scatter diagram analysis, a new computationally efficient two-channel algorithm for distinguishing monomorphic ventricular tachycardia (VT) from polymorphic ventricular tachycardia and ventricular fibrillation (VF). Scatter diagram analysis plots the amplitude from one channel versus the amplitude from another channel on a graph with a 15 x 15 grid. The fraction (percentage) of the 225 grid blocks occupied by at least one sample point is then determined. We found that monomorphic VT traces nearly the same path in space and occupies a smaller percentage of the graph than a nonregular rhythm such as polymorphic VT or VF. Scatter diagram analysis was tested on 27 patients undergoing intraoperative implantable cardioverter defibrillator testing. Passages of 4.096 seconds were obtained from rate (bipolar epicardial) and morphology (patch) leads, and digitized at 125 Hz. Scatter diagram analysis distinguished 13 episodes of monomorphic VT (28.6% +/- 4.0%) from 27 episodes of polymorphic VT or VF (48.0% +/- 8.2%) with P < 0.0005. There was overlap in only one monomorphic VT episode and one polymorphic VT or VF episode.

Algorithms↗
PubMed1989

Fast Fourier transformation of the entire low amplitude late QRS potential to predict ventricular tachycardia.

Signal-averaged electrocardiograms (X, Y and Z leads) were acquired from 24 patients with coronary artery disease and recurrent ventricular tachycardia, 24 control patients with coronary artery disease and 23 normal subjects to assess the discriminant value of fast Fourier transformation of the entire late potential period of the QRS complex. Analysis of the vector magnitude in the temporal domain (25 to 250 Hz bandpass filters) measured high frequency QRS duration, the duration of terminal signals less than 40 microV and the root mean square voltage of the last 40 ms. Late potentials were defined as terminal signals greater than 25 Hz that were less than 40 microV. Analysis in the frequency domain used a 120 ms window that encompassed (had onset with) all of the late potential, but the mean value was first subtracted to eliminate a direct current component. High frequency spectral areas (60 to 120 Hz) and the percent high frequency (100 x [60 to 120 Hz/0 to 120 Hz]) were calculated. Results in both temporal and frequency domains were similar in control patients with coronary artery disease and normal subjects. Patients with ventricular tachycardia had a longer high frequency QRS complex (p less than 0.0001) and longer high frequency terminal signals less than 40 microV (p less than 0.0004), but not significantly lower voltage in the last 40 ms. The most useful temporal domain measurement was high frequency QRS duration (if greater than or equal to 120 ms, odds ratio = 8.2). Patients with ventricular tachycardia had increased high frequency spectral areas (p less than 0.0002) in the late potential, and the percent high frequency was especially increased (p = 0.0000; if percent high frequency greater than 3.1%, odds ratio = 18.4). The odds ratio and the area under the receiver operating characteristic curve were both greater for percent high frequency than for high frequency QRS duration (p less than 0.03). All patients with ventricular tachycardia had a high frequency QRS complex greater than or equal to 107 ms or percent high frequency greater than or equal to 3.1% (sensitivity 100%). For a high frequency QRS complex greater than or equal to 107 ms and percent high frequency greater than or equal to 3.1%, specificity was 96%. Therefore, high frequencies in late potentials, not their duration or reduced voltage, most usefully identify patients with coronary artery disease who are prone to ventricular tachycardia.

Adult↗
PubMed1988

Intermittent preexcitation: marked enhancement of anterograde conduction in the atrioventricular accessory pathway with isoproterenol.

A 29-year-old man presented with intermittent preexcitation and exertional syncope. Electrophysiological evaluation in the control state demonstrated a single, left posterior free-wall atrioventricular accessory pathway. The anterograde and retrograde effective refractory periods and block cycle lengths were long in the control state. No tachycardias were induced during programmed electrical stimulation. After intravenous administration of isoproterenol, anterograde conduction of the accessory pathway was markedly enhanced (block cycle length shortened 45% to less than 240 ms) and rapid antidromic reciprocating tachycardia (CL = 250 ms) associated with syncope was observed. Following successful surgical dissection of the accessory pathway the patient has been without tachycardia or exertional symptoms. We conclude that, under the influence of exercise or emotion, patients with intermittent preexcitation may be at risk for serious arrhythmias.

Adult↗
PubMed1987

Effects of upright posture on anterograde and retrograde atrioventricular conduction in patients with coronary artery disease, mitral valve prolapse or no structural heart disease.

To assess the effects of posture on anterograde and retrograde atrioventricular conduction, electrophysiologic testing was performed in 25 patients in both the supine and 45 degrees upright positions on a tilt table. Retrograde conduction was present during ventricular pacing in 17 patients in the supine position; all 17 continued to manifest retrograde conduction in the upright position. In all patients with absent retrograde conduction while supine, retrograde conduction could not be demonstrated while upright. Upright posture significantly (p less than 0.05) shortened the sinus cycle length (from 808 +/- 34 to 678 +/- 26 ms, mean +/- standard error of the mean), AH interval during sinus rhythm (78 +/- 6 to 69 +/- 6 ms), and AH interval during atrial pacing at cycle length 500 ms (123 +/- 13 to 91 +/- 9 ms). Total atrioventricular conduction time during atrial pacing shortened significantly (from 169 +/- 13 to 136 +/- 10 ms), as did ventriculoatrial conduction time during ventricular pacing (from 192 +/- 9 to 178 +/- 7 ms). Upright posture also significantly shortened both anterograde block cycle length (390 +/- 20 to 328 +/- 17 ms) and retrograde block cycle length (466 +/- 27 to 354 +/- 18 ms). However, the effect of upright posture on retrograde block cycle length was significantly greater than on anterograde block cycle length: a 21% decrease retrograde vs a 14% decrease anterograde (p less than 0.05). These effects may produce clinically important changes in characteristics of arrhythmias that depend on the properties of anterograde and retrograde conduction.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrioventricular Node↗
PubMed1987

Efficacy of class Ib (lidocaine-like) antiarrhythmic agents for prevention of sustained ventricular tachycardia secondary to coronary artery disease.

The effects of lidocaine, tocainide and mexiletine were examined in 17 patients with coronary artery disease and chronic, recurrent, sustained ventricular tachycardia (VT) or ventricular fibrillation and inducible VT. Eleven patients presented with sustained VT; 6 patients had had an episode of sudden death from which they had been resuscitated. All patients were refractory to conventional antiarrhythmic agents. Lidocaine prevented induction of VT in only 3 patients (18%). Tocainide prevented induction of VT in only 1 lidocaine-responsive patient. Mexiletine prevented VT induction in 1 patient who had responded to lidocaine but not tocainide. Neither tocainide nor mexiletine was effective in preventing induction of VT in any patient who did not respond to lidocaine. Lidocaine terminated VT in 3 patients, but this did not predict noninducibility with lidocaine, tocainide or mexiletine. Cycle length of VT was prolonged slightly by lidocaine (control 311 +/- 14 ms, lidocaine 361 +/- 26 ms, p less than 0.05), tocainide (344 +/- 16 ms, p less than 0.05) and mexiletine (371 +/- 27 ms, mean +/- standard error of the mean, p less than 0.05). Thus, class lb agents are infrequently effective in preventing induction of VT in this group of patients, electrophysiologic inefficacy of lidocaine is highly predictive of continued inducibility with tocainide and mexiletine, and termination of VT with lidocaine does not correlate with its ability to prevent VT induction.

Adult↗
PubMed1986

Electrophysiologic evaluation of pirmenol for sustained ventricular tachycardia secondary to coronary artery disease.

The efficacy and electrophysiologic effects of pirmenol were evaluated in 21 patients with a history of sustained ventricular tachycardia (VT) and coronary artery disease. Intravenous pirmenol (0.7- to 1.1-mg/kg bolus, followed by a 35- to 40-micrograms/kg/min infusion) significantly prolonged the PR, QRS, QT and corrected QT intervals, HV interval and right ventricular effective refractory period, and shortened the sinus cycle length and atrioventricular nodal block cycle length. All 21 patients had inducible VT (20 sustained, 1 nonsustained) during programmed stimulation in the control state. After intravenous pirmenol, 5 patients (24%) no longer had inducible VT. In those in whom VT was still inducible, the VT cycle length was prolonged significantly. The 5 patients who responded to intravenous pirmenol were given oral pirmenol (200 to 250 mg every 8 hours) for 1 to 3 days and retested with programmed stimulation. In 4 of these 5, VT could not be induced with oral pirmenol administration; in 1 patient sustained VT was induced and pirmenol therapy was discontinued. Oral pirmenol suppressed recurrent VT during a follow-up of 315 +/- 133 days in 4 patients. However, pirmenol therapy was discontinued in 2 patients because of possible deleterious effects (worsened heart failure in 1 patient and elevated liver function test results in 1). Thus, pirmenol, a type IA antiarrhythmic drug, had an overall efficacy of approximately 19% in patients with sustained VT secondary to coronary artery disease.

Adult↗