Biomedical subjects
E Lichstein
Publications and source records attributed to E Lichstein.
Transient atrioventricular standstill. Etiology and management.
Four patients with different clinical conditions had transient cardiac standstill for periods of up to 22.5 seconds. All patients showed signs of cerebral ischemia and required cardiac resuscitation. In one patient, the standstill was thought to be the result of a transient increase in the vagal tone, and no long-term therapy was required. In the second patient, cardiac standstill occurred during hospitalization for impending myocardial infarction. Coronary arteriography followed by coronary artery surgery was performed, and there was no further episodes of standstill. In the third patient, standstill was probably related to long-term ingestion of propranolol hydrochloride, and was not observed after this medication was discontinued. In the fourth patient, standstill was the result of the sick sinus syndrome, and a permanent pacemaker was inserted. Standstill of both atria and ventricles may occur under different clinical settings, and management of arrhythmia should be guided by thf etiology of the arrhythmia.
Refractory reentrant atrial tachycardia. Successful treatment with a permanent radio frequency triggered atrial pacemaker.
This 68 year old man had recurrent episodes of paroxysmal atrial tachycardia, probably due to chronic pericarditis, persisting over a 7 year period. These episodes were resistant to all conventional medical therapy and at times produced ischemic chest pain. There was no evidence of Wolff-Parkinson-White syndrome either on the standard electrocardiogram or on the His bundle electrogram performed with atrial pacing. Rapid atrial pacing at a rate of 200/min was found to promptly terminate the tachycardia and restore normal sinus rhythm. Because of the refractoriness of the patient's tachycardia, in addition to the presence of ischemic chest pain during these episodes, a permanent radio frequency triggered atrial pacemaker was inserted which enables him to initiate rapid atrial pacing by pressing an external control. The patient has been maintained on antiarrhythmic medications in an attempt to decrease the frequency of these episodes; during an 8 month follow-up period, he has done well with approximately one episode of tachycardia each month requiring radio frequency atrial pacing for termination.
Bradycardia-hypotension syndrome in acute myocardial infarction. Reappraisal of the overdrive effects of atropine.
Sixty-eight (17 per cent) of 380 patients with acute myocardial infarction had the bradycardia-hypotension syndrome (ventricular rate below 60/min and systolic blood pressure less than 100 mm Hg) during the first 24 hours of admission to a large general hospital. In 61 of the 68 patients, the administration of atropine significantly increased the heart rate (from 46 plus or minus 14 to 79 plus or minus 12/min) (p less than 0.01) and systolic blood pressure (from 70 plus or minus 15 to 105 plus or minus 13 mm Hg) (p less than 0.001). In 26 of the 68 patients, ventricular premature complexes decreased from 9.4 plus or minus 3/min to 2.4 plus or minus 0.7/min (p less than 0.001) after the administration of atropine. It is concluded that the bradycardia-hypotension syndrome is not an uncommon complication following acute myocardial infarction and that selected doses of atropine may have a beneficial effect without significant complications.
Incidence and description of accelerated ventricular rhythm complicating acute myocardial infarction.
One hundred and nineteen episodes of accelerated ventricular rhythm (less than 125/min) were noted in 37 patinets with acute myocardial infarction during a 1 year period. The incidence was 12.7 per cent. Twenty-seven episodes of fast ventricular tachycardia (less than 125/min) were noted in 16 of these patients. Eighteen patients had anterior myocardial infarction and 19 inferior myocardial infarction. The mechanism of onset of accelerated ventricular rhythm was classified as escape in 65 episodes. Ventricular premature beats were noted close to episodes of accelerated ventricular rhythm in 31 patients and fast ventricular tachycardia in 14 patients. The morphology of accelerated ventricular rhythm was similar to the ventricular premature beats in 27 patients and similar to the fast ventricular tachycardia in 12. In 11 patinets the morphology of ventricular premature beats, accelerated ventricular rhythm and fast ventricular tachycardia were all the same. In six patients the coupling time of the ventricular premature beats and the onset of the accelerated ventricular rhythm were the same. In seven patients the morphology of the accelerated ventricular rhythm and fast ventricular tachycardia were the same, and the rate of the accelerated ventricular rhythm was exactly half that of the fast ventricular tachycardia. There were three deaths due to shock and heart failure. Three episodes of fast ventricular tachycardia progressed to ventricular fibrillation and were successfully cardioverted. It is concluded that accelerated ventricular rhythm and fast ventricular tachycardia were all the same. In six patients the coupling time of the ventricular premature beats and the onset of the accelerated ventricular rhythm were the same. In seven patients the morphology of the accelerated ventricular rhythm and fast ventricular tachycardia were the same, and the rate of the accelerated ventricular rhythm was exactly half that of the fast ventricular tachycardia. There were three deaths due to shock and heart failure. Three episodes of fast ventricular tachycardia progressed to ventricular fibrillation and were successfully cardioverted. It is concluded that accelerated ventricular rhythm is a relatively common complication of both anterior and inferior myocardial infarction. The high incidence of concomitant fast ventricular tachycardia, the frequency of ventricular premature beats with similar morphology and coupling time, and the instances of two arrhythmias having common rate multiples, suggest that at least in some instances accelerated ventricular rhythm may represent an ectopic focus with exit block.
Long-term survival of patients with incomplete bundle-branch block complicating acute myocardial infarction.
Electrocardiograms and His bundle electrograms were reviewed in 28 patients with incomplete bilateral bundle-branch block complicating acute myocardial infarction. All had a His bundle electrogram at the time of pacemaker insertion; 10 had a second one. Of 23 patients with an initially abnormal HV interval (55 ms or greater), 15 died (65%), while only one died (20%) in the group of 5 with a normal HV interval. This difference is not statistically significant. Sequential His bundle electrograms were done in 6 of the 8 survivors with an initially abnormal HV interval, and 4 showed 10 to 15 ms decrease in HV interval. The disappearance of incomplete bilateral bundle-branch block occurred significantly more often in patients who survived (7 of 12) when compared with those who did not survive (2 of 16) (P less than 0.05). It is concluded that long-term survival is po-sible after incomplete bilateral bundle-branch block complicating acute myocardial infarction. The characteristics of the survivors include an initially normal HV interval, transient incomplete belateral bundle-branch block and a decreasing HV interval if it were initially abnormal.
Diagonal ear-lobe crease: prevalence and implications as a coronary risk factor.
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Pericarditis complicating acute myocardial infarction: incidence of complications and significance of electrocardiogram on admission.
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Appraisal of sinus nodal recovery time in patients with sick sinus syndrome.
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Lidocaine-induced heart block in patients with bundle branch block.
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Bifascicular block related to anginal episodes.
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Television set distortion of electrocardiogram.
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Complete right bundle branch block with left axis deviations: significance of vectorcardiographic morphology.
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Hypomagnesemia and refractory cardiac arrhythmia in a nondigitalized patient.
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Atrioventricular block with lidocaine therapy.
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Intraventricular conduction time (H-V interval) during antegrade conduction in patients with heart block.
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Findings of prognostic value in patients with incomplete bilateral bundle branch block complicating acute myocardial infarction.
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