Prospective randomized comparison of 50%/50% versus 65%/65% tilt biphasic waveform on defibrillation in humans.

It is unknown if there is a single optimal biphasic waveform for defibrillation. Biphasic waveform tilt may be an important determinant of defibrillation efficacy. The purpose of this study was to compare acute defibrillation success with a three-electrode configuration in humans using 50%/50% versus 65%/65% tilt truncated exponential, biphasic waveforms delivered through a 110-microF capacitor. Acute DFTs for biphasic waveforms with 50%/50% versus 65%/65% tilt were measured in random order in 60 patients using a binary search method. The electrode configuration consisted of a RV coil as the cathode, and a SVC coil plus a pectoral active can emulator (CAN) as the anode. The waveforms were derived from an external voltage source with 110-microF capacitance, and the leading edge voltage of phase 2 was equal to the trailing edge voltage of phase 1. Stored energy DFT (9.2 +/- 5.7 [50%/50%] vs 10.8 +/- 6.4 [65%/65%] J, P = 0.007), current DFT (10.9 +/- 4.0 [50%/50%] vs 12.0 +/- 4.4 [65%/65%] A, P = 0.002) and voltage DFT (391 +/- 118 [50%/50%] vs 424 +/- 128 [65%/65%] V, P = 0.004) were significantly lower for the 50%/50% tilt waveform versus the 65%/65% tilt waveform using this three-electrode configuration and a 110-microF capacitor. For an RV(-)/SVC plus CAN(+) electrode configuration and a 110-microF capacitor, a 50%/50% tilt biphasic waveform results in a 15% reduction in energy DFT, 9% reduction in current DFT, and 8% reduction in voltage DFT versus a 65%/65% tilt biphasic waveform.

Critical analysis of dual-chamber implantable cardioverter-defibrillator arrhythmia detection : results and technical considerations.

BACKGROUND: One of the perceived benefits of dual-chamber implantable cardioverter-defibrillators (ICDs) is the reduction in inappropriate therapy due to new detection algorithms. It was the purpose of the present investigation to propose methods to minimize bias during such comparisons and to report the arrhythmia detection clinical results of the PR Logic dual-chamber detection algorithm in the GEM DR ICD in the context of these methods. METHODS AND RESULTS: Between November 1997 and October 1998, 933 patients received the GEM DR ICD in this prospective multicenter study. A total of 4856 sustained arrhythmia episodes (n=311) with stored electrogram and marker channel were classified by the investigators; 3488 episodes (n=232) were ventricular tachycardia (VT)/ventricular fibrillation (VF), and 1368 episodes (n=149) were supraventricular tachycardia (SVT). The overall detection results were corrected for multiple episodes within a patient with the generalized estimating equations (GEE) method with an exchangeable correlation structure between episodes. The relative sensitivity for detection of sustained VT and/or VF was 100.0% (3488 of 3488, n=232; 95% CI 98.3% to 100%), the VT/VF positive predictivity was 88.4% uncorrected (3488 of 3945, n=278) and 78.1% corrected (95% CI 73.3% to 82.3%) with the GEE method, and the SVT positive predictivity was 100.0% (911 of 911, n=101; 95% CI 96% to 100%). CONCLUSIONS: A structured approach to analysis limits the bias inherent in the evaluation of tachycardia discrimination algorithms through the use of relative VT/VF sensitivity, VT/VF positive predictivity, and SVT positive predictivity along with corrections for multiple tachycardia episodes in a single patient.

Signal-averaged ECG prior to and serially after thrombolytic therapy for acute myocardial infarction.

Signal averaging has been performed to evaluate late potentials following infarction and the administration of thrombolytic therapy. Most studies have recorded signal-averaged electrocardiograms (SAECGs) at least 12 hours after the onset of the infarction. In this study, SAECGs were recorded before thrombolytic therapy and serially over 7-10 days following infarction in 21 patients. The high frequency QRS duration was significantly shortened at 1 and 24 hours compared to presentation (96.8 +/- 11.3 ms and 93.4 +/- 8.0 ms vs 103.3 +/- 14.3 ms, respectively, P < 0.05) and there was an increase in the terminal voltage over time, significant at 1 hour and 3 days (57.3 +/- 29.1 microV and 58.6 +/- 44.7 microV vs 44.4 +/- 35.5 microV, respectively, P < 0.01). Five patients met criteria for ventricular late potentials on at least one SAECG. The prevalence of late potentials was higher in patients with Q wave infarctions, or with occluded infarct related arteries. These changes in myocardial activation may be related to ischemia and reperfusion, and may not correlate with the development of a fixed substrate for reentry.

Effects of exercise on signal-averaged electrocardiogram.

Signal averaging can be used to assess changes in myocardial activation under a variety of physiological conditions including stress. This study prospectively evaluated patients who underwent rest and exercise recording of signal-averaged electrocardiograms. The 163 patients were divided into three groups based on thallium results: normal (group I), reperfusion (group II), and fixed defect (group III). Patients in group I showed shortening of the high frequency duration (P = 0.02) and the duration of the low amplitude signal (P = 0.024) after exercise. In these patients the terminal root mean square amplitude (RMSA) also increased significantly (P = 0.005). However, patients who were in either group II or group III showed little change in signal averaging measurements after exercise. The amplitude of the QRS in V5 and the RMSA of the total QRS also increased in all groups following exercise, with a lesser increase in the patients with reperfusion by thallium imaging (group II). There was no change among groups in the incidence of ventricular late potentials with exercise. This suggests that patients with ischemia or infarction may not have the same response to an increase in sympathetic tone with exercise as patients without abnormalities of cardiac perfusion. The clinical implications of these findings may include demonstration that an area of slow conduction exists in these latter two groups of patients.

Use-dependent prolongation of ventricular tachycardia cycle length by type I antiarrhythmic drugs in humans.

BACKGROUND: Type I antiarrhythmic drugs block the cardiac sodium channel in a use-dependent fashion. This use-dependent behavior causes increased drug binding and consequently increased sodium channel blockade at faster stimulation rates. Importantly, the kinetics of drug association and dissociation from the sodium channel differ for each type I antiarrhythmic drug. METHODS AND RESULTS: Thirty-five patients receiving type I antiarrhythmic drugs for the treatment of sustained monomorphic ventricular tachycardia (VT) were studied before and after drug therapy. A total of 41 drug studies were performed (lidocaine, n = 10; procainamide, n = 16; flecainide, n = 15). Sustained monomorphic VT of an identical electrocardiographic morphology was induced during the control and follow-up drug studies. During the control study, there was no significant change in the VT cycle length over time. Compared with control, significant prolongation of the onset VT cycle length was observed after treatment with procainamide and flecainide (increase of 52 +/- 24 and 80 +/- 49 msec, respectively) but not after treatment with lidocaine (increase of 8 +/- 37 msec). Additional drug-induced prolongation of the VT cycle length occurred during a 40-second observation period. This secondary "use-dependent" cycle length prolongation contributed significantly to the steady-state VT cycle length during treatment with flecainide (increase of 82 +/- 34 msec; p < 0.0001). Although a use-dependent increase in VT cycle length was observed with procainamide and lidocaine, the increase was not statistically significant (increase of 12 +/- 15 and 8 +/- 8 msec, respectively). The estimated time constants for the onset of use-dependent VT cycle length prolongation were distinctly different for the three drugs. Flecainide's prolongation of the VT cycle length occurred slowly, with an estimated time constant of 12.5 +/- 5.0 seconds. In contrast, the time course of VT cycle length prolongation was rapid during treatment with lidocaine and intermediate during treatment with procainamide (time constants of 0.52 +/- 0.51 and 4.0 +/- 1.3 seconds, respectively). CONCLUSIONS: Use-dependent prolongation of VT cycle length during treatment with type I antiarrhythmic drugs was observed in humans. This effect was clinically significant during treatment with flecainide (i.e., the use-dependent slowing of the heart rate improved the hemodynamic tolerance of the arrhythmia). Finally, the estimated time constants for the use-dependent prolongation of VT cycle length by the three test drugs are similar to their reported in vitro time constants for use-dependent sodium channel blockade.

Refusal of implantable cardioverter defibrillator generator replacement: the nurse's role.

An adult patient who is conscious and mentally competent has the right to refuse any medical or surgical procedure even when the best medical opinion deems it necessary for life. The doctrine of informed consent is grounded on the premise that a physician's judgment is subservient to the patient's right to self-determination. Some suggestions for the future are offered. It may be beneficial to have a formal doctrine of informed refusal incorporated into the existing system of informed consent thus having patients sign a refusal of treatment form just as they sign a form consenting to treatment. Even if the physician and patient share an ideal relationship that includes mutual respect and participation in decision making, the consent to treatment or refusal of treatment should be documented both on a form and in the physician's own words in the patient record to avoid any discrepancies that may arise later. Items that may eventually be added to the list of requirements for informed consent or refusal include the impact of the treatment or procedure on the patient's job or family situation, impact on quality of life, and the potential long-term cost to the patient or to public or private health care payers.

Rate-modulated pacemakers.

Rate-modulated pacing is an advancement in pacing technology that has opened the way for the development of a wide variety of pacemaker generators and pacing modes. Rate-modulated pacemakers use a physiologic sensor other than the sinus node to adjust the pacing rate according to the physiologic needs of the patient. As rate-modulated pacemakers become more widely used, nurses caring for patients with these devices need to understand pacing physiology as well as rate-modulated pacing technology to provide optimal patient care.

Differentiation of arrhythmias by measurement of intracardiac pressures in man.

Antitachycardia devices currently use sustained high rate, abrupt changes in cycle length, and probability density function to determine the onset of ventricular tachycardia. Hemodynamic changes occur with the onset of tachycardia and may provide a method of discriminating supraventricular from ventricular tachycardia. In this study, patients had atrial and ventricular pressures measured during rapid atrial and ventricular pacing. Right atrial pressure increased significantly with ventricular pacing but not with atrial pacing. Right ventricular pressures did not significantly differ with atrial or ventricular pacing. The change in atrial pressure compared to baseline was greater, with ventricular pacing compared to atrial pacing. Right ventricular pressure increased compared to baseline with atrial or ventricular pacing, but there was no significant difference between pacing modalities. Measurement of right atrial pressure might prove useful in discriminating supraventricular from ventricular tachycardia.

Spontaneous changes in ventricular tachycardia cycle length.

Understanding spontaneous fluctuations in ventricular tachycardia cycle length is required to develop algorithms for ventricular tachycardia detection and termination. Variations in cycle length, time to stable cycle length and the range of RR intervals during ventricular tachycardia were analyzed in 74 episodes of sustained monomorphic ventricular tachycardia induced in patients not taking antiarrhythmic medication. Linear regression demonstrated cycle length variability to decrease over time (41 +/- 24 to 17 +/- 19 ms, p less than 0.001). Slower ventricular tachycardia had more cycle length variability than faster ventricular tachycardia (p less than 0.001). Ventricular tachycardia that was initially more variable tended to remain more variable (p less than 0.001). Fifty-four percent of episodes stabilized within the first 15 beats, 75% by 30 beats and 93% by 50 beats. The number of beats to stable cycle length was independent of ventricular tachycardia rate. The average range in cycle length per episode was 127 +/- 72 ms; 12% of ventricular tachycardia episodes varied by less than 50 ms and 45% by less than 150 ms. The maximal range in RR intervals from a single episode of ventricular tachycardia was 290 ms. Therefore, ventricular tachycardia demonstrates a wide range of cycle lengths and has time-dependent changes in variability and stability. These cycle length changes should be considered in the algorithms for ventricular tachycardia detection and termination by automatic antitachycardia devices.

Complete atrioventricular block during cardiac catheterization: two cases reports in patients without pre-existing conduction abnormalities.

Third-degree atrioventricular block has been well documented during ventricular catheterization of patients with underlying conduction abnormalities. Two cases reported here describe patients with normal conduction at baseline who sustained complete heart block during ventricular catheterization. Catheterizing physicians should be aware of this risk, which has not been previously reported.

The effects of atrial pacing on the signal-averaged electrocardiogram in patients with coronary artery disease.

The effects of atrial pacing on the signal-averaged electrocardiogram were studied in 14 patients with remote myocardial infarction and a history of cardiac arrest or sustained ventricular tachycardia (group I) and in 13 patients with coronary artery disease and no history of sustained ventricular tachyarrhythmia (group II). Recordings of the signal-averaged electrocardiogram were obtained at control and during atrial pacing at rates of 80, 100, and 120 beats/min. All patients had recordings analyzed from at least two paced rates. At control, the mean high frequency total duration of the QRS complex (HFTD) was significantly longer in group I versus group II patients (123 +/- 5.6 versus 111 +/- 3.5 msec, p less than 0.05). Although the duration of the QRS signal under 40 microV (D40) was higher in group I versus group II patients (42 +/- 4.7 versus 32.4 +/- 3.5 msec) and the root mean square amplitude of the terminal 40 msec QRS (RMSA) was lower in the group I patients (27 +/- 7.5 versus 38.1 +/- 8.8 microV), these differences did not achieve statistical significance. There was no effect of atrial pacing on the measured signal-averaged parameters of HFTD, D40, and RMSA. Although there was a difference between group I and group II at each paced rate analyzed, atrial pacing did not help to further stratify the groups. In patients with coronary artery disease, atrial pacing is not a useful method of stratifying high-risk patients. Changes in serial signal-averaged electrocardiograms from the same patient are not due to heart rate variability.

Pacemaker-mediated tachycardia from a single chamber temperature sensitive pacemaker.

This report describes a case of pacemaker-mediated tachycardia from a single chamber temperature sensitive rate modulated pacemaker. The patient experienced diaphragmatic pacing that produced an increase in right ventricular blood temperature. This temperature increase was sensed by the pacemaker and led to sustained upper rate limit pacing. Decreasing the ventricular output to prevent diaphragmatic capture eliminated further episodes of pacemaker-mediated tachycardia.

VOOR--nondemand rate modulated pacing necessitated by myopotential inhibition.

This report describes the use of the temperature sensitive rate modulated nondemand pacing mode (VOOR) in a patient with significant myopotential inhibition of pacemaker output during exercise. The VOOR mode eliminated myopotential sensing which had prevented an exertion related increase in heart rate. The patient has done well with VOOR pacing for the past year. VOOR pacing is useful in selected cases.

Swallowing-induced tachycardia: electrophysiologic and pharmacologic observations.

A 38-year-old man developed palpitations after swallowing. Intracardiac recordings and esophageal manometry were obtained during episodes of swallowing-induced tachycardia. These studies demonstrated that the site of origin of the tachycardia was the high right atrium and that the onset of the tachycardia occurred prior to the arrival of the peristaltic wave in the esophagus. Evaluation of the tachycardia revealed that the likely mechanism for the tachycardia was triggered automaticity. Autonomic blockade and other pharmacologic interventions failed to prevent episodes of tachycardia. Swallowing-induced tachycardia is a rare disorder triggered by an undefined neural reflex arc.

Amiodarone therapy: role of early and late electrophysiologic studies.

Forty-two patients with a history of symptomatic ventricular tachycardia or cardiac arrest underwent electrophysiologic testing at control and early in the course of amiodarone therapy (mean 12 +/- 7 days). Late electrophysiologic studies (mean 17 +/- 4 weeks) were repeated in 23 patients on a maintenance dose of 400 mg/day. At control study, all patients had inducible ventricular tachyarrhythmias (sustained ventricular tachycardia in 35, nonsustained ventricular tachycardia in 4, ventricular fibrillation in 3), while after amiodarone loading (1,200 mg daily) 4 (10.5%) of the 42 patients developed noninducible ventricular arrhythmias. At late study, an additional 6 (26%) of the 23 patients with inducible arrhythmias at early study developed noninducible arrhythmias. The cycle length of induced ventricular tachycardia increased from 275 +/- 61 ms at control study to 340 +/- 58 ms at early study (p = 0.001). A further increase in ventricular tachycardia cycle length was noted in patients who underwent both early and late study (341 +/- 38 versus 375 +/- 63 ms, p less than 0.05). The percent of induced tachycardias that were clinically tolerated increased as patients were treated longer with amiodarone (control = 22%, early = 34%, late = 53%, p less than 0.001). Of the 23 patients who had both early and late electrophysiologic studies and were followed up for a mean of 21.7 months (range 4 to 47), there were no recurrences among the 6 patients with noninducible arrhythmias, but there were five recurrences among the 17 patients with persistently inducible arrhythmias. None of the four patients with noninducible arrhythmias at early study had a recurrence. On the basis of these findings, it is concluded that: 1) The timing of programmed electrical stimulation will affect the results of the study in patients treated with oral amiodarone.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of direct current countershock on ventricular late potentials.

Signal averaging is a noninvasive method of recording ventricular late potentials. These late potentials are present in many patients with sustained ventricular tachycardia. Analysis of ventricular late potential characteristics may develop as a useful marker of antiarrhythmic drug efficacy. Often antiarrhythmic drugs are tested acutely in the electrophysiology laboratory after direct current countershock (DC shock). The purpose of this study was to investigate the effects of DC shock delivered for cardioversion of sustained ventricular tachycardia or fibrillation on ventricular late potentials. Signal averaged electrocardiograms (SAEKGs) were recorded before and after 13 DC shocks. There was no significant change in QRS duration, duration of the high frequency filtered QRS, or duration of the high frequency signal under 40 microvolts. There was a small increase in the root mean square amplitudes of the terminal 40 milliseconds (41 microV to 49 microV). This degree of change is felt to be clinically insignificant. Except for one trial, no late potential appeared or disappeared after electrical cardioversion. We have shown that ventricular late potentials are only slightly altered by programmed ventricular stimulation, induced sustained ventricular tachycardia or ventricular fibrillation, and DC countershock. To analyze changes in ventricular late potentials after antiarrhythmic drug administration in the electrophysiology laboratory, in those patients requiring DC countershock, comparisons should be made to postshock SAEKGs rather than those obtained prestudy.