The balloon-borne cryogenic telescope testbed mission: Bulk cryogen transfer at 40 km altitude.

The balloon-borne cryogenic telescope testbed is a stratospheric balloon payload intended to develop technology for a future cryogenic suborbital observatory. A series of flights are intended to establish ultra-light dewar performance and open-aperture observing techniques for large (3 m-5 m diameter) cryogenic telescopes at infrared wavelengths. An initial flight in 2019 demonstrated bulk transfer of liquid nitrogen and liquid helium at stratospheric altitudes. An 827 kg payload carried 14 l of liquid nitrogen (LN2) and 268 l of liquid helium (LHe) in pressurized storage dewars to an altitude of 39.7 km. Once at float altitude, liquid nitrogen transfer cooled a separate, unpressurized bucket dewar to a temperature of 65 K, followed by the transfer of 32 l of liquid helium from the storage dewar into the bucket dewar. Calorimetric tests measured the total heat leak to the LHe bath within the bucket dewar. A subsequent flight will replace the receiving bucket dewar with an ultra-light dewar of similar size to compare the performance of an ultra-light design dewar to that of conventional superinsulated dewars.

Differential distribution of alpha subunits and beta gamma subunits of heterotrimeric G proteins on Golgi membranes of the exocrine pancreas.

Heterotrimeric G proteins are well known to be involved in signaling via plasma membrane (PM) receptors. Recent data indicate that heterotrimeric G proteins are also present on intracellular membranes and may regulate vesicular transport along the exocytic pathway. We have used subcellular fractionation and immunocytochemical localization to investigate the distribution of G alpha and G beta gamma subunits in the rat exocrine pancreas which is highly specialized for protein secretion. We show that G alpha s, G alpha i3 and G alpha q/11 are present in Golgi fractions which are > 95% devoid of PM. Removal of residual PM by absorption on wheat germ agglutinin (WGA) did not deplete G alpha subunits. G alpha s was largely restricted to TGN-enriched fractions by immunoblotting, whereas G alpha i3 and G alpha q/11 were broadly distributed across Golgi fractions. G alpha s did not colocalize with TGN38 or caveolin, suggesting that G alpha s is associated with a distinct population of membranes. G beta subunits were barely detectable in purified Golgi fractions. By immunofluorescence and immunogold labeling, G beta subunits were detected on PM but not on Golgi membranes, whereas G alpha s and G alpha i3 were readily detected on both Golgi and PM. G alpha and G beta subunits were not found on membranes of zymogen granules. These data indicate that G alpha s, G alpha q/11, and G alpha i3 associate with Golgi membranes independent of G beta subunits and have distinctive distributions within the Golgi stack. G beta subunits are thought to lock G alpha in the GDP-bound form, prevent it from activating its effector, and assist in anchoring it to the PM. Therefore the presence of free G alpha subunits on Golgi membranes has several important functional implications: it suggests that G alpha subunits associated with Golgi membranes are in the active, GTP-bound form or are bound to some other unidentified protein(s) which can substitute for G beta gamma subunits. It further implies that G alpha subunits are tethered to Golgi membranes by posttranslational modifications (e.g., palmitoylation) or by binding to another protein(s).

Modulation of conduction and refractoriness in atrioventricular junctional reentrant circuit. Effect on reentry initiated by atrial extrastimulus.

The importance of activation sequence of an atrioventricular junctional reentrant (AVJRe) circuit, before delivery of an extrastimulus, has received little attention in studies concerned with clinical tachycardias. In this study a change in activation sequence was accomplished using bidirectional activation (V-A sequential pacing) during the basic drive (V1A1-V1A1). It was noted that, compared with an atrial extrastimulus (A2) after an atrial drive (A1-A1), earlier activation (by V1 impulse of the V1A1-V1A1 drive) consistently improved conduction, or decreased refractoriness, or both, in the anterograde as well as the retrograde pathway of the AVJRe circuit. In all patients, five with AV nodal reentry and six with Wolff-Parkinson-White syndrome, reentrant tachycardia could be prevented during V-A sequential pacing. In four of eleven patients, reentry was prevented despite achieving the so-called critical atrioventricular nodal delays that had previously caused reentry during control study. This finding suggested that conduction delay necessary for reentry was related to the site of block, which in turn was affected by V-A sequential pacing. We concluded that changing the activation sequence during basic drive modulates conduction and refractoriness in AVJRe circuits, and allows the study of a wide range of electrophysical factors that prevent or permit reentry.

Electrophysiologic characteristics of sudden QRS axis deviation during orthodromic tachycardia. Role of functional fascicular block in localization of accessory pathway.

We analyzed the effect of functional fascicular block (FFB) on ventriculoatrial conduction time (VACT) during orthodromic tachycardia (OT) in 32 patients with single accessory pathway (AP) of the Kent bundle type. The location of AP was left free wall (LFW-AP) in 21 patients, left posteroseptal in 6, right free wall in 2, and right anteroseptal in 3. FFB either alone or in combination with functional left or right bundle branch block (LBBB or RBBB) occurred predominantly at the onset of OT and was initiated with ventricular extrastimulus technique more often than with atrial extrastimulation. In patients with LFW-AP, isolated functional left anterior fascicular block (LAFB) produced significant prolongation in VACT (15-35 ms). A similar magnitude of VACT increase (20-35 ms) was also observed when LAFB was associated with RBBB. Although 25-45-ms prolongation in VACT occurred with functional LBBB and normal axis, an additional 20-55-ms VACT increase was seen when LAFB accompanied LBBB. Functional LAFB, alone or in combination with bundle branch block, however, did not prolong VACT in patients with other AP locations. Furthermore, left posterior fascicular block did not produce prolongation of VACT in any of the cases. It is concluded that in patients with the Wolff-Parkinson-White syndrome, evaluation of VACT during functional LAFB provides important information regarding AP localization and a clear separation of LFW-AP from all other locations.

Effects of alternating cycle lengths on refractoriness of the His-Purkinje system.

The effects of alternating cycle lengths (bigeminal rhythm) on His-Purkinje system refractoriness were studied in 14 patients using His bundle and right bundle recordings. Programmed atrial stimulation at constant cycle length (method I) was scanned using the atrial extrastimulus technique (A2) and compared with an atrial cycle length of identical duration coupled to A2 on alternate beats (method II). The results showed that (a) despite shorter cycle length of the His-Purkinje system with method II due to effect of A2 on atrioventricular nodal conduction (699 +/- 90 vs. 743 +/- 87 ms, P less than 0.001), the relative refractory period of the His-Purkinje system was always longer with method II (463 +/- 52 vs. 440 +/- 43 ms, P less than 0.001). A similar increase also occurred in effective refractory period of the His-Purkinje system; (b) while functional right bundle branch block occurred in eight patients and functional left bundle branch block in two patients with method I, functional right bundle branch block occurred in all 14 patients and left bundle branch block in seven patients with method II; (c) in two patients where both functional right and left bundle branch block occurred with method I this never was manifest at identical degree of abbreviation of His-Purkinje system cycle length but was manifest at identical abbreviation in each of seven patients with method II; (d) site of conduction delay and/or block during functional right bundle branch block was always proximal, i.e., between the His bundle and right bundle recordings with both methods. During method II this resulted in shortening of the subsequent right bundle cycle length relative to the subsequent His bundle (and of necessity left bundle) cycle length. The finding of increased His-Purkinje system refractoriness despite shorter preceding cycle length of the His-Purkinje system during atrial bigeminy has never been previously described and suggests that classical concepts of His-Purkinje system behavior may require revision in this setting. Secondly, during atrial bigeminy the occurrence of alternating functional bundle branch block cannot be accounted for solely by the degree of abbreviation of His-Purkinje system cycle length, but may be explained by a relative shortening of the next ipsilateral bundle branch cycle length in the bundle manifesting block.

Electrophysiologic mechanisms of functional bundle branch block at onset of induced orthodromic tachycardia in the Wolff-Parkinson-White syndrome. Role of stimulation method.

The mechanisms of aberrant conduction at the onset of induced orthodromic tachycardia in the Wolff-Parkinson-White syndrome were analyzed in 20 consecutive patients in whom this tachycardia was initiated by the atrial (A2) and/or right ventricular (V2) extrastimulus techniques. Of 13 patients in whom orthodromic tachycardia was induced by the A2 method, functional right bundle branch block occurred at tachycardia onset in four (31%) and left bundle aberrancy in two (15%), one of whom also manifested right bundle aberrancy. The occurrence of bundle branch block at the onset of tachycardia was linked to aberrant conduction of the initiating A2 impulse which, in turn, was associated with attainment of relatively short His1His2 intervals within the tachycardia initiation zone. Aberrant conduction of A2 was also more common in patients without manifest preexcitation. In contrast, of 14 patients in whom orthodromic tachycardia was induced by the V2 method, left bundle aberrancy occurred at the onset of tachycardia in 11 (79%), one of whom manifested right bundle branch block as well. Left bundle aberrancy was more likely to occur when the interval from the initiating V2 (or macro-reentrant V3) impulse to the first anterograde His deflection was less than 300 ms. This suggests that left bundle aberrancy at the onset of orthodromic tachycardia induced by the V2 method results from concealed retrograde penetration of the His-Purkinje system, with the left bundle being last to recover. Our findings provide the conceptual basis for a physiologic approach to the deliberate induction of specific types of aberrant conduction at onset of orthodromic tachycardia in patients with Wolff-Parkinson-White syndrome.

Evaluation of new laboratory tests to discriminate bacterial from nonbacterial chronic obstructive pulmonary disease exacerbations.

INTRODUCTIONS: Discriminating bacterial from nonbacterial acute exacerbations of chronic obstructive pulmonary disease (AECOPD) is difficult, causing antibiotics overuse and bacterial resistance. Sputum cultures are of limited use because results take time. In our hospital, only leukocyte concentration and CRP are laboratory parameters evaluated in AECOPD. We evaluated additional tests to discriminate bacterial vs. nonbacterial AECOPD: 5-part leukocyte differentiation (hematology analyzer), leukocyte differentiation using flow cytometry (Leukoflow, Cytodiff), Leuko64 kit, and procalcitonin. METHODS: Retrospectively, patients were classified as bacterial or nonbacterial AECOPD. ROC analyses tested how the additional tests discriminate these groups. RESULTS: Twenty-two AECOPD were classified as bacterial and 23 as nonbacterial. From the additional tests, basophil percentage (Cytodiff) has superior AUC (0.800). At a cutoff resulting in ≥90% sensitivity, neutrophil/lymphocyte ratio (AUC:0.755) and CD4-positive T cells (Leukoflow, AUC:0.747) have the highest specificity (57%). Both neutrophil mean volume and standard deviation (Cell Population Data, DxH800 hematology analyzer) had good combined sensitivity and specificity (AUC:0.846/0.804, 91% sensitivity, 69% specificity). Addition of leukocyte populations and procalcitonin to CRP in regression models (AUC: 0.907/0.876/0.890) increased specificity compared to CRP alone (71% or 73% vs. 39%). CONCLUSION: No additional test has sufficient accuracy on its own to predict bacterial AECOPD. Combining CRP with several parameters from the additional tests may improve this.

Efficacy and safety of ibutilide fumarate for the conversion of atrial arrhythmias after cardiac surgery.

BACKGROUND: Atrial arrhythmias occur commonly after cardiac surgery and are a cause of significant morbidity and increased hospital costs, yet there is no well-studied treatment strategy to deal with them expeditiously. The purpose of this study was to determine the efficacy and safety of ibutilide fumarate, an approved drug for the rapid conversion of atrial fibrillation and flutter, in patients after cardiac surgery. METHODS AND RESULTS: Patients with atrial fibrillation or flutter occurring 1 to 7 days after surgery and lasting 1 hour to 3 days were randomized to receive two 10-minute blinded infusions of placebo or 0.25, 0.5, or 1.0 mg of ibutilide fumarate. Treatment was considered successful if sinus rhythm was restored for any period of time by hour 1.5. A total of 302 patients were randomized, 201 with fibrillation and 101 with flutter. Treatment with ibutilide resulted in significantly higher conversion rates than placebo, and efficacy was dose related (placebo 15%; ibutilide 0.25 mg 40%, 0.5 mg 47%, and 1.0 mg 57%). Conversion rates at all doses were higher for atrial flutter than for atrial fibrillation. Mean time to conversion decreased as the dose was increased. Polymorphic ventricular tachycardia was the most serious adverse effect and occurred in 1.8% of the ibutilide-treated patients compared with 1.2% of patients who received placebo. CONCLUSIONS: Ibutilide is a useful and safe treatment alternative for the atrial arrhythmias that occur after cardiac surgery.

Effect of amiodarone on conduction and refractoriness of the His-Purkinje system in the human heart.

Although the antiarrhythmic aspect of amiodarone has been extensively studied, its effects on His-Purkinje system conduction and refractoriness have not been systematically investigated in human beings. In 24 patients, anterograde His-Purkinje system conduction (HV intervals) and variables of His-Purkinje system refractoriness using the ventricular extrastimulus (V2) technique were analyzed before and after long-term therapy with amiodarone. The mean duration of amiodarone therapy at the time of repeat study was 16.2 +/- 7.7 weeks (range 11 to 42). The anterograde His-Purkinje system conduction time (HV interval) measured 49.6 +/- 9.5 ms (range 40 to 80) before and 60.6 +/- 10.7 ms (range 45 to 90) after amiodarone (p less than 0.005). During retrograde refractory period studies, the longest V1V2 interval at which a retrograde His bundle potential (H2) emerged from the V2 electrogram (relative refractory period of the His-Purkinje system) was consistently longer after amiodarone as compared with the control period (376.4 +/- 46.6 versus 318.8 +/- 33.1 ms, p less than 0.005). Similarly, the shortest and longest His-Purkinje system conduction times ( V2H2 interval) at comparable V1V2 intervals were uniformly and significantly prolonged after administration of the drug. Amiodarone also abolished macroreentry in the His-Purkinje system in six of the nine patients who showed such reentry during the control period. The effective refractory period of the ventricular myocardium was also increased from a mean of 227.1 +/- 13.9 to 259.2 +/- 20.2 ms (p less than 0.005) in this series of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of atrioventricular sequential pacing in patients with no ventriculoatrial conduction.

Candidates for the dual chamber "universal" (DDD) pacemaker are frequently tested for the presence of intact ventriculoatrial (VA) conduction to identify those at risk for developing endless loop tachycardia. However, recent reports have cited instances where clinical endless loop tachycardia has occurred even when no VA conduction could be demonstrated during ventricular pacing. A pacing protocol was designed to assess the effect of atrioventricular (AV) sequential pacing on VA conduction in 13 patients who showed no evidence of VA conduction during routine electrophysiologic testing. The absence of VA conduction was inferred by pacing the ventricle at several cycle lengths without obtaining a retrograde atrial capture. With the AV sequential method, which consisted of an AV sequential drive with a programmed AV interval of 100 to 160 ms, the presence or absence of VA conduction was tested utilizing a premature ventricular stimulus (V2) over a wide range of coupling intervals. During the AV sequential method, the V2 effectively propagated to the atria in 5 of 13 patients with V2A2 intervals ranging from 200 to 460 ms (mean 304 +/- 97). It is concluded that in patients showing absent VA conduction during routine testing, the ability of a paced ventricular impulse to propagate retrogradely can be demonstrated in a significant number of cases with AV sequential pacing. Although the exact mechanism could not be determined, it is postulated that as compared with ventricular pacing alone, a longer input into the AV node (first anterogradely during the AV sequential drive and then retrogradely with V2) may be partly responsible for the facilitative effect of the AV sequential method.

Functional characteristics of retrograde conduction in a pacing model of "endless loop tachycardia".

A pacing model was designed that stimulated "endless loop tachycardia," a complication found in the new generation of DDD (atrioventricular [AV] universal) pacemakers. The functional characteristics of the train of ventricular impulses simulating endless loop tachycardia were studied during both AV sequential pacing and basic ventricular drive. AV sequential pacing, by causing a decrease in ventriculoatrial (VA) conduction time of the first beat of the endless loop tachycardia, was associated with a decrease in the cycle length at which VA block occurred in 9 of 12 patients. The site of block was the His-Purkinje system in 4 of these 12 patients and the AV node in the remaining 8. At a cycle length with 1:1 VA conduction, a steady state VA conduction time was achieved in 2 to 4 beats (VA conduction time accommodation). The pattern of such accommodation depended on the site (His-Purkinje system versus AV node) of the maximal conduction delay. The steady state VA conduction time itself was altered with AV sequential pacing in patients showing His-Purkinje system delay, but not in patients with AV nodal delay. The results suggest that in most patients, the cycle length of VA block and the longest steady state VA conduction time will depend on the retrograde conduction time of the first beat of the tachycardia. In addition, pharmacologic measures to prevent or terminate endless loop tachycardia will have to take into account the fact that both the His-Purkinje system and the AV node can be the site of initial block.

Electrophysiologic mechanisms of orthodromic tachycardia initiation during ventricular pacing in the Wolff-Parkinson-White syndrome.

Orthodromic tachycardia is the most common arrhythmia in patients with Wolff-Parkinson-White syndrome. It is often initiated during incremental ventricular pacing that requires the onset of retrograde block along the normal pathway (that is, atrioventricular [AV] node-His-Purkinje system) with concomitant retrograde atrial activation by way of the accessory pathway. However, the site of retrograde block, that is, the AV node versus the His-Purkinje system, during incremental ventricular pacing and, hence, the mechanism of orthodromic tachycardia initiation have not been systematically elucidated. The mechanisms of orthodromic tachycardia induction were studied in 17 patients with Wolff-Parkinson-White syndrome using a specially designed pacing protocol. A beat by beat analysis indicated that the retrograde His-Purkinje system block was the most common initiating mechanism of orthodromic tachycardia in 14 of the 17 cases. In two cases, AV node block preceded the onset of orthodromic tachycardia, whereas the data in the remaining case suggested that both mechanisms were operative but at different pacing cycle lengths. The orthodromic tachycardia induction with His-Purkinje system block occurred within the first two cycles in most cases. When orthodromic tachycardia initiation was delayed beyond the first two cycles of the ventricular train it represented either a 2:1 block in the His-Purkinje system; a linking phenomenon in the His-Purkinje system; or a block in the AV node. These data have methodologic, mechanistic and therapeutic implications for patients with the Wolff-Parkinson-White syndrome.

Functional characteristics of human macro-reentry: a study of "pre-excited" circuits by extrastimulus method.

The effect of improved conduction in areas of delay was tested during macro-reentry within the His-Purkinje system, in an attempt to separate the role of conduction delay from that of prematurity of the extrastimulus as the key determinant of reentry. Using the right ventricular extrastimulus technique (S1S2 method), both the critical His-Purkinje system delays and the zone of S1S2 intervals causing His-Purkinje system reentry were determined. Then, using a previously described technique of atrioventricular (AV) sequential pacing during the basic drive, the potential site of His-Purkinje system conduction delay was (anterogradely) excited earlier (pre-excitation), as compared with the control S1S2 method. This produced a decrease in retrograde His-Purkinje system delay (S2H2), as compared with the same S1S2 interval during the control method. Changing the degree of pre-excitation at each S1S2 interval allowed for determination of the critical (or shortest) S2H2 delay necessary for His-Purkinje system reentry at each coupling interval. Of importance was the observation that the critical delay was not specific for each case but varied with the prematurity of S2. For example, the critical S2H2 delay required for reentry was actually less at shorter S1S2 intervals as compared with longer S1S2 intervals (from 206 +/- 25 to 187 +/- 20 ms, p less than 0.01). These data suggest that manifestation of reentry is a complex interplay between degree of prematurity and conduction delay. The so-called critical conduction delay can be readily modified by altering the site of block, which in turn may be dependent on prematurity of the extrastimulus.

Useful clinical criteria for the diagnosis of ventricular tachycardia.

Misdiagnosis occurs upon initial presentation to medical attention in a considerable number of patients referred for evaluation of wide QRS tachycardia. In order to improve diagnostic accuracy (ventricular versus supraventricular tachycardia), the answers to two key bedside questions were prospectively evaluated: (1) Had the patient experienced a prior myocardial infarction? (2) Did symptoms of tachyarrhythmia start only after the infarction? A patient presenting with a wide QRS tachycardia was considered to have ventricular tachycardia if he or she answered in the affirmative to both of these questions. Of 31 consecutive patients referred with electrocardiographically documented sustained wide QRS tachycardia that was reproduced in the electrophysiology laboratory, the diagnoses made when the patients first presented to medical attention were ventricular tachycardias in 17 patients and supraventricular tachycardias in 14 patients. Following electrophysiologic evaluation, 29 were diagnosed as having ventricular tachycardia and two as supraventricular tachycardia. If the diagnoses were made solely on the basis of responses to the bedside questions mentioned earlier, 28 of the 29 patients having a final diagnosis of ventricular tachycardia would have been correctly identified. It is concluded that the use of these two questions can be very helpful in improving the clinical diagnosis of ventricular tachycardia.

Patterns of human atrioventricular nodal accommodation to a sudden acceleration of atrial rate.

Atrioventricular nodal (AVN) accommodation to an abrupt increase in atrial rate was systematically studied in 10 patients using a pacing protocol incorporating a programmable pause (S1S2) between the last beat of basic atrial drive (S1S1) and the onset of an 18-beat paced atrial train (S2S2) of shorter constant cycle length (CL) than that of S1S1. Pacing was repeated, varying S1S2 while keeping S1S1 and S2S2 CLs fixed. In all patients there existed a zone of 1 or more critical S1S2 intervals for which the new steady-state AVN conduction time (S2H2) was attained "instantaneously," that is, with the first beat, and maintained for subsequent beats of the S2S2 train. At S1S2 intervals that exceeded or were less than critical values, S2H2 progressively increased (crescendo pattern) or decreased (decrescendo pattern), respectively, until the steady-state value was achieved. The zone of S1S2 intervals that resulted in decrescendo or instantaneous AVN accommodation contracted when either the S1S1 CL was increased or the S2S2 CL was shortened. These findings have relevance to the interpretation of electrophysiologic studies and explain the spectrum of AVN accommodation patterns observed at the onset of supraventricular tachycardia.

Facilitation of ventricular tachycardia induction with abrupt changes in ventricular cycle length.

The effect of abrupt short-to-long changes in cycle length (CL) on the postulated reentrant circuit of ventricular tachycardia (VT) was evaluated. This was performed using single and double ventricular extrastimuli in a group of 21 patients clinically suspected of having VT in whom VT could not be induced at comparable or shorter constant CLs. A second group of 10 patients without suspected VT was similarly studied. Compared with constant CLs of equal or shorter duration preceding the single or double ventricular extrastimuli, abrupt short-to-long CL changes resulted in (1) initiation of sustained VT in 13 of 21 patients in whom VT could not be induced at constant CLs despite the use of shorter S1S3 by 66 +/- 17 ms; (2) increased incidence of initiation of sustained VT after the V3 phenomenon resulting from macroreentry within the His-Purkinje system (Re-HPS); (3) a small but higher incidence of sustained VT due to sustained Re-HPS; and (4) no induction of sustained or nonsustained VT with either method in the second group of patients. These results provide additional support for reentry as the basis for sustained ventricular tachyarrhythmias. Abrupt short-to-long CL changes may be effective for initiating sustained VT in patients at risk for these arrhythmias.

Incidence and clinical significance of ventricular fibrillation induced with single and double ventricular extrastimuli.

Of 718 patients evaluated for suspected or documented ventricular tachyarrhythmias, ventricular fibrillation (VF) was induced in 28 (incidence 3.9%) by single and double extrastimuli. Nine of the 28 patients had suspected but no clinically documented ventricular tachycardia (VT) or VF (group 1), 11 had documented VT (group 2) and 8 had out of hospital VF (group 3). In group 1, electropharmacologic control was achieved in 8 patients with the initial agent tested; however, symptoms recurred in 6 patients. In 4 patients the drug was discontinued. After a follow-up of 26 +/- 11 months in group 1, no patient had died. In only 2 of 19 patients in groups 2 and 3 were arrhythmias controlled with the initial agent; 15 patients had VT and 2 VF. Control with class I agents was achieved in 9 of 19 patients and none died until the drug regimen was changed empirically in 3 of these 9. Ten patients, all from groups 2 and 3, were treated empirically with amiodarone; 3 died. All patients died either suddenly or in VT. The mortality rate in groups 2 and 3 after a mean follow-up of 24 +/- 9 months was 32% (p less than 0.05). Continued symptoms and no deaths in group 1 suggests a nonclinical nature of induced VF. Control of induced VF on serial drug testing in group 2 and 3 also indicates a false-negative drug efficacy response, as pharmacologic control of emergent VT on subsequent studies appeared essential to their survival despite control of induced VF. Thus, even with single or double premature stimuli, induction of VF can be a nonclinical response, especially in patients without clinical VF.

Value of preexisting bundle branch block in the electrocardiographic differentiation of supraventricular from ventricular origin of wide QRS tachycardia.

The relation between the morphologic configuration of QRS complexes during wide QRS tachycardia induced during electrophysiologic studies and sinus rhythm was examined in 18 patients who had preexisting left or right bundle branch block. Representative QRS complexes during sinus rhythm and during tachycardia were isolated from each patient and juxtaposed for comparison. The QRS complexes that constituted each pair were judged by 4 observers as being identical, different or, if the decision was equivocal, similar. Nine patients had supraventricular tachycardia (SVT). In 8 of the 9 patients, all 4 observers found the QRS complexes during sinus rhythm and SVT identical in morphologic configuration. In the other patient, 2 observers found the QRS complexes identical and 2 found them similar. In 12 patients ventricular tachycardia (VT) was induced. In 11 of these 12, all 4 observers found the QRS complexes during VT different from their respective sinus beats. In the other patient, 3 observers found the QRS complexes different, whereas the fourth found them similar. During SVT, the QRS duration was unchanged from the corresponding value during sinus rhythm, whereas in patients with VT, QRS width increased by a mean of 56 +/- 20 ms (p less than 0.001). The results of our study suggest that the electrocardiographic differentiation of wide QRS tachycardia in patients with preexisting bundle branch block can be accomplished easily and accurately by comparing the QRS complexes during tachycardia with those during sinus rhythm: If the complexes are identical, the tachycardia is supraventricular, but if they are different, the arrhythmia is ventricular in origin.

Normal electrophysiologic responses of the human heart.

A thorough understanding of physiologic behavior of the human conduction system is essential to define the abnormalities. This article deals with normal responses of the cardiac conduction system to both antegrade and retrograde direction. Responses to electrical as well as mechanical stimulation are discussed.