Right bundle branch block updated.
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Biomedical subjects
Publications and source records attributed to L N Horowitz.
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Clinical cardiac electrophysiologic testing has been employed in the evaluation and treatment of patients with tachyarrhythmias. In patients with recurrent supraventricular tachyarrhythmias, electrophysiologic study is indicated when the arrhythmia is life-threatening or significantly disruptive to lifestyle, when empiric therapy has failed to control the arrhythmia, or when supraventricular tachycardia complicates the Wolff-Parkinson-White syndrome. In patients with ventricular tachyarrhythmias, electrophysiologic study should be undertaken when life-threatening sustained ventricular tachyarrhythmias are documented or when a substantial risk of developing these arrhythmias is noted.
The relationship of apparent steady-state serum concentrations of amiodarone and its metabolite, desethylamiodarone, to therapeutic and toxic effects was assessed in 127 patients who had treatment-resistant ventricular or supraventricular arrhythmias or were intolerant to other agents. After at least 2 months (mean, 9.8) of treatment with daily maintenance doses of 200 to 600 mg, arrhythmias were effectively suppressed in 78% of patients. Arrhythmias recurred in 47% of patients with serum amiodarone concentrations of less than 1.0 mg/L, whereas only 14% of patients with higher concentrations had recurrences (p less than 0.005). Side effects, most of them mild, occurred in 57%; only 9 patients required discontinuation of drug therapy. The risk of developing adverse reactions was related to serum amiodarone concentrations (p less than 0.0001). Adverse reactions were common in patients with serum values exceeding 2.5 mg/L, although pulmonary complications did occur at lower concentrations. Monitoring serum amiodarone concentrations may differentiate failure of drug therapy from suboptimal dosing and reduce the incidence of concentration-related side effects.
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The relation between low-amplitude, late potentials on the body surface and directly recorded electrograms in 8 patients with and 11 patients without ventricular tachycardia (VT) was studied. Bipolar X,Y,Z leads were signal-averaged and filtered with a digital technique. All patients had catheter endocardial left ventricular maps. The VT group had medically intractable VT and an endocardial excision was performed for control of VT. Before bypass, epicardial maps were obtained in the operating room. All studies were performed during normal sinus rhythm. Four patients without VT, each with a previous myocardial infarction, had fragmented endocardial electrograms recorded at 2.0 +/- 1.2 sites. The latest electrogram for each patient ended 87 +/- 8 ms after QRS onset, within the high-amplitude portion of the filtered QRS complex. All patients with VT had fragmented electrograms recorded at 6.1 +/- 3.1 sites/patient. Eighty-eight percent of the fragmented electrograms were endocardial. The latest fragmented electrogram for each patient ended 161 +/- 43 ms after QRS onset, significantly later than the fragmented electrograms from the patients without VT (p = 0.002). Six VT patients had low-amplitude, late potentials at the end of the filtered QRS complex. In these patients, the last 40 ms of the filtered QRS complex contained a higher proportion of fragmented electrograms compared with earlier segments of the QRS complex (68% versus 27%, p less than 0.001). Two patients with VT did not have late potentials. One patient with left bundle branch block had delayed left ventricular epicardial activation which masked the fragmented electrograms. The other had fragmented electrograms of brief duration which ended 80 +/- 12 ms after QRS onset, during the time of normal ventricular activation. It is concluded that the late potential corresponds to delayed, fragmented electrographic activity. Failure to record a late potential may arise from delayed ventricular activation at other sites from bundle branch block or fragmented electrograms of a brief duration.
The clinical utility of electrophysiologic testing in assessing the long-term efficacy of amiodarone for treatment of life-threatening ventricular arrhythmias is controversial, most investigators reporting little or no correlation between the early effects of the drug on arrhythmia inducibility and subsequent prognosis. We have evaluated 69 consecutive patients given amiodarone for ventricular tachycardia (VT) or fibrillation (VF). All patients underwent provocative electrophysiologic testing with programmed electrical stimulation before and after amiodarone loading. After a standardized amiodarone loading regimen, the patients' arrhythmias were not inducible in 22 patients (group 1) and remained inducible in 47 patients (group 2). No patient in group 1 has had a recurrence of VT/VF, whereas 15 (32%) of 47 patients in group 2 have had recurrences. The characteristics of the arrhythmia induced by programmed stimulation in group 2 accurately predicted the severity of the recurrence. We conclude that electrophysiologic testing may be useful in evaluating the efficacy of amiodarone for the long-term treatment of VT/VF and that its precise role in this context should be further investigated by stringently controlled studies.
To identify predictors of the success or failure of medical therapy in chronic recurrent sustained ventricular tachycardia, univariate and multivariate statistical techniques were used to retrospectively analyze data in 84 patients with this arrhythmia. By univariate analysis, four factors were associated with successful medical treatment: age less than 45 years, ejection fraction greater than 50%, hypokinesia as the only contraction abnormality and the absence of organic heart disease. Four other findings, the induction of ventricular tachycardia with a single ventricular extrastimulus, an HV interval greater than 60 ms, the presence of a left ventricular aneurysm and Q waves on a baseline electrocardiogram, correlated with medical failure. However, none of these variables alone accurately predicted treatment results in more than 75% of cases. By discriminant analysis, a function incorporating eight variables was constructed which correctly classified 81% of patients. Moreover, three-quarters of the patients could be classified into groups with a high or low probability of success where accuracy increased to 90%. When the discriminant function was tested prospectively in 31 similar patients, 25 (81%) fell into the groups with a high or low probability of success. In the latter group, of 20 patients predicted to fail medical therapy, 19 (95%) did fail a complete trial of medical therapy. The overall accuracy remained a high 92%. In clinical application this function would allow patients with a high probability of responding to medical therapy to be selected for serial electrophysiologic drug testing. In patients with a low probability of responding to medical therapy, serial studies could be avoided and alternate forms of therapy explored.
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A definite diagnosis of anterior myocardial infarction is often difficult to make in patients when a pattern of poor R wave progression in the precordial leads is present on the electrocardiogram. The purpose of this study was to determine whether a mathematical model could be devised to identify patients with anterior infarction among 102 consecutive patients with poor R wave progression. Each patient underwent exercise testing with thallium scanning. The diagnosis of anterior infarction was established in 20 (20%) of the 102 patients by the presence of fixed thallium-201 perfusion defects in the anterior wall or septum, or both. With the use of a multivariate stepwise discriminant analysis of clinical and electrocardiographic variables, five variables (sex, ST-T changes, S wave amplitude in leads V2 and V3 and the sum of the R wave amplitude in leads V3 and V4) that were statistically significant by univariate analysis were selected by the model to identify patients with anterior infarction (sensitivity 85%, specificity 71%). The discriminant model was subsequently applied prospectively to an additional 21 patients with poor R wave progression and provided a sensitivity of 85% and a specificity of 88%. Thus, anterior infarction (fixed thallium-201 defects in the anteroseptal segments) was present in 20% of patients with poor R wave progression in the precordial leads; and a mathematical model can be used to identify a subset of patients with anterior infarction in a group of patients with poor R wave progression.
Surgical resection of the endocardium and subendocardium often abolishes chronic recurrent sustained ventricular tachycardia in patients with healed myocardial infarcts or ventricular aneurysms, presumably by interrupting the reentrant pathway. To define the morphologic characteristics of cells in the reentrant pathway, we studied the histology and ultrastructure of the endocardial resections of 23 patients who underwent this procedure. Bundles of apparently viable myocardial fibers embedded in dense fibrous tissue were identified throughout the endocardial resections from all patients. These bundles of cells were separated from one another by fibrous tissue but extended uninterrupted to the margins of the surgical resection. In 14 patients Purkinje fibers were identified beneath the thickened endocardium whereas the remaining bundles were composed of ventricular muscle. The Purkinje fibers appeared to have normal ultrastructure and ventricular cells with both normal and abnormal ultrastructures were present. The abnormal muscle cells were characterized by loss of contractile elements, aggregates of dilated sarcoplasmic reticulum, and osmiophilic dense bodies. The sarcolemma was intact and the nuclear chromatin was evenly dispersed suggesting that these cells were still viable. The abnormal structure and arrangement of the surviving cardiac fibers in the endocardium may cause the abnormal electrophysiologic function that results in ventricular tachycardia.
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The ECG changes resulting from endocardial resection, with or without aneurysmectomy and coronary artery bypass grafting (CABG), are reported in 82 patients. Angiographic and surgical features and peak creatine kinase (CK) levels are correlated with ECG findings. Twenty-three of 82 patients (28%) had the following ECG changes postoperatively: decreased ST segment elevation = 3 (4%), loss of R wave amplitude = 4 (5%), increased R wave amplitude = 5 (6%), new Q wave = 4 (4%), axis shift greater than or equal to 45 degrees = 6 (7%), and new bundle branch block = 6 (7%). Five of six new cases of bundle branch block were left bundle type and resulted from resection of the inferoposterobasal and contiguous septal endocardium. ECG anterior infarction, anterior aneurysm, and anteroseptal endocardial resection were associated with a significantly lower incidence of postoperative ECG changes. Aneurysmectomy and the performance of CABG were not significantly associated with postoperative ECG changes, but more bypass grafts per patient grafted appeared in the group with postoperative ECG changes, suggesting that coronary artery disease may be more severe in that group. Peak CK did not correlate with postoperative ECG findings. We conclude that ECG changes occur infrequently after endocardial resection and that the factors responsible are not clear, although severity of coronary artery disease may be contributory. Left bundle branch block is a significant complication of inferoposterobasal resection, but complete heart block appears not to be. The diagnosis of myocardial necrosis is difficult in these patients.
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Programmed electrical stimulation can now be safely performed in humans for the evaluation of therapy for recurrent ventricular tachyarrhythmia. Such studies may also eventually be found useful in predicting the risk of developing life-threatening ventricular tachyarrhythmias. The repetitive ventricular response phenomenon has been evaluated. Although an association between the intraventricular reentrant phenomenon and sustained ventricular tachyarrhythmias has been found, its predictive value in a population at risk is not sufficient for use in clinical decision making. On the other hand, the initiation of sustained ventricular tachycardia or fibrillation appears closely related to its actual spontaneous clinical occurrence. Serial electrophysiologic studies can be performed and are effective in prospectively evaluating the response to antiarrhythmic drugs. The efficacy of therapy based on the results of programmed stimulation appears to be good.
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Sixty patients with recurrent sustained ventricular tachycardia (VT) refractory to medical therapy underwent subendocardial resection. There were 52 men and 8 women, ranging in age from 39 to 74 years, all of whom had coronary disease. Each patient had had a prior infarction 1 week to 11 years prior to surgery and 52 had left ventricular aneurysms. The mean ejection fraction was 27%. All 60 patients underwent endocardial resection with or without aneurysmectomy guided by intraoperative and/or catheter endocardial mapping. Thirty-seven endocardial resections were from the interventricular septum, 14 from the interoposterior free wall, and 16 were from the anteroapical and anterolateral free wall. There were five (8%) surgical deaths. The 55 survivors underwent programmed stimulation in the control state 28 days following the operation. VT was not inducible in 42 patients (group A) and was inducible in 13 patients (group B). The group B patients underwent drug testing and were discharged on the antiarrhythmic agent that made the VT noninducible or more difficult to induce. There have been only four recurrences in sustained VT with a follow-up of 19 +/- 11 months. There have also been nine late nonarrhythmic deaths. The actuarial survival curve predicted 62% survival at 40 months. We conclude that activation guided endocardial resection provides long-term effective therapy for drug-resistant ventricular tachycardia.
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