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Biomedical subjects

B Olshansky

Publications and source records attributed to B Olshansky.

At least 73 records · Page 4Linked to original sources
PubMed1992

Ventricular tachycardia rate and morphology determine energy and current requirements for transthoracic cardioversion.

BACKGROUND: The electrical current and energy required to terminate ventricular tachyarrhythmias are known to vary by arrhythmia: Ventricular tachycardia (VT) is generally considered to require less energy than ventricular fibrillation (VF). The hypothesis of our study was that current requirements for transthoracic termination of VT are further determined by VT rate and QRS complex morphology. METHODS AND RESULTS: We prospectively studied 203 patients who received a total of 569 shocks for VT or VF by following a current-based protocol. This protocol recommended shocks for VT beginning at 18 A (70 +/- 22 J) and shocks for VF beginning at 25 or 30 A (137 +/- 52 J or 221 +/- 70 J). The ventricular tachyarrhythmias were subclassified as monomorphic VT (MVT): uniform QRS complex morphology on surface electrocardiogram and heart rate greater than 100 beats per minute; polymorphic VT (PVT): nonuniform QRS complex morphology and heart rate less than or equal to 300 beats per minute; or VF: nonuniform QRS complex morphology and heart rate greater than 300 beats per minute. We found that shocks of 18 A and 25 A for terminating MVT had success rates of 69% and 82%, respectively, whereas such low-current shocks were less successful for PVT (33% at 18 A) and for VF (19% at 18 A, 53% at 25 A). High-current shocks of 35 A and 40 A were equally successful for the three ventricular tachyarrhythmias. Subdividing MVT revealed that slower MVT (heart rate less than 200 beats per minute) had a significantly better success rate with low-current shocks of 18 A and 25 A than did faster MVT (greater than 200 beats per minute) (89% versus 72% success, p less than 0.01). Bundle branch block morphology, QRS axis, and duration of ventricular tachyarrhythmia did not alter current requirements. CONCLUSIONS: Heart rate and electrocardiographic degree of organization of ventricular tachycardia are important determinants of transthoracic energy and current requirements for cardioversion and defibrillation. Transthoracic termination of MVT requires relatively low current or energy, but PVT behaves more like VF and requires higher electrical current or energy.

Electric Countershock↗
PubMed1991

Control of refractory ventricular tachycardia with biventricular assist devices.

A 65-year-old man developed incessant ventricular tachycardia following coronary artery bypass grafting while being weaned from cardiopulmonary bypass. The arrhythmia was refractory to procainamide, lidocaine, bretylium, and magnesium. Ventricular tachycardia subsided following reinitiation of cardiopulmonary bypass. Ultimately, the patient required ventricular assist devices to control his arrhythmia. This case is unique as the ventricular assist devices were used not for hemodynamic support, but for arrhythmia control. The mechanism of arrhythmia suppression may be related to contraction-excitation coupling.

Aged↗
PubMed1991

Electrocardiographic body surface potential mapping in the Wolff-Parkinson-White syndrome. Noninvasive determination of the ventricular insertion sites of accessory atrioventricular connections.

BACKGROUND: A reliable, noninvasive procedure to determine the location of accessory atrioventricular connections in patients with Wolff-Parkinson-White syndrome would add an important diagnostic tool to the clinical armamentarium. METHODS AND RESULTS: Body surface potential mapping (BSPM) using 180 electrodes in various-sized vests and displayed as a calibrated color map was used to determine the ventricular insertion site of the accessory atrioventricular (AV) connections in 34 patients with Wolff-Parkinson-White syndrome. Attempts were made to determine the 17 ventricular insertion sites described by Guiraudon et al. All 34 patients had an electrophysiologic study (EPS) at cardiac catheterization, and 18 had surgery so the ventricular insertion sites could be accurately located using EPS at surgery. A number of physiologic observations were also made with BSPM. CONCLUSIONS: The following conclusions were drawn: 1) BSPM using QRS analysis accurately predicts the ventricular insertion site of accessory AV connections in the presence of a delta wave in the electrocardiogram; 2) the ventricular insertion sites of accessory AV connections determined by BSPM and by EPS at surgery were identical or within one mapping site (1.5 cm or less) in all but four of 18 cases; three of the four exceptions had more than one accessory AV connection, and the other had a very broad ventricular insertion; 3) BSPM and EPS locations of the accessory AV connections correlated very well in the 34 cases despite the fact that BSPM determines the ventricular insertion site and EPS determines the atrial insertion site of the accessory AV connection; 4) as suggested by the three cases of multiple accessory AV connections, EPS and BSPM may be complementary since BSPM identified one pathway and EPS identified the other (in the case with a broad ventricular insertion, BSPM and EPS demonstrated different proportions of that insertion); 5) BSPM using ST-T analysis is very much less accurate in predicting the ventricular insertion site of accessory AV connections unless there is marked preexcitation; 6) standard electrocardiography using the Gallagher grid methodology (but with no attempt at stimulating maximal preexcitation) was not as accurate as QRS analysis of BSPM in predicting the ventricular insertion site of the accessory AV connection; however, exact comparison is hampered by the different number and size of the Gallagher and Guiraudon insertion sites; 7) BSPM using QRS analysis appears to be very accurate in predicting right ventricular versus left ventricular posteroseptal accessory AV connections; 8) typical epicardial right ventricular breakthrough, indicative of conduction via the specialized AV conduction system, occurs in all patients with left ventricular free wall accessory AV connections; 9) epicardial right ventricular breakthrough was not observed in cases with right ventricular free wall or anteroseptal accessory AV connections; 10) epicardial right ventricular breakthrough can occur in the presence of posteroseptal accessory AV connections, whether right or left ventricular; and 11) the delay in epicardial right ventricular breakthrough in cases with left ventricular insertion may provide a marker to estimate the degree of ventricular preexcitation.

Adult↗
PubMed1990

Characterization of double potentials in human atrial flutter: studies during transient entrainment.

Double potentials, defined as atrial electrograms with two discrete deflections per beat separated by an isoelectric interval or a low amplitude baseline, have been observed during right atrial endocardial mapping of human atrial flutter. In this study, bipolar atrial electrograms were recorded during atrial flutter (mean cycle length 235 +/- 27 ms [+/- SEM]) from the high right atrium, the His bundle region, the coronary sinus and at least 30 right atrial endocardial mapping sites in 10 patients. Double potentials were recorded from the right atrium in all patients during atrial flutter. Double potentials were evaluated during transient entrainment of atrial flutter by rapid high right atrial pacing in 5 of the 10 patients. In four of these five patients during such transient entrainment 1) one deflection of the double potential was captured with a relatively short activation time (mean interval 89 +/- 45 ms) and the other deflection was captured with a relatively long activation time (mean interval 233 +/- 24 ms), producing a paradoxical decrease in the short interdeflection interval from a mean of 75 +/- 20 ms to a mean of 59 +/- 24 ms; and 2) the configuration of the double potential remained similar to that observed during spontaneous atrial flutter. On pacing termination 1) the two double potential deflections were found to be associated with two different atrial flutter complexes in the electrocardiogram (ECG); 2) the previous double potential deflection relation resumed; and 3) when sinus rhythm was present, the double potentials were replaced by a broad, low amplitude electrogram recording at the same site.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Demonstration of an area of slow conduction in human atrial flutter.

Ten patients with chronic atrial flutter were studied prospectively using electrophysiologic mapping and pacing techniques to assess the mechanism of atrial flutter and the presence of an area of slow conduction in the atria. Electrograms recorded from greater than or equal to 30 right atrial sites for each patient during atrial flutter demonstrated that right atrial free wall activation was craniocaudal and that the interatrial septum activation was caudocranial, consistent with a reentrant circuit involving the right atrium. In six patients, slow conduction occurred during atrial flutter in the inferior right atrium and was spatially associated with fractionated electrographic recordings. In the other four patients, a "missing" interval of electrical activity occurred in the inferior right atrium for an average of 40% of the atrial flutter cycle. Transient entrainment criteria were demonstrated in each patient during rapid high right atrial pacing. The mean activation time from the high right atrial pacing site to the coronary sinus (inferior left atrial) recording site was long (228 ms) and consistent with activation through an area of slow conduction. During rapid pacing of atrial flutter from the coronary sinus site, no transient entrainment criteria could be demonstrated. The mean activation time from the coronary sinus pacing site to the high right atrial recording site was relatively short (134 ms) and consistent with orthodromic activation of the high right atrium not through an area of slow conduction. High right atrial pacing during sinus rhythm at rates similar to atrial flutter demonstrated a short activation time to the coronary sinus and low right atrial sites (mean 169 and 88 ms, respectively), indicating activation that did not traverse an area of slow conduction. Coronary sinus pacing during sinus rhythm demonstrated the same phenomena. Low right atrial electrograms recorded during sinus rhythm and during rapid pacing of sinus rhythm were not fractionated, although they were during atrial flutter. Thus, atrial mapping and pacing data were complementary, indicating that human atrial flutter in the patients studied was generated by a reentrant circuit in the right atrium, with an area of slow conduction in the low right atrium present only during atrial flutter.

Atrial Flutter↗
PubMed1990

Surgical ablation of ventricular tachycardia in the normothermic heart.

Nineteen patients with ventricular tachycardia were subjected to surgery using a normothermic map-guided approach. Surgical ablation was performed by endocardial resection and cryoablation. Eleven patients had multiple distinct morphologies, and eight patients needed concomitant coronary artery bypass surgery. Seventeen patients survived the perioperative period, and all but one patient had a successful surgical ablation of all documented morphologies. Ventricular tachycardia surgery can be accomplished with the sequential map-guided approach on the normothermic beating heart, and in this era of the implantable defibrillator should remain a mainstay of the surgical treatment for ventricular tachycardia.

Aged↗
PubMed1990

Electrophysiological testing and nonsustained ventricular tachycardia. Use and limitations in patients with coronary artery disease and impaired ventricular function.

Electrophysiological testing was performed in 100 consecutive patients with spontaneous asymptomatic nonsustained ventricular tachycardia, chronic coronary artery disease, and ejection fraction of less than 40%. Fifty-seven patients without inducible sustained ventricular arrhythmias were discharged on no antiarrhythmic therapy. Sustained monomorphic ventricular tachycardia was induced in 37 patients, and polymorphic ventricular tachycardia or ventricular fibrillation was induced in six patients. Of the 43 patients with inducible sustained ventricular arrhythmias, three had spontaneous cardiac arrest during serial drug testing and were excluded from further analysis. Twenty patients were discharged on drug therapy, resulting in suppression of inducible sustained ventricular arrhythmias. The remaining 20 patients with persistently inducible sustained arrhythmias were discharged on drug therapy, resulting in maximal rate slowing of the induced tachycardia. During a mean follow-up of 16.7 months, there were 10 recurrent cardiac arrests or sudden deaths. The 1- and 2-year actuarial incidence of these events was 2% and 6%, respectively, in patients without inducible sustained ventricular arrhythmias; 0% and 11%, respectively, in patients in whom inducible arrhythmias were suppressed; and 34% and 50%, respectively, in patients with persistently inducible sustained ventricular arrhythmias. Multivariate Cox analysis identified only the persistence of inducible sustained ventricular arrhythmias as a significant independent predictor of sudden death or recurrent sustained arrhythmias (p less than 0.001; relative risk, 3.5; 95% confidence intervals, 2.1-4.9). In this population, therapeutic intervention to prevent sudden death is unnecessary in patients without inducible sustained ventricular arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

Usefulness of isoproterenol in facilitating atrioventricular nodal reentry tachycardia during electrophysiologic testing.

In some patients with documented atrioventricular (AV) nodal supraventricular tachycardia (SVT), the arrhythmia is not inducible during a standard stimulation protocol. In these patients the level of sympathetic activity may be an important factor. This study evaluates the influence of isoproterenol on anterograde and retrograde pathway properties in patients with AV nodal SVT and the mechanism by which this SVT is facilitated. Group 1 consisted of 8 consecutive patients, ages 23 to 85 years (mean +/- standard error, 57 +/- 8) who had no inducible AV nodal SVT during electrophysiologic testing until isoproterenol (0.5 to 3.0 micrograms/min) was infused. These patients were compared with 6 patients in the same age range (45 to 78 years, mean +/- standard error, 64 +/- 5) who had inducible AV nodal SVT without isoproterenol and who comprised group 2. In comparing group 1 (before isoproterenol) with group 2, there was no significant difference in the refractory periods of the anterograde slow and fast pathways, although the anterograde block cycle length was longer in group 1 patients (421 +/- 18 vs 362 +/- 14 ms, p less than 0.05). The retrograde block cycle length was also longer in 7 of the 8 group 1 (before isoproterenol) patients in whom it could be measured versus those in group 2 (411 +/- 14 vs 318 +/- 27 ms, p less than 0.05). During isoproterenol, the anterograde and retrograde block cycle lengths in group 1 were not different from group 2. Therefore, AV nodal SVT may not be inducible in some patients during routine electrophysiologic testing.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1988

Ventricular tachycardia masquerading as supraventricular tachycardia: a wolf in sheep's clothing.

It is generally assumed that if a wide QRS complex tachycardia has the same morphology on the 12-lead electrocardiogram as during sinus rhythm, the tachycardia is supraventricular. The author presents unique electrocardiographic data on four patients with QRS complex morphologies that are nearly identical during ventricular tachycardia and during sinus rhythm. The QRS complex duration during sinus rhythm was 140-180 msec and was the same as that of the tachycardia. The QRS complex morphology on the electrocardiogram was a right bundle branch block, left axis in three patients and right bundle branch block, normal axis in one patient. The mean ventricular tachycardia cycle length was 345 msec. The diagnosis of ventricular tachycardia was established by electrophysiologic testing in two patients and by atrial electrograms demonstrating AV dissociation in two patients. Thus, if the 12-lead electrocardiogram morphology of a wide QRS complex tachycardia is similar to that during sinus rhythm, it does not necessarily imply that the tachycardia is supraventricular. Ventricular tachycardia can occur with the same QRS complex morphology as occurs during sinus rhythm.

Adult↗
PubMed1988

Use of procainamide with rapid atrial pacing for successful conversion of atrial flutter to sinus rhythm.

Rapid atrial pacing is a useful technique and often the therapy of choice to terminate atrial flutter in patients. However, interruption of atrial flutter by rapid atrial pacing may not always produce sinus rhythm, but rather may result in atrial fibrillation. Twelve patients with spontaneous atrial flutter that had been present for greater than 24 h were studied to assess the efficacy of atrial pacing, alone and in combination with procainamide, to convert atrial flutter to normal sinus rhythm. Rapid atrial pacing for greater than or equal to 15 s from selected atrial sites at selected pacing rates were performed during atrial flutter. The initial pacing rate was always at a cycle length 10 ms shorter than the atrial flutter cycle length. If atrial flutter persisted after cessation of pacing, it was repeated at progressively shorter cycle lengths until either a rate of 400 beats/min was achieved or atrial fibrillation was induced. In two patients, atrial flutter was converted to sinus rhythm with pacing alone. Three patients developed sustained atrial fibrillation as a result of the rapid atrial pacing, this rhythm ultimately reverting back to atrial flutter in two. Ten patients received procainamide and 9 of the 10 had lengthening of the atrial flutter cycle length by a mean of 68 ms (1 patient continued to have atrial fibrillation). Then, using the same atrial pacing protocol, high right atrial pacing alone at a mean cycle length of 227 ms interrupted atrial flutter in all these patients, returning their rhythm to sinus rhythm. It is concluded that intravenous procainamide effectively augments the efficacy of rapid atrial pacing to convert atrial flutter to sinus rhythm.

Adolescent↗
PubMed1988

A fourth criterion for transient entrainment: the electrogram equivalent of progressive fusion.

Prior data pertaining to transient entrainment and associated phenomena have been best explained by pacing capture of a reentrant circuit. On this basis, we hypothesized that rapid pacing from a single site of two different constant pacing rates could constantly capture an appropriately selected bipolar electrogram recording site from one direction with a constant stimulus-to-electrogram interval during pacing at one rate, yet be constantly captured from another direction with a different constant stimulus-to-electrogram interval when pacing at a different constant pacing rate. To test this hypothesis, we studied a group of patients, each with a representative tachycardia (ventricular tachycardia, circus-movement tachycardia involving an atrioventricular bypass pathway, atrial tachycardia, and atrial flutter). For each tachycardia, pacing was performed from a single site for at least two different constant rates faster than the spontaneous rate of the tachycardia. We observed in these patients that a local bipolar recording site was constantly captured from different directions at two different pacing rates without interrupting the tachycardia at pacing termination. The evidence that the same site was captured from a different direction at two different pacing rates was supported by demonstrating a change in conduction time to that site associated with a change in the bipolar electrogram morphology at that site when comparing pacing at each rate. The mean conduction time (stimulus-to-recording site electrogram interval) was 319 +/- 69 msec while pacing at a mean cycle length of 265 +/- 50 msec, yet only 81 +/- 38 msec while pacing at a second mean cycle length of 233 +/- 51 msec, a mean change in conduction time of 238 +/- 56 msec. Remarkably, the faster pacing rate resulted in a shorter conduction time. The fact that the same electrode recording site was activated from different directions without interruption of the spontaneous tachycardia at pacing termination is difficult to explain on any mechanistic basis other than reentry. Also, these changes in conduction time and electrogram morphology occurred in parallel with the demonstration of progressive fusion beats on the electrocardiogram, the latter being an established criterion for transient entrainment.(ABSTRACT TRUNCATED AT 400 WORDS)

Atrial Flutter↗
PubMed1988

Energy, current, and success in defibrillation and cardioversion: clinical studies using an automated impedance-based method of energy adjustment.

The purposes of this study were two. First, we wanted to evaluate in patients a technique for automated adjustment of selected energy for defibrillation or cardioversion based on transthoracic impedance. Second, we wanted to define the relationship of peak current and shock success in various arrhythmias. Applying a previously validated method of predicting transthoracic impedance in advance of any shock, we modified defibrillators to automatically double the operator-selected energy if the predicted impedance exceeded 70 omega. Success rates of shocks given for ventricular and atrial arrhythmias from these modified energy-adjusting defibrillators were compared with success rates for shocks given from standard defibrillators. We prospectively collected data on 347 patients who received a total of 1009 shocks. Low-energy (100 J) shocks given to high-impedance (greater than or equal to 70 omega) patients had a poor success rate; in such high-impedance patients significant improvement in shock success rate was achieved by the energy-adjusting defibrillators. For example, when 100 J shocks were selected for high-impedance patients in ventricular fibrillation the energy-adjusting defibrillators achieved a shock success rate of 75%, whereas standard defibrillators achieved a shock success rate of only 36% (p less than .01). Similar improvements were seen for ventricular tachycardia and atrial fibrillation. Thus, automated energy adjustment based on transthoracic impedance is a beneficial approach to defibrillation and cardioversion. For ventricular fibrillation, atrial fibrillation, and atrial flutter there was a clear relationship between peak current and shock success.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1987

Usefulness of isoproterenol facilitation of ventricular tachycardia induction during extrastimulus testing in predicting effective chronic therapy with beta-adrenergic blockade.

Previous studies indicate that programmed extrastimulus testing (PES) during isoproterenol infusion facilitates induction of clinical ventricular tachycardia (VT) in some patients. This study attempts to determine if VT inducible only during isoproterenol infusion predicts suppression of VT with chronic oral beta-adrenergic blockade. Nine patients, aged 23 to 77 years, with symptomatic VT or syncope not necessarily provoked by exercise or stress were evaluated. Extrastimuli did not induce VT in any patient. However, during isoproterenol infusion (1 to 4 micrograms/min), all patients had reproducibly inducible VT corresponding to their spontaneously occurring VT (recordings available in 7 patients). Coupling intervals inducing tachycardia during isoproterenol were similar to intervals that did not induce VT without isoproterenol. No patient had VT with isoproterenol infusion alone (without extrastimuli). In only 4 of 8 patients who underwent exercise tests while not taking medications was VT provoked. With propranolol therapy (160 mg/day) or its equivalent, only 1 patient had recurrent symptoms during a mean follow-up of 39 months (range 23 to 52). VT inducible with extrastimuli only during isoproterenol infusion predicts that oral beta-adrenergic blockade will prevent spontaneous VT or syncope long term. These data suggest that occurrence of VT in some patients depends on premature depolarizations in the setting of beta-adrenergic influence.

Adrenergic beta-Antagonists↗
PubMed1987

Demonstration of the presence of slow conduction during sustained ventricular tachycardia in man: use of transient entrainment of the tachycardia.

To test the hypothesis that an area of slow conduction is present during reentrant ventricular tachycardia in man, and that the earliest activation site during ventricular tachycardia is within or orthodromically just distal to the area of slow conduction in the reentry loop, we studied 12 episodes of ventricular tachycardia (mean rate 185 +/- 32 beats/min) that were induced in nine patients with ischemic heart disease. Rapid ventricular pacing was performed at selected sites during ventricular tachycardia while recording electrograms from an early activation site relative to the onset of the QRS complex (site A) and from a site close to the pacing site (site B). Rapid pacing from the right ventricular apex during ventricular tachycardia with a right bundle branch block pattern and from selected left ventricular sites during ventricular tachycardia with a left bundle branch block pattern (mean pacing rate 202 +/- 38 beats/min) resulted in constant ventricular fusion beats on the electrocardiogram except for the last captured beat (i.e., the ventricular tachycardia was entrained) in 11 of 12 episodes. During entrainment: sites A and B were activated at the pacing rate, conduction time from the last pacing impulse to the last captured ventricular electrogram at site A (St-A interval) was 359 +/- 69 msec and spanned the diastolic interval, while that at site B (St-B interval) was only 28 +/- 13 msec, site A had the same ventricular electrogram morphology as that during ventricular tachycardia, while site B had a different electrogram morphology, indicating that site A was activated in the same direction during entrainment as during ventricular tachycardia. Eight episodes of ventricular tachycardia were entrained at two or more different pacing rates. The St-A interval increased during pacing at the faster rate(s) in four of eight episodes, while the St-B interval remained unchanged. Rapid ventricular pacing performed from the same site during sinus rhythm (mean pacing rate 201 +/- 37 beats/min) resulted in an St-A interval of 103 +/- 37 msec (p less than .001 vs the value during entrainment) and an St-B interval of 31 +/- 15 msec (p = NS vs the value during entrainment). It is concluded that an area of slow conduction not demonstrable during sinus rhythm exists during ventricular tachycardia, and that the earliest activation site during ventricular tachycardia is at or orthodromically distal to this area of slow conduction.

Aged↗
PubMed1985

Significance of inducible tachycardia in patients with syncope of unknown origin: a long-term follow-up.

The frequency of inducible tachycardia was assessed in patients presenting with syncope whose noninvasive evaluation did not reveal a cause for syncope. It was also determined whether treatment of tachyarrhythmias during programmed electrical stimulation would prevent recurrence of syncope. One hundred five patients were studied and 97 were followed up for a mean period of 25.8 months. Sixty-eight patients (65%) did not have inducible tachycardia. Sixty of these 68 patients could be followed up; 12 (20%) had recurrent syncope. Ventricular or supraventricular tachycardia was inducible in 37 patients (35%). The frequency of organic heart disease was not higher in this group or in those with inducible ventricular tachycardia as compared with those with inducible supraventricular tachycardia. Three patients with inducible ventricular tachycardia died suddenly or were resuscitated from cardiac arrest, and an additional seven had recurrent syncope; thus, the total recurrence rate was 27%. Of 23 patients undergoing effective therapy as predicted by electrophysiologic testing, 3 (14%) had a recurrent event. Results were significantly different in patients receiving ineffective therapy as judged by electrophysiologic testing. Of 13 patients in this latter category, 7 patients (54%) had recurrence of syncope or cardiac arrest (p less than 0.05). In three patients, recurrence took place a mean of 5 months after cessation of therapy; on resumption of effective therapy, no syncope recurred for 15.6 months (p less than 0.025). Tachycardia is frequently induced in patients with syncope of unknown origin, whether or not organic heart disease is present. Treatment of inducible tachycardia may prevent recurrence of syncope.

Adolescent↗
PubMed1985

Echocardiographic assessment of schizophrenics and manics: a reexamination of early necropsy findings.

Postmortem evaluation of schizophrenic patients earlier this century demonstrated relatively consistent findings of hypoplasia of the heart and great vessels. No recent attempts have been made, to our knowledge, to replicate these results. In vivo assessment of the left heart and aorta by M-mode echocardiographic examination seemed likely to provide an opportunity to investigate the relationship of major psychiatric illness to heart size and aortic diameter. Twenty-two chronic schizophrenics (mean age 31.5 years), 17 manics (mean age 30.9 years), and 14 normal volunteers (mean age 29.1 years) consented to echocardiographic examination. Patients were diagnosed by DSM-III criteria. Individuals with any history of cardiovascular disease or alcohol abuse were excluded. No statistically significant differences emerged among the groups in measures of left atrial, aortic root, or end-diastolic left ventricular diameters. Our results did not support previously reported autopsy findings. Implications of the relationship of chronic institutionalization and chronic neuroleptic treatment to heart and great vessel dimensions are discussed.

Adult↗