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Biomedical subjects

D L Kuchar

Publications and source records attributed to D L Kuchar.

At least 19 recordsLinked to original sources

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.

Electrocardiography↗

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.

Anticoagulants↗

Idiopathic right ventricular tachycardia: electrophysiology and response to catheter ablation.

BACKGROUND: Ventricular tachycardia (VT) originating in the right ventricle may be seen in the absence of structural heart disease. Although this is thought to be associated with a benign course, it may cause intolerable symptoms and be difficult to control with antiarrhythmic drugs. AIMS: To assess the value of radiofrequency ablation of right ventricular tachycardia and to characterise the clinical and electrophysiologic features predictive of successful ablation. METHODS: Nine patients (aged 20-49 years) with clinical VT underwent cardiac mapping which localised the site of origin of VT in the right ventricle. At least three separate areas of VT origin were identified in these patients. Ablation of VT was defined as suppression of VT at the time of hospital discharge. RESULTS: Five patients had successful ablation of the tachycardia focus with long term suppression of the arrhythmia. Patients with successful ablation were characterised by inability to induce VT with extrastimuli, a distinct VT morphology with a rS pattern in lead 1, right axis deviation, facilitation of VT with isoprenaline and site of origin in the lateral outflow tract. During VT, an earlier site of presystolic activation was found in successful patients compared with unsuccessful ablations. Right ventricular tachycardia in patients without structural heart disease is a heterogeneous disorder with varied clinical and electrophysiologic features. Successful ablation of VT may be predicted by consideration of these variables.

Action Potentials↗

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)

Electrocardiography↗

Late potentials on the signal-averaged electrocardiogram after canine myocardial infarction: correlation with induced ventricular arrhythmias during the healing phase.

Signal-averaged electrocardiograms (ECGs) and programmed ventricular stimulation were serially performed in 12 dogs (3 weeks of age) after experimental anteroapical myocardial infarction. At electrophysiologic study, sustained ventricular tachyarrhythmia was induced in seven dogs on at least one occasion. Of a total of 39 electrophysiologic studies, sustained monomorphic ventricular tachycardia was induced in seven studies and ventricular fibrillation in eight studies. In the remaining studies, no ventricular arrhythmia could be induced with triple ventricular extrastimuli. There was considerable day to day variability in the response to programmed stimulation and the results of the signal-averaged ECG. The signal-averaged QRS complex was significantly longer in dogs with inducible ventricular tachycardia or fibrillation (61 +/- 5 versus 57 +/- 3 ms, p = 0.02), had a lower terminal QRS amplitude (24 +/- 20 versus 46 +/- 33 microV, p = 0.04) and a longer late potential duration (19 +/- 4 versus 15 +/- 3 ms, p = 0.003) compared with that in animals with no inducible ventricular arrhythmia. Late potentials were defined as a total QRS duration greater than 58 ms, a terminal QRS amplitude less than 20 microV and a late potential duration greater than 18 ms. Using this definition, late potentials were seen in two distinct phases--immediately after coronary ligation and then beyond the first 72 h after infarction. The appearance of late potentials coincided with a change in arrhythmia inducibility from no ventricular arrhythmia to initiation of sustained monomorphic ventricular tachycardia. There is a close relation between inducibility of ventricular tachycardia in experimental canine myocardial infarction and the appearance of late potentials on the surface ECG.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Usefulness of sotalol in suppressing ventricular tachycardia or ventricular fibrillation in patients with healed myocardial infarcts.

The electrophysiologic effects and antiarrhythmic efficacy of oral sotalol were investigated in 42 patients with coronary artery disease and prior myocardial infarction who presented with ventricular tachycardia (VT), ventricular fibrillation (VF) or syncope. The mean left ventricular ejection fraction was 36 +/- 9%. Baseline programmed cardiac stimulation initiated sustained VT (26 patients) or VF (16). The induced arrhythmia was not suppressed by conventional antiarrhythmic drugs in any patient (3 +/- 2 trials/patient). The mean daily dosage of sotalol was 221 +/- 84 mg. The right ventricular effective refractory period increased from 247 +/- 25 to 273 +/- 26 ms with sotalol (p = 0.0001) and the corrected QT interval increased from 431 +/- 35 to 456 +/- 62 ms (p = 0.02). Arrhythmia suppression was defined as no sustained VT or VF in response to programmed cardiac stimulation using up to 3 extrastimuli. Induced VT or VF was suppressed by sotalol therapy in 10 (24%) patients (group 1). Group 1 patients had faster induced arrhythmias at the baseline study than patients whose induced ventricular arrhythmia was not suppressed (group 2). The mean left ventricular ejection fraction tended to be higher in group 1 patients (p = 0.07). Fourteen patients (including 9 group 1 patients) continued receiving sotalol after discharge. In 2 group 2 patients, sotalol was combined with a class IA antiarrhythmic drug. During a mean follow-up period of 7.9 +/- 4.9 months, 2 patients had recurrent VT and in 2 others sotalol was discontinued due to side effects.

Aged↗

Electrocardiographic localization of the site of origin of ventricular tachycardia in patients with prior myocardial infarction.

The utility of the 12 lead electrocardiogram (ECG) in identifying the site of origin of sustained ventricular tachycardia in patients with previous myocardial infarction was studied. A new mapping grid, based on biplanar fluoroscopic imaging of the heart, was utilized for the definition of left ventricular endocardial sites. On the basis of QRS configurations resulting from left ventricular endocardial pacing at disparate sites in 22 patients (Group I), ECG features that were specific for particular sites were identified and used to construct an algorithm. Apical and basal sites were differentiated by the QRS configuration in leads V4 and aVR, anterior and inferior sites by that in leads II, III and V6 and septal and lateral sites were differentiated using leads I, aVL and V1. The algorithm was used to predict the site of earliest endocardial activation during 44 episodes of sustained ventricular tachycardia in a second group of 42 patients (Group II) in a blinded fashion. Anterior sites were correctly predicted in 83% of cases, inferior sites in 84%, septal sites in 90% and lateral sites in 82% of cases. Apical and basal sites were each correctly predicted in 70% of cases, whereas intermediate sites were less well predicted (29 to 55%) on the basis of QRS configuration. Precise localization of the site of origin of ventricular tachycardia (in all three planes) was achieved in 17 cases (39%), and in 16 cases (36%) the site of origin was immediately adjacent to the predicted site. Prediction of the site of origin of ventricular tachycardia from the 12 lead ECG may serve as a useful, time-saving adjunct to, but not a substitute for, activation sequence mapping during ventricular tachycardia.

Algorithms↗

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.

Electrocardiography↗

Electrophysiologic evaluation of antiarrhythmic therapy for ventricular tachyarrhythmias.

The use of electrophysiologic studies has contributed significantly to our understanding of the mechanisms of ventricular tachyarrhythmias and enhanced our ability to assess objectively the efficacy of various therapeutic interventions in modifying or preventing their recurrence. The basis on which electrophysiologic testing techniques is founded is the ability reproducibility to initiate ventricular arrhythmias by programmed electrical stimulation in patients with a history of recurrent ventricular tachycardia or fibrillation. Ventricular tachycardia can be initiated by electrophysiologic studies in approximately 90% of patients with clinically documented recurrent, sustained ventricular tachycardia related to coronary artery disease and in 60% of patients with nonsustained ventricular tachycardia. Reports indicate that electrophysiologic testing is highly specific as well (99% for sustained monomorphic ventricular tachycardia). Studies in patients with recurrent ventricular tachycardia demonstrate that prevention by antiarrhythmic drugs of the ability to initiate tachycardias that were previously inducible by comparable stimulation techniques in the absence of therapy is highly predictive of freedom from recurrent episodes of spontaneous ventricular tachycardia and ventricular fibrillation. This end point can be achieved in 35 to 75% of patients. This wide range of success rates results from differences in the patient populations studied, as well as major differences in the programmed stimulation and antiarrhythmic drug protocols used among laboratories. The positive predictive value of this technique (defined as the percentage of patients in whom complete suppression of inducible ventricular tachycardia or ventricular fibrillation is achieved during electrophysiologic testing with antiarrhythmic drugs and in whom no spontaneous arrhythmia occurs at 1- to 2-year follow-up) ranges between 80 and 95%.

Anti-Arrhythmia Agents↗

Prediction of successful suppression of sustained ventricular tachyarrhythmias by serial drug testing from data derived at the initial electrophysiologic study.

This study investigated whether data available after the initial electrophysiologic study in patients with sustained ventricular tachyarrhythmia could identify those patients in whom serial drug testing is likely to be efficacious. One hundred six patients with inducible sustained ventricular tachyarrhythmia, whose initial study included short-term drug testing with intravenous procainamide, were evaluated. The baseline arrhythmia induced (in the absence of all antiarrhythmic drugs) was monomorphic tachycardia with a cycle length greater than 200 ms in 81 patients and ventricular flutter or fibrillation in the remaining 25 patients. After intravenous infusion of procainamide (1,250 +/- 300 mg), a ventricular tachyarrhythmia could still be induced in 80 patients during testing with up to three extrastimuli. Serial drug testing with one to four trials of oral conventional and investigational agents was then undertaken. Evaluation of 15 clinical, hemodynamic and electrophysiologic variables by stepwise logistic regression identified two independent predictors of successful response to oral antiarrhythmic drugs: 1) noninducibility of ventricular tachycardia after intravenous procainamide (p less than 0.001), and 2) left ventricular ejection fraction greater than or equal to 40% (p less than 0.05). Subgroup analysis combining each of these variables identified patients with a high, intermediate or low probability of finding a successful oral drug regimen. Patients whose arrhythmia was suppressed by intravenous procainamide had a 100% likelihood (if left ventricular ejection fraction was greater than or equal to 40%) or an 87% likelihood (if ejection fraction was less than 40%) of responding to an oral regimen.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

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.

Arrhythmias, Cardiac↗

Long-term survival after counterpulsation for medically refractory heart failure complicating myocardial infarction and cardiac surgery.

Intra-aortic balloon counterpulsation (IABP) was performed in 225 patients over a 12-year period for the treatment of severe left ventricular failure following acute myocardial infarction and cardiac surgery, and which had failed to respond to conventional therapy. Of these patients, 97 (43%) were discharged alive from hospital. Patients were followed-up for a mean of 5.8 years (3 months to 11 years) and assessment of functional status was made. In patients with shock after myocardial infarction, the most favourable outcome was seen in patients who had mechanical cardiac defects which were corrected after institution of IABP and in those treated within 8 hours of the onset of shock; of those patients without shock, best results were seen in patients who had evidence of continuing ischaemia prior to IABP. In patients treated after cardiac surgery, long-term results were favourable in patients with good pre-operative left ventricular function and in those who underwent coronary artery bypass grafting or aortic valve replacement. Long-term results in patients treated with IABP for refractory cardiac failure are encouraging and suggest that IABP should have a continuing role in certain high risk patient groups.

Adult↗

Enhanced prediction of major cardiac events after myocardial infarction using exercise radionuclide ventriculography.

Exercise radionuclide ventriculography (RVG) was performed 7-12 days after acute myocardial infarction (MI) in 153 patients to assess its value in identifying those at risk of serious recurrent cardiac events. In addition to electrocardiogram (ECG) features of the exercise test, clinical and hemodynamic features were also considered: the exercise test was abnormal if there was a fall in blood pressure of 10 mmHg or more, development of angina, or inability to complete three minutes of exercise. RVG was used to measure left ventricular ejection fraction and to assess wall motion at rest and at peak exercise. After a median follow-up of 14 months, there were 18 cardiac events: six deaths and 12 patients with recurrent MI. In addition, 18 patients underwent coronary artery bypass surgery; the decision to perform surgery was predicted by ST segment depression or a fall in blood pressure during exercise (p less than 0.005). The sensitivity of the exercise test for identifying patients with a cardiac event increased progressively as additional parameters were considered in a cumulative fashion; hence, ST depression identified 28% of patients with events, whereas addition of clinical and hemodynamic parameters increased this to 61%. The addition of RVG increased the sensitivity further to 88%, but with a specificity of 50%. Although exercise-induced ST depression of up to 1 mm did not predict outcome significantly, a positive exercise RVG did predict cardiac events: 17% of patients with a positive test had an event, compared with 6% of those with a normal study (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗