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C D Gottlieb

Publications and source records attributed to C D Gottlieb.

53 records · Page 3Linked to original sources
PubMed1995

Benefits and lessons learned from stored electrogram information in implantable defibrillators.

Implantable defibrillators have evolved from simple event counters to sophisticated diagnostic monitoring units capable of storing electrocardiographic information surrounding arrhythmia events and device therapy. In this review, the nature and characteristics of these stored electrocardiographic recordings are discussed and examples displayed. Potential benefits and limitation of stored electrogram analysis are described with respect to both clinical utility and the ability to enhance our understanding of ventricular arrhythmogenesis. Finally, future developments to improve data storage, retrieval, and analysis are identified.

Defibrillators, Implantable↗
PubMed1995

Postshock sensing performance in transvenous defibrillation lead systems: analysis of detection and redetection of ventricular fibrillation.

INTRODUCTION: The sensing performance of transvenous lead systems may be adversely affected by the delivery of high-energy shocks. This may be due to the proximity of the sensing and energy-delivery electrodes on transvenous leads. METHODS AND RESULTS: The time required for detection of ventricular fibrillation and redetection after a failed first shock was compared in 93 patients with five different lead system-pulse generator combinations: Cadence--Endotak 60 series, Ventak P--Endotak 60 series, Jewel--Transvene, Cadence--TVL, and Cadence--Transvene. A total of 418 successful and 204 failed first shocks were delivered during induced ventricular fibrillation. Redetection times (RED) were consistently shorter than detection times (DET) in the Jewel-Transvene (RED minus DET: -1.9 +/- 0.8 sec, P < 0.0001), the Cadence-TVL (-1.6 +/- 1.0 sec, P < 0.0001), and the Cadence-Transvene combinations (-2.0 +/- 0.9 sec, P < 0.0004). Redetection times were not significantly different than detection times in the Cadence-Endotak combination (0.9 +/- 3.1 sec; P = 0.09). Redetection times were significantly longer than detection times in the Ventak-Endotak combination (1.2 +/- 2.3 sec; P = 0.034). Prolonged individual redetection episodes (> 8.2 sec) were observed in the Cadence-Endotak (7 [10%] of 73 episodes) and the Ventak-Endotak (4 [10%] of 39 episodes), but not in the Jewel-Transvene, the Cadence-TVL, and the Cadence-Transvene combinations. CONCLUSIONS: Redetection of ventricular fibrillation may be delayed in some transvenous lead-pulse generator combinations. Successful redetection of ventricular fibrillation following a failed first shock should be demonstrated prior to hospital discharge of patients with implantable defibrillators.

Adolescent↗
PubMed1995

Insights into the electrophysiology of atrial arrhythmias gained by the catheter ablation experience: "learning while burning, Part II".

Although the development and wide-scale application of catheter ablative techniques has drastically changed the practice of electrophysiology, catheter ablation does not preclude physiologic investigation. On the contrary, given the precise and directed nature of this technique and the increased attention to detailed cardiac mapping that it requires, catheter ablation may be viewed as a tool to provide unique information about arrhythmia substrates. In this article, the insights provided by the catheter ablation experience into the pathophysiology of the focal atrial arrhythmias, atrial tachycardia, sinus node reentrant tachycardia, and inappropriate sinus tachycardia will be reviewed. Atrial arrhythmias were initially difficult to treat with ablative therapy, particularly because they can occur anywhere within the atria and the experience with mapping for surgical ablation was quite limited. A number of novel approaches to atrial mapping have been developed in response to this challenge, and presently, catheter ablation provides effective therapy for the majority of patients with focal atrial arrhythmias. In addition, deliberate attempts at "learning while burning" have already begun to enhance our understanding of the interaction of the structural and electrophysiologic aspects of the substrate for atrial arrhythmias.

Arrhythmias, Cardiac↗
PubMed1994

Insights into the electrophysiology of ventricular tachycardia gained by the catheter ablation experience: "learning while burning".

The success of catheter ablation has significantly improved the treatment of patients with cardiac arrhythmias and has established electrophysiology as an increasingly interventional subspecialty. Some members of the electrophysiology community have expressed concern that this success has been purchased at the cost of undermining what had been our primary concern: understanding the anatomic and physiologic basis of arrhythmia syndromes. In many laboratories, endpoints such as case load and primary success have eclipsed physiologic investigation. Despite these trends, however, catheter ablation is not inherently at odds with investigation and education. On the contrary, because the lesions delivered with current techniques are much more discrete than the effects of antiarrhythmic agents or surgical ablation, catheter ablation can be used as a research tool directed toward a more precise understanding of arrhythmia substrates. Conscious attempts at "learning while burning" have already provided important and unique information about arrhythmia pathogenesis.

Cardiomyopathy, Dilated↗
PubMed1993

ICD data storage: value in arrhythmia management.

Sophisticated diagnostic information is provided by the latest generation of implantable defibrillators. The success of therapy and the type of therapy successful in terminating ventricular arrhythmias is provided by interrogating the ICD device. In addition, R to R interval information can be retrieved. In selected devices, either local bipolar electrograms from the rate sensing leads or wide bipolar electrograms from the energy delivering leads provide visual confirmation of the presence of ventricular tachyarrthythmic events leading to therapy. The value and limitations of this sophisticated diagnostic information in providing insight into the electrical events triggering therapy and the events triggering ventricular arrhythmias are discussed.

Arrhythmias, Cardiac↗
PubMed1992

Late potentials in an ovine model of acute transmural myocardial infarction.

The development of slow conduction during the first hours of acute transmural myocardial infarction (ATMI) was studied by signal-averaged electrocardiograms (SAE) in 19 adult anesthetized sheep. SAEs were recorded before and after intravenous infusions of lidocaine and bretylium were begun and 10, 30, and 60 min after ATMI produced by ligation of the left anterior descending and second diagonal coronary arteries. Four sheep died promptly of ventricular tachyarrhythmias; two others developed sustained ventricular arrhythmias, which precluded additional data. Biphasic changes in QRS duration, root mean square voltage of the terminal 40 ms of the QRS complex, and duration of terminal low-amplitude (less than 30 microV) signal were observed. Peak changes in conduction occurred 30 min after infarction and regressed toward baseline thereafter. At 30 min, all animals developed late potentials, which were defined as signals that exceeded both after-drug QRS duration and duration of terminal low-amplitude signal less than 30 microV by more than two standard deviations. At 60 min, only 3 of 13 (23%) animals had late potentials. Conduction is slowest 30 min after ATMI in sheep but may not be related to development of ventricular arrhythmias. In five of six sheep (83%), ventricular arrhythmias occurred within 15 min of infarction before peak slowing was observed by SAE.

Animals↗
PubMed1991

Usefulness of the delta HA interval to accurately distinguish atrioventricular nodal reentry from orthodromic septal bypass tract tachycardias.

Surface electrocardiographic criteria may be inadequate to distinguish some cases of atrioventricular (AV) nodal reentrant supraventricular tachycardia (SVT) from those with orthodromic SVT incorporating a posterior septal bypass tract (orthodromic SVT) because of similarities in P-wave morphology and timing during SVT. Invasive electrophysiologic studies may occasionally leave uncertainty in the correct diagnosis, using currently accepted criteria. A new criterion for distinguishing these 2 forms of SVT was therefore devised and tested based on differences in the sequence of activation of the His bundle and atrium during SVT and ventricular pacing. Eighty-four patients underwent invasive electrophysiologic studies (60 with proved AV nodal SVT, 24 with proved orthodromic SVT), during which His to atrial (HA) intervals were measured during SVT as well as ventricular pacing at the same rate. The newly devised criterion, the delta HA interval (HApace-HAsvt) was found to accurately distinguish AV nodal SVT (delta HA greater than 0 ms) from orthodromic SVT (delta HA less than -27 ms). An intermediate value of delta HA = -10 ms was chosen which had a 100% sensitivity, specificity and predictive accuracy in differentiating the 2 forms of SVT. A clear retrograde His potential during ventricular pacing, which is essential for application of this criterion, was present in 78 of 84 (93%) cases. In summary, patients with delta HA intervals greater than -10 ms separate AV nodal reentry from orthodromic SVT incorporating a septal bypass tract, and no overlap exists between the 2 groups. This criterion may be useful in differentiating the mechanism of SVT in cases in which distinction is not possible by other methods.

Adolescent↗
PubMed1990

A quantitative evaluation of refractoriness within a reentrant circuit during ventricular tachycardia. Relation to termination.

Programmed ventricular stimuli introduced during sustained monomorphic ventricular tachycardia frequently reset the tachycardia, resulting in a less than fully compensatory pause. A resetting response curve is generated when the set of return cycles is evaluated as the function of the coupling intervals of the extrastimuli delivered during the ventricular tachycardia. If the stimulated wave front encounters tissue within the tachycardia circuit that is not fully recovered, interval-dependent conduction changes should occur producing an increasing resetting response pattern. We quantified the magnitude of this interval-dependent conduction slowing in 17 morphologically distinct ventricular tachycardias. The slope of the increasing limb of the resetting response curve was determined by linear regression analysis and ranged from -0.30 to -1.14 (mean +/- SD, 0.70 +/- 0.25). Seven of the 17 ventricular tachycardias (41%) terminated during introduction of ventricular extrastimuli. The slope of the resetting response pattern in those ventricular tachycardias that terminated were significantly steeper than in those that did not terminate (-0.85 +/- 0.15 versus -0.61 +/- 0.21, respectively, p = 0.025). Six of the seven ventricular tachycardias terminated with programmed ventricular stimuli had a slope steeper than -0.75, whereas only one of 10 ventricular tachycardias that did not terminate exceeded this value. In conclusion, the slope of the increasing portion of the resetting response curve correlates with ability to terminate uniform sustained ventricular tachycardia by timed extrastimuli. This slope is the quantification of the magnitude of interval-dependent conduction slowing. Additionally, tissue within the reentrant circuit displaying greater degrees of interval-dependent conduction slowing may also have relatively longer effective refractory periods.

Cardiac Pacing, Artificial↗
PubMed1989

Procainamide-induced slowing of ventricular tachycardia with insights from analysis of resetting response patterns.

To investigate the mechanism of slowing of the rate of ventricular tachycardias (VTs) by procainamide, resetting response patterns were characterized in 24 VTs in 22 patients. All patients had coronary artery disease and inducible sustained VT during procainamide therapy. Only tachycardias with the same surface QRS morphology before and after procainamide were studied: all were slowed by procainamide. The mean cycle length was 292 +/- 61 ms before and 374 +/- 61 ms after procainamide (p less than 0.05). The mean effective refractory period, measured at the right ventricle, was 241 +/- 21 ms before and 261 +/- 24 ms after procainamide (p less than 0.05). During procainamide therapy, single and double extrastimuli were delivered during VT and resetting response patterns identified. Patterns were characterized as flat, increasing or flat plus increasing. Resetting was seen in 17 (71%) of these VTs and resetting response patterns were identified in 16 (94%) of these. The resetting response pattern was flat in 7, flat plus increasing in 5 and increasing in 4. The finding of some flat portion at the end of resetting response patterns in 12 VTs after procainamide indicates that the reentrant impulse conducts through fully recovered tissue within the circuit. It suggests that procainamide slowed these VTs by slowing conduction velocity in fully recovered tissue due to sodium channel blockade and not by prolongation of action potentials and refractory periods.

Cardiac Pacing, Artificial↗
PubMed1988

Relation of the intraoperative defibrillation threshold to successful postoperative defibrillation with an automatic implantable cardioverter defibrillator.

To determine the relation between the intraoperative defibrillation threshold and successful postoperative termination of induced ventricular fibrillation (VF) with the automatic implantable cardioverter defibrillator (AICD), 33 patients who underwent AICD implantation were studied. The defibrillation threshold, determined after at least 10 seconds of VF, was 5 J in 2, 10 J in 6, 15 J in 10, 20 J in 10 and 25 J in 5 patients. The AICD energy rating on the first discharge was 28 +/- 1.8 J. Defibrillation of induced VF was demonstrated postoperatively in 29 of 33 (88%) patients. The AICD terminated VF postoperatively in all 18 patients with a defibrillation threshold less than or equal to 15 J. Only 11 of the 15 (73%) patients with a defibrillation threshold greater than or equal to 20 J (p less than 0.04) had VF terminated postoperatively. In all 4 patients in whom the AICD failed to terminate induced VF, the energy difference between the AICD rating and the defibrillation threshold was less than or equal to 10 J. Among the 14 patients with a difference of less than or equal to 10 J between the AICD energy rating and the defibrillation threshold, there were no significant differences between the 4 patients with and the 10 without successful VF termination with respect to the duration of VF induced postoperatively or the AICD lead system. In summary, failure to terminate VF with the AICD is not uncommon (27%) when the defibrillation threshold approaches the energy delivering capacity of the AICD.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Coupling intervals of ventricular extrastimuli causing resetting of sustained ventricular tachycardia secondary to coronary artery disease: relation to subsequent termination.

Single and double ventricular extrastimuli (VE) delivered during sustained, uniform ventricular tachycardia (VT) are able to reset or terminate the tachycardia. The relation between the coupling intervals of single and double VE resetting VT and those terminating it was examined in 80 uniform, morphologically distinct VT occurring in 52 patients. Of the 80 tachycardias receiving single VE, 41 were reset and 8 terminated. The corrected coupling interval of single VE first causing resetting was 0.81 +/- 0.08 compared with 0.66 +/- 0.06 for termination (p less than 0.001). Forty-two tachycardias received double VE with 33 being reset and 13 terminating. The corrected coupling interval of double VE at which resetting was first seen was 0.86 +/- 0.08 compared with 0.73 +/- 0.05 for termination (p less than 0.001). If the longest corrected coupling interval causing resetting was greater than or equal to 0.75, then 7 of 34 tachycardias terminated with single VE and 13 of 31 terminated with double VE compared with only 1 of 46 terminating with single VE and 0 of 10 with double VE if resetting was not observed by a corrected coupling interval of 0.75 (p less than 0.01 and p less than 0.02, respectively). If the longest corrected coupling interval at which resetting occurred was greater than or equal to 0.75, the predictive value for VT termination was 21% with single VE and 42% with double VE compared with only 2% with single VE and none with double VE if resetting was not observed by this corrected coupling interval.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗
PubMed1988

Entrainment of ventricular tachycardia: explanation for surface electrocardiographic phenomena by analysis of electrograms recorded within the tachycardia circuit.

Transient entrainment was demonstrated during 59 pacing events in 18 episodes of sustained uniform ventricular tachycardia (VT) while recording electrograms from the site of origin of tachycardia (LE-SOO). During entrainment, the morphology of the initial component of the LE-SOO was identical to the morphology observed during the tachycardia in 13 VTs (group I), but in five VTs (group II), the initial component changed at a "critical" paced cycle length. The presence of the proposed surface electrocardiographic criteria for entrainment--fixed fusion and a first postpacing complex without fusion but occurring at the paced cycle length--were integrally dependent on the morphologic changes in the local presystolic electrogram. Fixed fusion of the surface electrocardiogram at one or more paced cycle lengths was detected during entrainment at 35 of 59 paced cycle lengths in 12 of 18 tachycardias, 10 of which were group I and two of which were group II VTs. Fixed fusion demonstrated by analysis of the LE-SOO was observed at one or more pacing cycle lengths in 17 of 18 VTs. In five tachycardias in which surface electrocardiographic fusion was not observed, fixed fusion was evident on analysis of the left ventricular LE-SOO during right ventricular pacing. The first postpacing interval, as measured at the surface electrocardiogram, was consistently equal to the paced cycle length in only one of 18 tachycardias and was greater than the VT cycle length in eight of 17 tachycardias. A pathway with a long conduction time was demonstrated during entrainment. However, in those 12 VTs in patients in whom pacing was performed at more than one cycle length and there was preservation of the LE-SOO morphology, the conduction time between the stimulus and presystolic electrogram remained constant. Thus, no evidence for "atrioventricular nodal-like" decremental conduction was observed over a wide range of pacing cycle lengths. We conclude that: (1) two of the previously proposed criteria for diagnosis of entrainment (fixed fusion on the surface electrocardiogram and a first postpacing interval equal to the paced cycle length) are overly restrictive criteria for definition of "entrainment" of VT, (2) analysis of endocardial recordings from the site of origin of tachycardia during attempted entrainment of VT is useful for documenting the presence of entrainment, and (3) such analysis provides a basis for the understanding of surface electrocardiographic phenomenon associated with entrainment.

Cardiac Pacing, Artificial↗
PubMed1988

Resetting of ventricular tachycardia with electrocardiographic fusion: incidence and significance.

The incidence and significance of fusion of the QRS complex during resetting of sustained ventricular tachycardias (VTs) was determined in 53 VTs induced by programmed stimulation in 46 patients with prior myocardial infarction. All 53 VTs were reset with one or two extrastimuli delivered at the right ventricular apex (RVA); 29 (54.7%) demonstrated fusion of the VT QRS complex coincident with the extrastimulus resetting the VT. Activation time at the RVA during VT (measured from the onset of the VT QRS complex to the first rapid deflection of the RVA electrogram) was longer in VT reset with fusion compared with those without fusion (91 +/- 30 vs 33 +/- 32 msec; p less than .001). A right bundle branch block VT QRS morphology and a rightward and inferior axis were more common in VT reset with electrocardiographic (ECG) fusion. Additionally, the shortest return cycle following the extrastimulus resetting the VT was shorter in VT reset with ECG fusion compared with those without (327 +/- 66 vs 423 +/- 84 msec; p less than .001). Fusion of the endocardial electrogram recorded at the site of VT origin was noted in 11 of 15 VTs that were reset while a recording catheter was positioned at this site, including all eight VTs with evidence of surface ECG fusion and three of seven VTs without fusion. Seventeen VTs were reset from the right ventricular outflow tract as well as the RVA; eight demonstrated QRS fusion at both sites, five from the right ventricular outflow tract only, and four from neither site.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗
PubMed1988

Comparison of individual and combined effects of procainamide and amiodarone in patients with sustained ventricular tachyarrhythmias.

To compare the individual and combined electrophysiological effects of amiodarone and procainamide, 35 patients with sustained ventricular arrhythmias underwent programmed stimulation in the control state, after procainamide (mean concentration, 8.7 +/- 2.8 micrograms/ml), after 13 +/- 2 days of amiodarone (1,400 mg/day x 7 days, then 400 mg/day), and after amiodarone with procainamide (mean procainamide concentration, 7.8 +/- 2.2 micrograms/ml). Sustained ventricular tachycardia (VT) was inducible in all 35 patients during treatment with procainamide alone and with amiodarone alone. Procainamide and amiodarone similarly increased the VT cycle length (+68 vs. +61 msec), the corrected QT interval (+63 vs. +49 msec), and the ventricular effective refractory period measured at paced cycle lengths of 600-550 msec (+23 vs. +21 msec) and 400 msec (+25 vs. +23 msec). Procainamide had a more pronounced effect on QRS duration than amiodarone during sinus rhythm (+18 vs. +8 msec, p less than 0.01) and during paced cycle lengths of 600-550 msec (+32 vs. +23 msec, p less than 0.01) and 400 msec (+37 vs. +28 msec, p less than 0.1) but a similar effect on the QRS duration during VT (+32 vs. +29 msec). During combination therapy, VT initiation was prevented in only two (6%) patients. The combination therapy produced a greater increase (p less than 0.001) than individual therapy in all the electrophysiological intervals assessed, with the exception of the sinus cycle length. On each drug regimen, a cycle length-dependent increase (p less than 0.05) in paced QRS duration was noted (400 more than 600-550 msec).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗