Biomedical subjects

M E Rosenthal

Publications and source records attributed to M E Rosenthal.

13 recordsLinked to original sources

PubMed1992

Results of electrophysiological testing and long-term follow-up in patients sustaining cardiac arrest only while receiving type IA antiarrhythmic agents.

UNLABELLED: Therapeutic management of patients sustaining a cardiac arrest while receiving antiarrhythmic agents can be difficult since the role of the drug in possibly facilitating the arrhythmia is often difficult to define. To determine if the response to programmed stimulation could give insight into which patients may have experienced a drug-induced cardiac arrest, we studied 29 patients (61 +/- 9 years) with no prior history of sustained ventricular tachyarrhythmias (VT) who suffered a cardiac arrest only while receiving type Ia antiarrhythmic agents. Patients with documented myocardial infarction, acute ischemia, electrolyte abnormalities, or torsade de pointes were excluded from the study. Twenty-four patients had coronary artery disease with prior myocardial infarction (ejection fraction 28% +/- 9%) and five patients had idiopathic dilated cardiomyopathy (ejection fraction 31% +/- 6%). During baseline electrophysiological testing, 19 patients (66%) had inducible sustained ventricular arrhythmias: uniform VT, n = 14 (group I), polymorphic VT or ventricular fibrillation, n = 5 (group II). Ten patients (group III) had no inducible sustained ventricular arrhythmias. To determine if rechallenge with a type Ia agent could facilitate induction of a sustained ventricular arrhythmia in group III, eight patients underwent ten electrophysiological studies during therapy with either procainamide or quinidine. Only two patients developed sustained VT in response to programmed stimulation. Patients in groups I and II received therapy guided by electrophysiological testing, including antiarrhythmic agents alone (n = 8), subendocardial resection (n = 4), or an implantable cardioverter defibrillator (n = 7). Patients in group III received antiarrhythmic agents empirically (n = 3), or for treatment of atrial tachyarrhythmias (n = 2) or nonsustained VT (n = 1). In addition, four patients in group III received an implantable cardioverter defibrillator. During a mean follow-up of 28 +/- 27 months (range: 1 day-84 months) 13 patients died suddenly or received a defibrillator shock preceded by syncope or presyncope: group I: n = 5; group II: n = 2; group III: n = 6. IN CONCLUSION: (1) most patients sustaining a cardiac arrest only in the presence of type Ia antiarrhythmic agents have inducible sustained VT in the absence of antiarrhythmic agents, and (2) the risk of recurrent VT persists in patients without inducible sustained arrhythmias in the drug-free state, regardless of whether they manifest inducible arrhythmias after rechallenge with a type Ia agent.

Aged↗

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↗

PubMed1991

Usefulness of the electrophysiology laboratory for evaluation of proarrhythmic drug response in coronary artery disease.

Two potential manifestations of proarrhythmic responses to type IA antiarrhythmic agents in the electrophysiology laboratory were evaluated in 122 patients with chronic coronary artery disease and previous myocardial infarction: (1) conversion of uniform nonsustained ventricular tachycardia (VT) into sustained VT after drug administration, and (2) induction of sustained VT by fewer extrastimuli after drug administration. Forty-two patients were evaluated for nonsustained VT. Eighty patients were evaluated for sustained VT: 30 of these had spontaneous sustained VT only while receiving empiric therapy with quinidine or procainamide, whereas the remaining 50 developed spontaneous VT in the absence of antiarrhythmic drugs. All patients underwent programmed stimulation in the baseline state and after procainamide. Four patients had conversion of induced uniform nonsustained VT into the same morphology, but sustained VT after procainamide administration. These responses only occurred in patients evaluated for nonsustained VT. Over 90% of patients presenting with sustained VT had uniform sustained VT induced at the baseline study and after procainamide, regardless of whether the spontaneous arrhythmia occurred only in the presence or absence of antiarrhythmic drugs. There was no significant difference in the change in mode of induction from baseline to procainamide study, regardless of whether patients had developed spontaneous VT only in the presence or absence of antiarrhythmic drugs. One patient with no inducible VT at the baseline study had inducible uniform sustained VT after procainamide administration, and 1 patient with inducible VT at baseline developed spontaneous sustained uniform VT after procainamide administration. Both patients had developed spontaneous sustained VT only while receiving therapy with type IA agents.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Complexes, Premature↗

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↗

PubMed1990

Current status of antitachycardia devices.

With the limitations of currently available modalities for treating clinically important tachycardias, the role of implanted antitachycardia devices will continue to expand. The challenge of the future will not only involve continued technological advances but the socioeconomic impact of this efficacious but expensive mode of therapy in an era of increasing financial restraints. Further studies to definitively prove the efficacy of more widespread use of antitachycardia device therapy will be needed.

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↗

PubMed1989

Sinus mapping in patients with cardiac arrest and coronary disease--results and correlation with outcome.

Electrophysiological testing and left ventricular endocardial mapping in sinus rhythm were performed in 61 patients with coronary artery disease who presented with cardiac arrest in an attempt to relate the results of these studies to clinical outcome. Forty-one patients (67%) had inducible sustained arrhythmias (18 uniform ventricular tachycardia, 23 polymorphic ventricular tachycardia/ventricular fibrillation) and 20 had no inducible arrhythmia. Patients with inducible arrhythmia had 45% abnormal and 6% fractionated electrograms versus 31% and 0% for those without inducible arrhythmia (P greater than 0.05 for both comparisons). Sixteen of 59 patients (27%) with adequate follow-up had arrhythmia recurrence (11/39 [31%] with inducible arrhythmia and 5/20 [25%] without inducible arrhythmia) over a mean follow-up period of 27 months. Of five patients without inducible arrhythmia who experienced recurrence, two did so despite the anti-ischemic therapy. In the 20 patients without inducible arrhythmia, the 15 who remained arrhythmia-free had a mean of 78 +/- 22% normal sites versus 46 +/- 24% normal sites in those with recurrence (P greater than 0.05). We conclude that in patients with coronary artery disease and cardiac arrest: 1) patients without inducible arrhythmia have less marked endocardial electrical abnormality than those with inducible arrhythmia, 2) those patients who have marked endocardial abnormality despite the lack of inducible arrhythmia are at risk for clinical recurrence which suggests that these abnormalities may represent an anatomic substrate for arrhythmia which cannot be identified by programmed stimulation. These patients are candidates for AICD implantation and 3) patients with relatively normal endocardial electrograms do well with anti-ischemic therapy alone.

Aged↗

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

Automatic implantable defibrillator discharge resulting from routine pacemaker programming.

A middle-aged gentleman with an idiopathic dilated cardiomyopathy, drug-refractory sustained ventricular arrhythmia, and high-degree AV block was managed with an automatic implantable cardioverter-defibrillator (AICD) and a Cordis Multicor II VVI pacemaker. During a routine follow-up visit, the pacemaker threshold was determined. Seven seconds after reprogramming the Cordis pacemaker to the "stat" VVI mode, the AICD discharged. The time to discharge after reprogramming the pacemaker equalled the previously determined AICD charge time. No other rhythm disturbance was documented and the rate with double counting of pacemaker stimulus and QRS complex was less than the triggering rate for the AICD. In conclusion, the AICD can be triggered by pacemaker programming signals unrelated to subsequent pacemaker function.

Electric Countershock↗

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↗

PubMed1986

Wide QRS tachycardia due to AV nodal reentry and a "bystander" bypass tract with slow conduction properties.

An unusual mechanism for recurrent, wide QRS complex supraventricular tachycardia is described in this report. A 25-year-old man with normal PR and QRS intervals during sinus rhythm was shown to have preexcitation with a left bundle branch block pattern during tachycardia and during atrial pacing. Electrophysiologic studies demonstrated slow and decremental conduction properties in an accessory "bystander" AV pathway utilized for antegrade conduction during AV nodal reciprocating tachycardia. The differential diagnosis of this tachycardia is discussed in detail.

Adult↗