Pacemaker programming in patients with first-degree AV-block: Programming pattern and possible consequences.

BACKGROUND: The optimal way of pacing in patients with an indication for pacing and concomitant first-degree atrioventricular (AV)-block is not known, and consequently, firm guidelines on this topic are lacking. This study explored the current pacemaker programming pattern in patients with first-degree AV-block who have a dual chamber pacemaker without cardiac resynchronization. METHODS: The study was a retrospective chart review conducted at Duke University Hospital. Patients receiving a pacemaker due to sinus node dysfunction with coexistent first-degree AV-block were studied. Baseline demographics and characteristics, as well as pacemaker programming parameters and follow-up data, were collected through chart review. Preimplantation and postimplantation electrocardiograms were analyzed. RESULTS: A total of 74 patients were included (mean age, 75 ± 11 y; 53% men). The mean ± SD preimplant PR interval and QRS duration was 243 ± 46 and 110 ± 30 milliseconds, respectively. A history of atrial fibrillation was present in 49% of the patients, and 77% had a normal left ventricular ejection fraction. The majority of patients (65%) had their pacemakers programmed to atrial pacing (AAI/DDD +/-R), whereas 32% and 2.7% of the pacemakers were programmed to AV-sequential pacing (DDD) and ventricular pacing (VVI), respectively. There were no significant differences in baseline characteristics or electrocardiogram measures between patients programmed to the 3 pacing modes. Patients with pacemakers programmed to AAI had a lower ventricular pacing percentage at follow-up (8 vs 55, and 46% [DDD and VVI, respectively]; P < .001). CONCLUSIONS: There was no evident association between baseline characteristics and programmed pacing mode in patients with first-degree AV-block. The choice of pacing mode affects long-term pacing burden, which in turn has been shown to influence outcome.

Fractal correlation properties of heart rate dynamics and adverse events in patients with implantable cardioverter-defibrillators.

The aim of this study was to determine the prognostic significance of nonlinear and standard heart rate (HR) variability parameters in predicting future adverse events (AEs) in patients with implantable cardioverter-defibrillators. In postinfarction studies, nonlinear measures of HR variability obtained from long-term electrocardiographic recordings have been suggested to be better predictors of adverse outcomes than conventional HR variability measures. Fifty-five high-risk patients with reduced left ventricular function and an implantable cardioverter-defibrillator had a 10-minute, high-resolution electrocardiographic recording after which they were followed for 25 months on average. Implantable cardioverter-defibrillator shock or death was determined as the end point. The SD of all normal-to-normal RR intervals, the square root of the mean squared differences of successive normal-to-normal RR intervals, and the proportion of interval differences of successive normal-to-normal RR intervals >50 ms, low-frequency and high-frequency powers of the power spectrum and their ratio were calculated as conventional measures of HR variability. The short-term scaling exponent (alpha(1)) and approximate entropy were determined as nonlinear measures of HR variability. AEs occurred in 23 patients (42%). Patients with AEs had significantly lower alpha(1) than event-free patients: 0.81 +/- 0.29 (mean +/- SD) versus 1.01 +/- 0.30 (p = 0.02). None of the other HR variability parameters differed significantly between patients with and without AEs. In the Cox proportional-hazards model including age, gender, ejection fraction, occurrence of ventricular tachyarrhythmia before defibrillator implantation, beta-blocker usage, and alpha(1), only alpha(1) was an independent predictor of AEs: hazard ratio 1.20 (95% confidence interval 1.03 to 1.39) for every 0.10 decrease in alpha(1) (p = 0.020). In conclusion, alpha(1) obtained from a 10-minute electrocardiographic recording yields important prognostic information about the risk of AEs in patients with implantable cardioverter-defibrillators.

Efficacy of implantable cardioverter-defibrillators for the prevention of sudden death in patients with hypertrophic cardiomyopathy.

BACKGROUND: Hypertrophic cardiomyopathy is a genetic disease associated with a risk of ventricular tachyarrhythmias and sudden death, especially in young patients. METHODS: We conducted a retrospective multicenter study of the efficacy of implantable cardioverter-defibrillators in preventing sudden death in 128 patients with hypertrophic cardiomyopathy who were judged to be at high risk for sudden death. RESULTS: At the time of the implantation of the defibrillator, the patients were 8 to 82 years old (mean [+/-SD], 40+/-16), and 69 patients (54 percent) were less than 41 years old. The average follow-up period was 3.1 years. Defibrillators were activated appropriately in 29 patients (23 percent), by providing defibrillation shocks or antitachycardia pacing, with the restoration of sinus rhythm; the average age at the time of the intervention was 41 years. The rate of appropriate defibrillator discharge was 7 percent per year. A total of 32 patients (25 percent) had episodes of inappropriate discharges. In the group of 43 patients who received defibrillators for secondary prevention (after cardiac arrest or sustained ventricular tachycardia), the devices were activated appropriately in 19 patients (11 percent per year). Of 85 patients who had prophylactic implants because of risk factors (i.e., for primary prevention), 10 had appropriate interventions (5 percent per year). The interval between implantation and the first appropriate discharge was highly variable but was substantially prolonged (four to nine years) in six patients. In all 21 patients with stored electrographic data and appropriate interventions, the interventions were triggered by ventricular tachycardia or fibrillation. CONCLUSIONS: Ventricular tachycardia or fibrillation appears to be the principal mechanism of sudden death in patients with hypertrophic cardiomyopathy. In high-risk patients with hypertrophic cardiomyopathy, implantable defibrillators are highly effective in terminating such arrhythmias, indicating that these devices have a role in the primary and secondary prevention of sudden death.

Y2K: effects on pacemaker and implantable defibrillator programmers.

All permanent pacemakers and implantable defibrillators (PPM/ICDs) will continue to function as programmed without regard to the date in the year 2000 (Y2K). All manufacturers contacted reassured us that some of these devices incorporate a day/year clock in the circuitry; however, these are not involved in sensing or delivering programmed therapy. Some manufacturers' device programmers will roll over to the year 2000 without any problems at all, whereas others may have difficulty with date and time stamping on printed reports. We tested 14 different types of PPM/ICD programmers for Y2K compliance using 8 tests. Five of the 14 models passed each test and were labeled at our institution with a green "Y2K" sticker to identify them as Y2K compatible and needing no special attention after December 31, 1999. The most common test failed was the ability to roll the date forward from December 31, 1999, with the programmer power off. Organizations should consider testing and replacing noncompliant device programmers or placing a red sticker with "Y2K" crossed out on noncompliant pieces. The red sticker alerts the advanced practice nurse or physician to the need to confirm the appropriate date and time in the programmer after startup in the year 2000 and before interrogating or programming any PPM/ICD, to avoid inappropriate date and time stamping on printed reports from that programmer.

Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. Multicenter Automatic Defibrillator Implantation Trial Investigators.

BACKGROUND: Unsustained ventricular tachycardia in patients with previous myocardial infarction and left ventricular dysfunction is associated with a two-year mortality rate of about 30 percent. We studied whether prophylactic therapy with an implanted cardioverter-defibrillator, as compared with conventional medical therapy, would improve survival in this high-risk group of patients. METHODS: Over the course of five years, 196 patients in New York Heart Association functional class I, II, or III with prior myocardial infarction; a left ventricular ejection fraction < or = 0.35; a documented episode of asymptomatic unsustained ventricular tachycardia; and inducible, nonsuppressible ventricular tachyarrhythmia on electrophysiologic study were randomly assigned to receive an implanted defibrillator (n = 95) or conventional medical therapy (n=101). We used a two-sided sequential design with death from any cause as the end point. RESULTS: The base-line characteristics of the two treatment groups were similar. During an average follow-up of 27 months, there were 15 deaths in the defibrillator group (11 from cardiac causes) and 39 deaths in the conventional-therapy group (27 from cardiac causes) (hazard ratio for overall mortality, 0.46; 95 percent confidence interval, 0.26 to 0.82; P=0.009). There was no evidence that amiodarone, beta-blockers, or any other antiarrhythmic therapy had a significant influence on the observed hazard ratio. CONCLUSIONS: In patients with a prior myocardial infarction who are at high risk for ventricular tachyarrhythmia, prophylactic therapy with an implanted defibrillator leads to improved survival as compared with conventional medical therapy.

Ventricular tachycardia induced cardiomyopathy: improvement with radiofrequency ablation.

Cardiomyopathy and congestive heart failure due to ventricular and supraventricular tachycardia is a well-recognized phenomenon. The mechanism of such cardiomyopathy is not clear. Ablation of the supraventricular tachycardia focus, either surgically or electrically, has been reported to result in the resolution of the left ventricular dysfunction. Similarly, the treatment of ventricular tachycardia with surgery or antitachycardia pacing has also been reported to result in improved ventricular systolic function. We present here a case of improvement in left ventricular systolic function after successful radiofrequency ablation of the ventricular tachycardia focus in the right ventricular outflow tract. We postulate that cardiomyopathy was due to the incessant or frequent ventricular tachycardia. To the best of our knowledge, this is the first such case being reported.

Antiarrhythmic agents in older patients. Current state of knowledge.

The treatment of ventricular arrhythmias in the elderly population is a challenging problem. Elderly patients are more predisposed to arrhythmias, are less responsive to antiarrhythmic agents and are more susceptible to the adverse effects of antiarrhythmic agents. Results from recent trial have altered the general approach to management of ventricular arrhythmias. The results of the Cardiac Arrhythmia Suppression Trials (CAST I and II) exemplified the disappointing results from numerous other studies, revealing the overall lack of efficacy of class I agents in reducing mortality in patients with coronary artery disease and asymptomatic premature ventricular complexes (PVCs). The results of CAST I and II also demonstrated the higher likelihood of older patients developing ventricular arrhythmias and toxicity to antiarrhythmic agents. Combined results of these studies have discouraged empirical antiarrhythmic therapy, especially in older patients with asymptomatic PVCs. In contrast, secondary prevention trials with beta-blockers in post-myocardial infarction patients have shown definitive survival benefit and reduction in ventricular arrhythmias, especially in the older patient population. Smaller trials with amiodarone have also shown survival benefit in post-myocardial infarction patients with or without PVCs. Management of ventricular tachycardia and fibrillation has become less empirical and more systematic with use of electrophysiologically guided and/or Holter monitor-guided therapy. Sotalol and amiodarone are especially effective agents. The efficacy of implantable cardioverter/defibrillators are also being compared with medical therapy systematically in multicentre trials. In general, empirical antiarrhythmic therapy is discouraged especially in the treatment of asymptomatic PVCs and should be reserved for systematic use in life-threatening arrhythmias.

Strength-interval curves in canine myocardium at very short cycle lengths.

While ventricular electrophysiological properties have been intensively studied at normal heart rates, little is known about these properties at the very short cycle lengths (approximately 100 msec), which are present in ventricular fibrillation. We examined refractoriness in the right ventricles of six dogs at stimulation intervals of 80 to 300 msec. Starting at 300 msec, the basic (S1) cycle length was decremented by 10 msec each beat to 200, 150, or 125 msec. A 1-msec premature (S2) stimulus of 1, 5, 10, or 20 mA was then introduced. The S1-S2 interval was decremented until capture was lost. The refractory period was considered to be the shortest interval that captured the heart for each S2 strength. Only pacing episodes that did not induce fibrillation were included. Strength-interval curves maintained the same hyperbolic shape but shifted to very short refractory periods as the S1-S1 interval was decreased. At the shortest S1-S1 intervals, premature stimuli were capable of capturing the heart without inducing ventricular fibrillation for S1-S2 intervals as short as 83 +/- 3 msec. Thus, decremental rapid pacing can produce refractory periods shorter than the cycle length during ventricular fibrillation. This finding suggests that there is no need to postulate a discontinuous jump to new electrophysiological properties or relationships at the onset of fibrillation, but that the capability for fibrillation is an integral part of normal electrophysiological parameters when they are pushed to values that do not occur normally. The results of this study should be useful in the further development of active membrane models and cellular automata models of cellular electrical behavior.

Complete heart block complicating retrograde left ventricular catheterization: case report and review.

Complete heart block (CHB) following retrograde left ventricular catheterization is uncommon. We report a case of transient CHB in a patient with severe aortic stenosis and bifascicular block on the baseline surface electrocardiogram during retrograde left ventricular catheterization. The block resolved spontaneously without sequelae. A review of the literature using MedLine was performed and recommendations for temporary and permanent pacing are outlined.

A fatal case of constrictive pericarditis due to a marked, selective pericardial accumulation of amyloid.

Distinguishing constrictive pericarditis from restrictive cardiomyopathy, usually due to amyloidosis, is a relatively frequent and difficult diagnostic problem. This report describes, for the first time, a patient with constrictive pericarditis caused by direct, extensive infiltration of the pericardium by amyloid, with only minimal amyloid in the myocardium, and a normal heart weight of 320 g. This patient demonstrates that amyloid may be predominantly deposited in the pericardium and actually cause constrictive pericarditis, as well as simulate its hemodynamic presentation by myocardial deposition. Given a clinical and hemodynamic presentation compatible with either constrictive or restrictive disease, an endomyocardial biopsy or other biopsy revealing amyloidosis does not necessarily rule out pericardial constriction that may be due to amyloid infiltration. The relationship between constrictive pericarditis, seen in this patient, and the other more common manifestations of amyloid heart disease, and the hemodynamic profiles of amyloid cardiomyopathy and constrictive pericarditis are reviewed.

Epicardial mapping of ventricular defibrillation with monophasic and biphasic shocks in dogs.

To study the mechanism of defibrillation and the reason for the increased defibrillation efficacy of biphasic waveforms, the potential gradient in a 32 x 30-mm region of the right ventricle in 15 dogs was progressively lowered in four steps while a strong potential gradient field was maintained throughout the rest of the ventricular myocardium. The volume of right ventricle beneath the plaque was 10 +/- 2% of the total ventricular mass. A 10-msec monophasic (eight dogs) or 5/5-msec biphasic (seven dogs) truncated exponential shock 30% above the defibrillation threshold voltage was given via electrodes on the left ventricular apex and right atrium to create the strong potential gradient field. Simultaneously, a weaker shock with the same waveform but opposite polarity was given via mesh electrodes on either side of the small right ventricular region to cancel part of the potential difference in the region and to create one of the four levels of potential gradient fields. Shock potentials and activations were recorded from 117 epicardial electrodes in the small region, and in one dog global epicardial activations and potentials were recorded from a sock containing 72 electrodes. Each gradient field was tested 10 times for successful defibrillation after 10 seconds of electrically induced fibrillation. For both monophasic and biphasic shocks, the percentage of successful defibrillation attempts decreased (p < 0.05) as the potential gradient decreased in the small region. Defibrillation was successful approximately 80% of the time for a mean +/- SD potential gradient of 5.4 +/- 0.8 V/cm for monophasic shocks and 2.7 +/- 0.3 V/cm for biphasic shocks (p < 0.05). No postshock activation fronts arose from the small region for eight waveform when the gradient was more than 5 V/cm. For both waveforms, the postshock activation fronts after the shocks were markedly different from those just before the shock and exhibited either a focal origin or unidirectional conduction.(ABSTRACT TRUNCATED AT 400 WORDS)

High and low strength nonsynchronized shocks given during canine ventricular tachycardia.

UNLABELLED: Cardioversion shocks given during ventricular tachycardia may cause ventricular fibrillation or acceleration of ventricular tachycardia, or arrest the tachycardia. A recently proposed theory may explain why the former two phenomena may occur. Briefly, this theory states that potential gradient shock fields of a critical strength delivered to tissue with a critical degree of refractoriness will cause circulating wave fronts of ventricular activation ("rotors") manifest as ventricular arrhythmia. We tested this theory by delivering nonsynchronized shocks 50% higher than defibrillation threshold or 50% lower than defibrillation threshold during 275 episodes of ventricular tachycardia in eight dogs with 5- to 7-day-old myocardial infarcts. Shocks stronger than the defibrillation threshold are likely to create shock fields in the ventricles everywhere stronger than this critical value, and therefore would not generate rotors. Shocks less strong than the defibrillation threshold may create shock fields within the ventricles that include the critical value, and therefore cause rotors if given when critically refractory tissue is present. Nonsynchronized shocks were used to increase the likelihood of encountering tissue with a critical degree of refractoriness. Ventricular fibrillation or acceleration of ventricular tachycardia occurred following 83 of 138 (60%) low strength shocks and following 20 of 137 (14.6%) high strength shocks. The pooled odds ratio for induction of ventricular fibrillation or accelerated ventricular tachycardia after low strength shocks as compared to high strength shocks was 8.9. CONCLUSION: when given during ventricular tachycardia, low strength shocks are much more likely to cause ventricular fibrillation or accelerated ventricular tachycardia than are high strength shocks (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Response of relatively refractory canine myocardium to monophasic and biphasic shocks.

BACKGROUND: Certain biphasic waveforms defibrillate at lower energies than monophasic waveforms, although the mechanism is unknown. METHODS AND RESULTS: The relative ability of monophasic and biphasic shocks to stimulate partially refractory myocardium was compared because defibrillation is thought to involve stimulating relatively refractory myocardial tissue. Shocks of 25-125 V were given during regularly paced rhythm in 11 open-chest dogs. Computerized recordings of shock potentials, and of activations before and after the shocks, were made at 117 epicardial sites. To quantify the shock field strength, the shock potential gradients were calculated at the electrode sites. Monophasic action potential (MAP) electrode recordings, obtained in five dogs, confirmed direct myocardial excitation by the shock, that is, activations beginning during the shock. Tissue was directly excited up to 4 cm from the shocking electrode, and the area directly excited increased as the shock was made stronger or given less prematurely. In six dogs, strength-interval curves for direct excitation were determined from plots of potential gradient versus refractoriness at each electrode site. The biphasic curves were located to the right of the monophasic curves by 8 +/- 4 msec, indicating a lesser ability to excite refractory myocardium. When the gradient at the directly excited border was at least 3.8 +/- 1 V/cm, conduction failed to propagate away from the directly excited zone after the shock, and MAP recordings made near the border showed a shock-induced graded response. This graded response, which prolonged repolarization, may have been responsible for the failure of conduction from the directly excited zone. Although better for defibrillating, the biphasic waveform was thus less effective than the monophasic one in exciting relatively refractory myocardium. CONCLUSIONS: These results indicated that waveform selection for defibrillation should not be guided solely by the ability of the waveform to stimulate tissue, as these two properties can be discordant.

Conduction disturbances caused by high current density electric fields.

During internal defibrillation, potential gradients greater than 100 V/cm occur near defibrillation electrodes. Such strong fields may cause deleterious effects, including arrhythmias. This study determined 1) the effects of such strong fields on the propagation of activation and 2) whether these effects were different for monophasic and biphasic shocks. Voltages and potential gradients during the shock, as well as activation sequences before and after the shock, were mapped from 117 epicardial electrodes placed over a 3 x 3-cm area on the right ventricle in six dogs. Pacing at a cycle length of 350 msec was given from a long narrow electrode on the right side of the mapped area to generate parallel activation isochrones. A monophasic shock, 10 msec in duration, or a biphasic shock with both phases 5 msec in duration was delivered 300 msec after the last paced stimulus via a mesh electrode on the left side of the mapped area as the cathode, with the anode on the right atrium. Shocks of 70-850 V were given, and the potential gradient and current density at each recording electrode were calculated from the measured potentials and fiber orientation by using a finite element method. Pacing was resumed 200 msec after the shock, and activation sequences were mapped for up to 5 minutes. Potential gradients ranged from 1 to 189 V/cm with high fields on the left side and low fields on the right side of the mapped area. Where the potential gradient was weak, the first activation sequence after the shock was similar to that before the shock, but activation blocked without conducting into areas where the gradient was greater than 64 +/- 4 (mean +/- SD) V/cm for monophasic and greater than 71 +/- 6 V/cm for biphasic shocks. These values are significantly different (p less than 0.003). The higher the potential gradient, the longer was the duration of block before conduction returned. Block duration, however, was generally shorter for biphasic than for monophasic waveforms of the same field strength. In conclusion, conduction block can follow either waveform, but biphasic waveforms cause less block than monophasic waveforms. This effect may partially explain the increased defibrillation efficacy of biphasic shocks.