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Biomedical subjects

M M Scheinman

Publications and source records attributed to M M Scheinman.

At least 19 recordsLinked to original sources

Electrocardiographic and electrophysiologic characteristics of anterior, midseptal and right anterior free wall accessory pathways.

OBJECTIVES: The objective of this study was to define the electrocardiographic (ECG) and electrophysiologic characteristics of midseptal, anteroseptal and right anterior free wall accessory pathways. METHODS: The fully pre-excited 12-lead surface ECGs and ECGs during orthodromic atrioventricular (AV) reentrant tachycardia were compared for 13 patients with an anteroseptal, 7 with a midseptal and 7 with a right free wall accessory pathway. Routine electrophysiologic studies were performed in all and stimulation of the right ventricular summit during tachycardia was accomplished in 10 patients. RESULTS: Differences in the surface ECGs were not sufficiently sensitive to distinguish among accessory pathway locations. Premature ventricular complexes induced from the right ventricular septal summit during ventricular activation either advanced the succeeding atrial depolarization or terminated the tachycardia in three of six patients with a septal pathway and in none of the four with a right anterior pathway. The change in ventriculoatrial (VA) interval with the development of right bundle branch block during orthodromic AV tachycardia proved most helpful in distinguishing these pathways. Patients with a right anterior free wall pathway showed a change in VA interval > or = 40 ms, whereas those with an anteroseptal pathway showed changes of 20 to 30 ms and those with a midseptal pathway showed no change. CONCLUSIONS: Anteroseptal, midseptal and right anterior free wall pathways may be distinguished by using programmed stimulation of the summit of the right ventricular septum and especially with changes in the VA interval with development of right bundle branch block during orthodromic AV reentrant tachycardia.

Adolescent

Comparison of a vectorcardiographically derived 12-lead electrocardiogram with the conventional electrocardiogram during wide QRS complex tachycardia, and its potential application for continuous bedside monitoring.

Previous investigators published conflicting reports comparing a vectorcardiographically derived electrocardiogram (ECGD) with the conventional 12-lead one (ECG). Prior comparisons were obtained in adults during sinus rhythm, but never in patients with wide QRS complex tachycardia. The ECGD was evaluated during baseline rhythms in patients with varying cardiac diagnoses, and the diagnostic accuracy of the 2 methods was compared during 64 episodes of wide QRS complex tachycardia in 49 patients during cardiac electrophysiologic study. All leads of the 12-lead ECGD closely resembled the conventional ECG in baseline and tachycardia tracings, except leads V3 and V4. QRS voltages were less in the ECGD, resulting in an inability to detect left ventricular hypertrophy in one third of patients with that diagnosis. There was excellent agreement between the ECGD and ECG in diagnosing prior myocardial infarction (92%), ventricular preexcitation patterns (100%), bundle branch and fascicular blocks (100%), and axis deviation. The ECGD was equally as valuable as the ECG in the diagnosis of wide QRS complex tachycardia. There was perfect agreement between the 2 lead systems in application of the morphologic criteria differentiating supraventricular tachycardia with aberration from ventricular tachycardia in leads V1, V2 and V6, and for criteria requiring axis determination and measurement of RS intervals in the precordial leads. The ECGD tracings contained less muscle artifact during body movements (e.g., after direct-current defibrillation). In conclusion, the ECGD's close correlation with the ECG, and its technical superiority and simple 5 torso-positioned electrode configuration make it worth pursuing as an option for continuous bedside monitoring.

Adult

Active compression-decompression resuscitation: a novel method of cardiopulmonary resuscitation.

Chest compression is an important part of cardiopulmonary resuscitation (CPR), but it only aids circulation during a portion of the compression cycle and has been shown to only minimally increase blood flow to vital organs. The purpose of this study was to quantitate the short-term hemodynamic effects of CPR with a hand-held suction device that incorporates both active compression and decompression of the chest. The suction device was applied to the middle of the sternum and compared with standard manual CPR in eight nonventilated anesthetized dogs. Coronary perfusion pressure, systolic and diastolic aortic pressures, right atrial diastolic pressure, and the velocity time integral (an analog of cardiac output), which were obtained by means of transesophageal pulsed wave Doppler echocardiography from the main pulmonary artery, were measured every 30 seconds during CPR. Minute ventilation was measured over the last minute of each CPR technique. Both active compression-decompression CPR and standard CPR were sequentially performed for 2 minutes in random order 30 seconds after induced ventricular fibrillation. The CPR techniques consisted of 100 compressions per minute, with a compression depth of 1.5 to 2 inches and a 50% duty cycle. Coronary perfusion pressure, velocity time integral (cardiac output analog), minute ventilation, and systolic arterial pressure were all significantly improved by active compression-decompression CPR when compared with standard CPR. We conclude that active compression-decompression CPR is a simple technique that appears to improve coronary perfusion pressure, systolic arterial pressure, cardiac output, and minute ventilation in nonventilated animals when compared with standard CPR.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

Combined use of beta-adrenergic blocking agents and long-term cardiac pacing for patients with the long QT syndrome.

OBJECTIVE: The objective of this study was to review our current experience using a combination of beta-adrenergic blocking agents and long-term cardiac pacing to treat patients with the idiopathic long QT syndrome. BACKGROUND: Patients with the idiopathic long QT syndrome are at high risk for sudden cardiac death. Before combination therapy, 20 of the 21 study patients experienced either cardiac arrest (n = 8) or syncope (n = 18) and 11 had documented polymorphous ventricular tachycardia. Nine of these patients had not responded to isolated beta-blocker therapy and five had not responded to isolated left cervicothoracic sympathectomy. METHOD: All patients were treated with combined beta-blocker therapy and long-term cardiac pacing at a rate designed to normalize the QT interval. RESULTS: Cardiac pacing at rates of 70 to 125 beats/min resulted in shortening of the QT and corrected QT (QTc) intervals from 517 +/- 78 and 541 +/- 62 ms to 404 +/- 37 and 479 +/- 41 ms, respectively. The mean follow-up interval after institution of pacing was 55 +/- 45 months. The only sudden death occurred in a patient who had discontinued beta-blocker therapy. Syncope occurred in four patients, two of whom had interrupted pacemaker function due to lead fracture. Pacemaker problems, partly attributable to the specific rate required for QT interval shortening and to avoidance of T wave sensing, were relatively common. No patient who continued the combination therapy died, but 10% of these patients had a recurrence of symptoms. CONCLUSIONS: Combination therapy with a beta-blocker and cardiac pacing appears to be a highly effective primary therapy for symptomatic patients with the long QT syndrome and to provide excellent adjunctive therapy for patients who require insertion of an automatic internal defibrillator.

Adrenergic beta-Antagonists

Importance of recording the right bundle branch deflection in the diagnosis of His-Purkinje reentrant tachycardia.

Eight of 120 consecutive patients with inducible sustained ventricular tachycardia who were studied at our institution from September 1, 1988 to January 1, 1991, were found to have reentry within the His-Purkinje System as the mechanism of their tachycardias. Two of the eight patients (25%) required the recording of the right bundle branch potential to elucidate the tachycardia circuits. The electrophysiological findings of these two patients are described. In both instances, the diagnosis of supraventricular tachycardia with aberrancy was excluded. In patient 1, a His-bundle electrogram preceded each QRS complex during tachycardia and the His-to-His interval variation preceded changes in QRS intervals. However, recordings from the right bundle branch allowed for exclusion of bundle branch reentry and evidence was found for reentry restricted to the left fascicles. In patient 2, despite instances of dissociation of the His-bundle deflection from the tachycardia, a right bundle branch potential preceded each QRS and spontaneous changes in the interval between successive activation of the right bundle branch preceded changes in ventricular activation. Catheter ablation of the right bundle branch eliminated the tachycardia. It is concluded that the recording of a right bundle branch potential should be included in electrophysiology study of patients in whom there is suspicion of reentry within the His-Purkinje System. Clinically, recognizing these forms of tachycardias can be important because they can be effectively treated with catheter ablation.

Adult

Ablation of ventricular tachycardia using multiple sequential transcatheter application of radiofrequency energy.

Multiple sequential radiofrequency energy was applied in the left and right ventricles of 24 dogs to produce large ablated areas limited to endocardial and subendocardial regions. Endocardial ablation was performed in nine dogs with normal ventricles and 15 that had survived remote myocardial infarcts, three with inducible sustained monomorphic ventricular tachycardia. A quadripolar catheter was positioned either at the site of earliest ventricular activation during induced monomorphic ventricular tachycardia or at circumscribed areas of the left ventricle. Radiofrequency energy was delivered between two adjacent poles of the catheter, successively applying radiofrequency energy to the distal, middle, and proximal electrode pairs; this was repeated 9 to 11 times with the catheter in a slightly different position. A cumulative energy of 9,688 +/- 4,191 joules resulted in an ablated endocardial/subendocardial surface area of 4.7 +/- 2.2 cm2 (range 2.4-10 cm2, maximum depth 4 mm). Sustained tachycardia was not inducible by aggressive programmed ventricular stimulation in the dogs with previously inducible tachycardia, indicating successful ablation of the tachycardia foci. Only seven normal dogs were available for electrophysiological studies; three were used in acute and four in chronic studies. Ventricular tachycardia was not induced in the remaining dogs either before or after radiofrequency ablation, indicating the lack of an arrhythmogenic effect of this method. Histologic examination was performed in all nine normal dogs (five were sacrificed for acute pathological examination) as well as in the 15 with myocardial infarction. The late pathological examination of the radiofrequency lesion in these 19 animals showed homogeneous areas of coagulation necrosis and endocardial proliferation. Thus, this modified technique of radiofrequency ablation produced large homogeneous endocardial/subendocardial scars suitable for treating ventricular tachycardia and showed no evidence of an arrhythmogenic influence.

Animals

Effects of sympathetic stimulation on use dependence of lidocaine, mexiletine, and quinidine in an intact canine model.

The use- or rate-dependent effects of a continuous infusion of lidocaine (n = 6, serum level 3.1 +/- 0.34 micrograms/mL), mexiletine (n = 8, serum level 7.08 +/- 0.90 micrograms/mL), and quinidine (n = 6, serum level 6.8 +/- 1.22 micrograms/mL) were studied in an open chest canine preparation. A use-dependent effect on conduction was assessed by measuring the change in the His to surface ventricular activation (HV) time at differing atrial paced rates during drug infusion. Global sympathetic activation was achieved by nondecentralized left stellate ganglion stimulation (4-10 Hz, 6-12 V, 2 ms) and use dependence at the same cycle lengths was compared. Repolarization times were measured from epicardial monophasic action potentials recorded from the anterior left ventricle throughout the study. There was no significant change in the HV time during control studies with or without left stellate stimulation. Use-dependent slowing of conduction was seen in all studies during drug infusion. This was evident at cycle lengths of 300-190 ms for quinidine and at cycle lengths less than 250 ms for lidocaine and mexiletine. Stellate stimulation attenuated use dependence in all studies. This effect was significant from cycle lengths of 300-190 ms for lidocaine and quinidine and at cycle lengths shorter than 230 ms for mexiletine (p less than 0.05). Stellate stimulation significantly reduced use-dependent prolongation of the HV interval by an average of 60%. During stellate stimulation there was a nonsignificant trend towards cycle length independent shortening of action potential duration both at baseline and in the presence of drugs.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials

Electrophysiologic effects of disopyramide phosphate on sinus node function in patients with sinus node dysfunction.

The electrophysiologic effects of intravenously administered disopyramide (2 mg/kg) on three parameters of sinus node function were examined in 16 symptomatic patients with sinus node dysfunction. Based on their ECG data before study, patients were subdivided into group A (n = 8), those with sinus pauses and/or sinoatrial (SA) exit block; and group B (n = 8), those with sinus bradycardia. Disopyramide shortened spontaneous cycle length in 10 of 16 patients and lengthened it in six--markedly so (91%) in one patient. Estimated SA conduction time decreased in seven of 14 patients and increased in seven. Two patients developed second degree SA exit block after disopyramide. Maximum sinus node recovery time was prolonged by disopyramide in 11 of 16 patients and markedly so in four. For the group as a whole there was no significant difference in spontaneous cycle length, maximum sinus node recovery time or estimated SA conduction time. P-wave and QRS durations and H-V intervals were significantly lengthened by disopyramide. Marked depression of the three parameters of sinus node function occurred in three group A patients and in one group B patient who had persistent severe sinus bradycardia. These four patients also had secondary pauses after termination of rapid atrial pacing under control conditions. Disopyramide should be administered cautiously to patients with sinus node dysfunction, particularly those with sinus pauses, SA exit block or secondary pauses.

Adult

Determination of His-Purkinje refractoriness in man with His bundle pacing.

Consistent His bundle pacing was accomplished in one of 60 consecutive patients. Intracardiac electrophysiologic studies in this patient revealed rapid atrioventricular nodal conduction (AH = 55 msec). While the relative refractory period of the His-Purkinje system as a whole determined by His bundle pacing (using the extrastimulus technique) was identical to that determined by atrial pacing, changes in right bundle branch refractoriness differed. An atrial extrasystolic interval of 370 msec resulted in right bundle branch block, whereas direct His pacing at a shorter extrasystolic interval (360 msec) failed to produce a bundle branch block pattern. The effective refractory period of the His-Purkinje system could not be determined by atrial pacing because of atrial refractoriness, but was obtained by His bundle pacing. Theoretically, direct His bundle pacing may be of value in determining His-Purkinje system refractoriness when this parameter is unobtainable due to either atrial or atrioventricular nodal refractoriness. This technique appears to have limited clinical usefulness, however, because of the very small success rates. Finally, His-Purkinje system refractoriness may differ, depending on site of stimulation, presumably due to differing inputs into the His-Purkinje system.

Adult

Clinical and electrophysiologic findings in patients with paroxysmal slowing of the sinus rate and apparent Mobitz type II atrioventricular block.

Over five years, 13 patients with episodic apparent type II atrioventricular (AV) block associated with sinus slowing were seen. This phenomenon occurred only transiently during an acute illness in eight patients (group I) but recurred chronically in five (groupII). For the group as a whole, the mean spontaneous cycle length was 42% longer during the period of AV block compared with periods of 1:1 AV conduction (800 +/- 116 msec to 1138 +/- 489 msec) (P less than 0.05). Electrophysiologic studies in four group I patients showed no abnormalities, whereas abnormalities in AV nodal conduction and refractoriness or provocation of intranodal Mobitz type II AV block (during carotid massage) were observed in three patients in group II and were totally abolished by atropine. In group I patients, apparent type II AV block was self-limited. In the chronic group, recurrent symptoms required insertion of permanent pacemakers in two patients. Simultaneous type II block and sinus slowing appeared to be related to the effects of increased vagal tone on both nodal structures. Intracardiac pacing is not indicated for patients with transient episodes associated with an acute illness, but may be required for symptomatic patients with recurrent episodes.

Adult