Charles W. Thorburn

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.

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.

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.

Natural history of late potentials in the first ten days after acute myocardial infarction and relation to early ventricular arrhythmias

Serial signal-averaged electrocardiograms (ECGs) were performed every 48 hours in 50 patients admitted to the coronary care unit with acute myocardial infarction. The prevalence of late potentials was 32% at presentation (mean time to recording 12.4 +/- 6.6 hours after onset of chest pain) and increased progressively throughout the hospital stay. New late potentials were recorded in patients with no prior acute myocardial infarction as early as 3 hours after the onset of chest pain and as late as 8 days. Late potentials appeared transiently in only 3 patients. The detection of late potentials in the initial signal-averaged ECG identified patients with clinically significant early ventricular arrhythmias with a sensitivity of 80% and specificity of 72%. The predictive accuracy was 38% for a positive test and 94% for a negative test. Patients with early ventricular arrhythmias had significantly lower voltage in the terminal 40 ms of the filtered QRS complex (16 +/- 8 vs 32 +/- 19 microV, p less than 0.01) than those without arrhythmias. The signal-averaged ECG may be useful in identifying patients at high risk of developing clinically significant early ventricular arrhythmias after acute myocardial infarction.

Left Ventricular Mechanical Assist Devices and Cardiac Device Interactions: An Observational Case Series

Background: Nonpulsatile left ventricular assist devices (LVADs) are increasingly used for treatment of refractory heart failure. A majority of such patients have implanted cardiac devices, namely implantable cardioverter‐defibrillators (ICDs) or cardiac resynchronization therapy‐pacemaker (CRT‐P) or cardiac resynchronization therapy‐defibrillator (CRT‐D) devices. However, potential interactions between LVADs and cardiac devices in this category of patients remain unknown.

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 about 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 μA 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.

Permanent Pacing for Late-Onset Atrioventricular Block in Patients with Heart Transplantation: A Single Center Experience

Introduction: The incidence, mechanisms, clinical associations, and outcomes in patients with late‐onset (>3 months) atrioventricular (AV) block following heart transplantation are not well known. This study will characterize late‐onset AV block following cardiac transplantation.

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 seriai 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 1) at the time of hospital discharge. Of these patients, 23 no longer had late potentials at G‐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 μV to 31 ± 9 μV (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 of31 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 palients with no late potentials at discharge (group II, 2%). Of those patients with events beyond 6 weeks, a normal signal‐averaged ECG (either lost late potentials or group II) was observed in 6/11 (55%) patients on at least one occasion prior to the occurrence of the event. Hence, a significant number of arrhythmic events occurring ≥ 6 weeks after myocardial infarction occur in palients with a normal signal‐averaged ECG even when late potentials are initially present. “Loss’ of late potentials does not necessarily confer an improved prognosis in terms of risk of arrhythmic events.

Surface electrocardiographic manifestations of tachyarrhythmias: clues to diagnosis and mechanism.

Although major developments in the analysis of arrhythmias have occurred in recent years using invasive intracardiac electrophysiologic testing, it is prudent to acknowledge the information available from the surface electrocardiograph (ECG). Many electrophysiologic concepts derived from the surface ECG were based on deductive reasoning; these have now been confirmed by programmed stimulation studies and intracardiac mapping. Further, recent advances in signal processing have enhanced the interpretative power of the surface ECG. This review will attempt to present the current status of the surface ECG in elucidating the mechanisms and site of origin of both supraventricular and ventricular tachyarrhythmias.

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.