Recurrent atrial electrode displacement complicating a single lead VDD pacing system.

We describe an unusual complication of single-lead VDD pacing: recurrent advancement of the atrial bipole into the right ventricle. As a consequence, the patient experienced symptomatic pacemaker-mediated tachycardia and underwent two revision operations to achieve adequate fixation of the lead.

Inappropriate rate change in minute ventilation rate responsive pacemakers due to interference by cardiac monitors.

Observations of inappropriate rate increase in five patients with minute ventilation rate responsive implanted pacemakers (Telectronics Meta) are reported. Pacing rate increases were observed immediately upon connection of the resting patients to two brands of widely used cardiac monitors, and one commonly used echocardiograph. In some circumstances, the rate increase remained until monitor disconnection; in others the rate increase was transient, lasting and 20 seconds. A hardware thoracic resistance variation simulator was constructed and connected to one of the pacemakers to test sensitivity to rate modifying interference from external sources. This demonstrated that the sensitivity to interference is dependent upon the frequency of the interfering signal and is highest in the range 10-60 kHz, that peak currents as low as 10 microA can cause maximum rate increase, and that the signals injected into patients by several cardiac monitors, for purposes of lead-off detection or respiratory monitoring, fall into the frequency range at which the pacemaker is most susceptible to interference.

Transesophageal echocardiography before and during direct current cardioversion of atrial fibrillation: evidence for "atrial stunning" as a mechanism of thromboembolic complications.

OBJECTIVES: The purpose of this study was to evaluate the usefulness of transesophageal echocardiography before electrical cardioversion in patients with atrial fibrillation and to determine the mechanism of thromboembolism after cardioversion. BACKGROUND: Thromboembolic complications after electrical cardioversion of atrial fibrillation have been attributed to the dislodgment of preexistent left atrial thrombus during the resumption of atrial contraction. Transesophageal echocardiography has been proposed as a method of screening patients for left atrial thrombus before cardioversion. METHODS: Seventy transesophageal echocardiographic studies were performed in 66 patients, predominantly with nonvalvular atrial fibrillation, before direct current cardioversion. In addition, transesophageal echocardiography was performed during the cardioversion procedure in 15 patients and immediately after in 1 patient. RESULTS: Left atrial thrombus was detected in one patient (1.4%), and cardioversion was cancelled. Thromboembolic complications occurred in 4 patients, none of whom had evidence of left atrial thrombus before cardioversion. Within 10 s of successful cardioversion, left atrial spontaneous echo contrast appeared in five patients, increased in one patient and was unchanged in nine patients. Patients with new or increased spontaneous echo contrast had more impaired atrial contraction and slower initial heart rates after cardioversion than those without. Left ventricular contraction was also impaired transiently by cardioversion. CONCLUSIONS: Transesophageal echocardiographic detection of left atrial thrombus before direct current cardioversion is important but infrequent in patients with predominantly nonvalvular atrial fibrillation. The occurrence of thromboembolic complications in the absence of demonstrable left atrial thrombus and the new development of spontaneous echo contrast in association with the transient atrial dysfunction ("stunning") caused by cardioversion suggest that cardioversion may promote new thrombus formation, in which case all patients should receive full anticoagulant therapy at the time of cardioversion.

Prognostic implications of loss of late potentials following acute myocardial infarction.

The prognosis of patients following myocardial infarction is adversely affected by the finding of late potentials at the time of hospital discharge. Loss of late potentials has been previously reported during serial testing during the first year after infarction, but it is not known whether such patients remain at risk of arrhythmic events. This study prospectively followed 243 patients after myocardial infarction. Late potentials were observed in 92 patients (group I) at the time of hospital discharge. Of these patients, 23 no longer had late potentials at 6-week follow-up and 8 had had an arrhythmic event (sudden death or ventricular tachycardia). In patients with loss of late potentials, overall QRS duration had decreased from 109 +/- 11 msec at discharge to 104 +/- 11 msec (P < 0.01), terminal QRS voltage rose from 15 +/- 4 microV to 31 +/- 9 microV (P = 0.001), and late potential duration fell from 42 +/- 6 msec to 28 +/- 6 msec (P = 0.001) at the 6-week study. Predictors of loss of late potentials were: initial duration of the QRS duration (P < 0.001) and terminal voltage (P < 0.005); non-Q wave infarction (P < 0.001); and being a male (P < 0.05). After the 6-week assessment, 11 additional arrhythmic events occurred during median follow-up of 31 months. The risk of arrhythmic events was similar in patients with loss of late potentials and those who retained late potentials in group I (9% vs 11%, P = NS) but significantly greater than patients with no late potentials at discharge (group II, 2%).(ABSTRACT TRUNCATED AT 250 WORDS)

Noninvasive predictors of cardiac events after myocardial infarction. Complementary value of exercise testing and signal-averaged electrocardiography.

Signal-averaged electrocardiography, resting radionuclide ventriculography and Holter monitoring were performed prior to hospital discharge, to assess their value in predicting recurrent cardiac events in 210 survivors of acute myocardial infarction. In addition, 153 of these patients also underwent exercise radionuclide ventriculographic assessment. During median follow-up of 14 months (6-24 months), there were 16 cardiac deaths, 15 patients had recurrent infarction and 7 patients represented with symptomatic ventricular tachycardia. Cox regression analysis identified independent predictors of 'ischemic events' (death or re-infarction) as a previous history of infarction (p = 0.01), Killip class III-IV (p = 0.03) and an abnormal exercise radionuclide study (p = 0.04); and predictors of 'arrhythmic events' (sustained ventricular tachycardia or sudden death) as an abnormal signal-averaged electrocardiograph (p = 0.01) and left ventricular ejection fraction less than 40% (p = 0.03). Patients with an abnormal signal-averaged electrocardiograph and reduced left ventricular ejection fraction had a 34% incidence of arrhythmic events during the first 6 months compared with a 4% incidence among patients without late potentials. In those patients who underwent exercise testing and signal averaging, 85% of total cardiac events and all cardiac deaths were predicted by an abnormality of either noninvasive test. In addition, exercise testing and signal-averaged ECG were independent predictors of outcome. Hence, using a combination of noninvasive tests, patients can be stratified according to the risk of recurrent life-threatening cardiac events after myocardial infarction; such patients may be suitable for intensive investigation and considered for trials involving active intervention.

Prediction of serious arrhythmic events after myocardial infarction: signal-averaged electrocardiogram, Holter monitoring and radionuclide ventriculography.

Noninvasive assessment was undertaken before hospital discharge in 210 patients who had recovered from acute myocardial infarction. This comprised signal-averaged electrocardiography, Holter monitoring and radionuclide left ventriculography. An abnormal signal-averaged electrocardiogram was defined as the presence of a low voltage signal less than 20 microV in the terminal 40 ms of the filtered QRS complex or a long filtered QRS complex greater than 120 ms. During a follow-up period of 6 months to 2 years (median 14 months), 15 patients had arrhythmic events: eight died suddenly and seven presented with sustained, symptomatic ventricular tachycardia. Using univariate analysis, abnormalities in each of the three noninvasive tests were able to predict arrhythmic events. Stepwise logistic regression demonstrated that each test was independently significant in predicting outcome, with a left ventricular ejection fraction less than 40% being the most powerful variable (beta = 2.8, p less than 0.005). This process generated an algorithm that allowed assessment of combinations of variables: the finding of an abnormal signal-averaged electrocardiogram in the presence of an ejection fraction less than 40% identified patients with a 34% probability of arrhythmic events. By contrast, in patients with left ventricular dysfunction but a normal signal-averaged tracing, the risk of arrhythmic events was 4% (p less than 0.001). This combination of variables was associated with a sensitivity of 80% and a specificity of 89%. Hence, using a combination of noninvasive tests after myocardial infarction, patients can be stratified according to risk of serious arrhythmic events.

Late potentials detected after myocardial infarction: natural history and prognostic significance.

The risk of developing spontaneous ventricular tachycardia (VT) and/or sudden death ("arrhythmic events") was prospectively assessed in 165 patients who survived acute myocardial infarction. Signal-averaged electrocardiograms (ECGs) were performed before hospital discharge and then serially at regular intervals over the following year. In addition, 24 hr Holter monitoring was performed and left ventricular ejection fraction was determined. Sixty-five patients (group 1) had abnormal signal-averaged ECGs (voltage in the last 40 msec of the filtered QRS less than 20 microV or filtered QRS duration greater than 120 msec), 92 had normal signal-averaged ECGs (group 2), and eight had bundle branch block (excluded from analysis). In group 1, spontaneous normalization of the voltage in the last 40 msec of the QRS complex occurred in 30% of patients after 12 months, although total filtered QRS duration did not change overall. During follow-up of up to 20 months (median 11), seven patients died suddenly and six presented again with spontaneous, symptomatic VT. Eleven of 65 (17%) group 1 patients had an arrhythmic event compared with one of 92 patients (1%) in group 2 (p less than .001). The sensitivity of the signal-averaged ECG as a predictor of arrhythmic events was 92% with a specificity of 62%. Patients with subsequent arrhythmic events had considerably lower voltage in the last 40 msec of the QRS (11.0 +/- 8.3 vs 32.0 +/- 21.9 microV; p less than .001) than those without such events, and longer filtered QRS complexes (121 +/- 14 vs 105 +/- 12 msec; p less than .001). Multivariate logistic regression determined that the signal-averaged ECG provided independent prognostic information from the presence of complex ventricular ectopy and the degree of left ventricular dysfunction assessed at the time of hospital discharge. Signal-averaged ECGs provide important prognostic information in identifying patients at risk of arrhythmic events after myocardial infarction. Dynamic changes in the terminal QRS voltage are observed during the first year after myocardial infarction.

Signal-averaged electrocardiogram for evaluation of recurrent syncope.

Signal-averaged electrocardiography (ECG) was performed in 150 consecutive patients presenting with syncope, to determine its diagnostic role in identifying patients with ventricular tachycardia (VT) and in determining their long-term prognosis. Patients also underwent a standardized investigational protocol to independently determine a cause of syncope. Twenty-nine patients had a late potential, 107 had a normal signal-averaged electrocardiogram and 14 had bundle branch block on 12-lead ECG. Signal-averaged ECG identified a late potential in 16 of 22 patients with VT and was normal in 101 of 114 patients in whom syncope was attributed to causes other than VT or remained unexplained (sensitivity 73%, specificity 89%, predictive accuracy 55%). In patients with coronary artery disease, the predictive accuracy increased to 82%. Absence of a late potential identified a group of patients with a very low incidence of VT. During follow-up of 1 to 20 months (median 11), 15 patients (10%) died, 6 suddenly. There was no significant difference in survival or recurrence of syncope between patients with and without a late potential. Signal-averaged ECG can noninvasively identify patients with serious ventricular arrhythmias among an unselected group presenting with syncope.

High-frequency analysis of the surface electrocardiograms of patients with supraventricular tachycardia: accurate identification of atrial activation and determination of the mechanism of tachycardia.

Signal processing of the electrocardiogram (ECG) was performed during supraventricular tachycardia (SVT) in 24 patients in an attempt to locate the P wave and to characterize its morphology in three orthogonal planes. In patients with atrioventricular reciprocating tachycardia, a discrete atrial signal could be identified within the ST segment and/or T wave with inferior-to-superior orientation. Atrial activation was identified in patients with primary atrial tachycardia as long as there was a constant relationship between each QRS complex and the preceding atrial signal. Patients with atrioventricular nodal reentrant tachycardia were deduced to have simultaneous atrial and ventricular activation when no atrial signal could be seen elsewhere in the cycle. Mean maximum P wave amplitude was 25.4 +/- 6.3 microV during SVT, with a mean noise level below 1.0 microV. Signal processing of the ECG during SVT enhances the detection of the P wave and the appreciation of P wave morphology, both of which are important factors in the noninvasive determination of the electrophysiologic mechanisms of SVT.

The role of signal averaged electrocardiography in the investigation of unselected patients with syncope.

The cause of syncope is often not determined, despite extensive investigations, yet it is important to identify the high risk group who may be in danger of sudden death due to ventricular arrhythmias. Recent studies have shown that the signal averaged electrocardiogram (SA ECG) can identify low amplitude signals in the terminal portion of the QRS and ST segment (late potentials) recorded from the body surface, which represent areas of delayed conduction in small areas of diseased myocardium in patients with ventricular tachycardia (VT). Sixty-five consecutive patients presenting to hospital with syncope were prospectively evaluated to determine a cause of syncope; this included quantitative analysis of the terminal QRS complex using SA ECG. A cardiac cause of syncope was assigned to 49% of patients, a non-cardiac cause to 20%, and no cause was found in the remaining 31%. Initial history and physical examination established a diagnosis in 14% of patients. A prior history of heart disease was an important indicator to a cardiac cause for syncope. Continuous electrocardiographic monitoring was diagnostic in 23% and the yield for electrophysiological testing (in a selected subgroup) was 40%. Ancillary cardiac and neurological investigations were of little diagnostic value, although they were useful in defining the severity and extent of clinically suspected conditions. SA ECG identified a late potential in 11 of 13 patients with VT, but was normal in all except three of the remaining patients who were not considered to have VT (sensitivity 85%, specificity 94%). We conclude that high frequency analysis of the signal averaged ECG is a reliable non-invasive indicator of syncope due to VT.

Pacemaker reversion for suspected supraventricular tachycardia.

Overdrive atrial pacing was employed in twelve patients with suspected supraventricular tachycardia resistant to drug therapy. Eleven of these patients reverted to sinus rhythm with pacing either immediately or after a short episode of atrial fibrillation. In one patient, recordings from the atrial electrode indicated that a broad complex tachycardia was of ventricular rather than supraventricular origin. No complications were encountered and the procedure was well tolerated in all. Overdrive pacing is suggested as a safe alternative to DC cardioversion in drug-resistant supraventricular tachycardia, particularly in the presence of digitalis, in the elderly and in patients with chronic lung disease.

New electrocardiographic criteria for inferior myocardial infarction.

The sensitivity of existing electrocardiographic (ECG) Q-wave criteria for inferior myocardial infarction (IMI) is poor. New criteria were developed after prospective analysis of the ECGs of 300 consecutive subjects undergoing cardiac catheterization (group 1). These criteria were then prospectively tested in a second group of 300 consecutive subjects undergoing cardiac catheterization (group 2). Only patients with left bundle branch block were excluded from both groups. In each group, IMI subgroups were defined on the basis of angiographic inferior wall motion abnormalities associated with a 70% or greater stenosis of the supplying coronary artery. All subjects who did not satisfy these angiographic criteria were included in the non-IMI subgroups. The new ECG criteria defined in the group 1 subjects were: 'Q' waves in one or more of the ECG leads 2, 3, or a VF, where 'Q' waves are those at least 30 ms in duration (onset to nadir) or those with a Q:R ratio at least 1:4, provided the QRS amplitude is greater than or equal to 0.5 mV. The ECG pattern 'Q3qF', where 'q' waves are those not satisfying either of the above, is excluded from these criteria. When tested in the group 2 subjects, the proposed criteria were significantly (P less than 0.001) more sensitive (68%) than those of the New York Heart Association (28%), though less specific (84% versus 97%, P less than 0.001). Of 300 ECGs analysed by two independent observers, disagreements as to the diagnosis by the proposed criteria were encountered in 19 cases (6%).

Long-term results of tricuspid valve replacement and the problem of prosthetic valve thrombosis.

Observations in 71 patients having tricuspid valve replacement over a 14-year period are described. The operative mortality rate was 10% and the actuarial survival rate was 73% at 5 years and 47% at 10 years. Survival was unaffected by the number of valves replaced or the type used (27 Starr-Edwards, 32 Björk-Shiley, 8 Lillehei-Kaster, and 4 porcine xenografts). Complications were common: 3 deaths were related to anticoagulation and 1 was due to a systemic embolus. Six patients required permanent pacing. There was a very high incidence of thrombosis of the prosthetic tricuspid valve. Twenty percent of the tilting disc valves thrombosed, compared with 4% of the Starr-Edwards valves (p less than 0.05). Symptoms of thrombosis were usually insidious, and its diagnosis was often delayed. There was a continuing risk of this complication, and presentation occurred up to 12 years after the original operation. Thrombolytic therapy with streptokinase was successful in 1 of 2 patients. Replacement of the thrombosed prosthetic valves was carried out without mortality in 8 patients.

Effects of disopyramide on electrophysiological properties of specialized conduction system in man and on accessory atrioventricular pathway in Wolff-Parkinson-White syndrome.

Seven patients with normal specialized conduction system and three patients with the Wolff-Parkinson-White (WPW) syndrome were studied using programmed stimulation of the heart before and after the administration of intravenous disopyramide. The principal effect of this drug was to prolong the effective refractory period of the atria and ventricles, and to prolong the effective refractory period of the anomalous pathway in the WPW syndrome. In addition, it prolonged the conduction time in the anomalous pathway in the WPW syndrome. These findings suggest that disopyramide would be a useful and safe drug in the management of certain atrial and ventricular arrhythmias and in the management of the Wolff-Parkinson-White syndrome with atrial fibrillation.