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Biomedical subjects

M E Josephson

Publications and source records attributed to M E Josephson.

At least 127 records · Page 7Linked to original sources

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↗

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↗

Relationship between the 12-lead electrocardiogram during ventricular tachycardia and endocardial site of origin in patients with coronary artery disease.

Previous studies in patients with sustained ventricular tachycardia (VT) have demonstrated the efficacy of surgical and catheter-mediated ablative procedures based on activation mapping during VT. Since extensive preoperative or intraoperative mapping may be impractical due to time constraints or patient intolerance, we sought to define characteristics of the 12-lead electrocardiogram (ECG) during VT that could suggest a particular endocardial region of origin and thus facilitate mapping studies. Endocardial mapping was performed during 182 VTs in 108 patients with prior myocardial infarction of either the anterior or inferior wall. Endocardial sites of origin (sites from which greater than or equal to 40 msec of presystolic electrical activity was consistently recorded) were identified with use of catheter (154 VTs) or intraoperative (85 VTs) activation mapping (both methods used in 57 Vts). Twelve-lead ECGs obtained during these VTs were characterized by four features: location of infarction, bundle branch block type configuration, quadrant of QRS axis, and precordial R wave progression pattern. A specific combination of these four features was associated with a particular endocardial region containing the mapped site of origin in 87 VTs (48% of total). An association (greater than or equal to 70% positive predictive accuracy) was more likely to be found in the presence of left, as opposed to right, bundle branch block type patterns (53/73 [73%] vs 34/109 [31%]; p less than .001) and in the presence of VT related to inferior, as opposed to anterior, infarction (40/54 [74%] vs 47/128 [37%]; p less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Effects of lidocaine and procainamide on normal and abnormal intraventricular electrograms during sinus rhythm.

The effect of lidocaine (n = 6) and procainamide (n = 12) on electrogram characteristics from electrically normal right ventricular and electrically abnormal left ventricular endocardial sites was determined in 18 patients with prior myocardial infarction. Bipolar electrograms were recorded during sinus rhythm with No. 6F catheters positioned at a left ventricular abnormal site (electrograms fulfilling two of the following criteria: amplitude less than 3 mV, duration greater than 70 msec, or an amplitude to duration ratio less than .046) and normal sites at the right ventricular apex (RVA) and right ventricular outflow tract (RVOT). All electrograms were recorded from the same location before and after intravenous lidocaine or procainamide administered to obtain mean serum concentrations of 4.2 +/- 0.6 and 9.42 +/- 2 micrograms/ml respectively. Lidocaine and procainamide had no significant effect on sinus cycle length or electrogram amplitude. After lidocaine, no significant change in QRS width (112 +/- 23 vs 114 +/- 24 msec), left ventricular electrogram duration (76 +/- 21 vs 78 +/- 15 msec), or right ventricular electrogram duration (RVA 33 +/- 9 vs 33 +/- 10 msec, RVOT 31 +/- 9 vs 33 +/- 11 msec) was noted during sinus rhythm. At a paced cycle length of 600 msec, there was also no change in the paced QRS duration (197 vs 198 msec), the RVA electrogram duration (30 vs 32 msec), the RVOT electrogram duration (49 vs 52 msec), or the left ventricular electrogram duration (102 vs 108 msec).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Catheterization↗

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↗

Spontaneous compared with induced onset of sustained ventricular tachycardia.

Electrophysiological characteristics of the modes of initiation of 16 episodes of spontaneously occurring sustained ventricular tachycardia recorded in 16 patients by two-channel ambulatory electrocardiographic monitoring were compared with the characteristics of ventricular tachycardia induced by programmed electrical stimulation. Eleven episodes of spontaneous ventricular tachycardia began after a single ventricular premature depolarization (VPD), three episodes after two VPDs, and two episodes after five VPDs. By comparison, only four episodes of sustained ventricular tachycardia were induced with a single VPD. Each episode of spontaneous ventricular tachycardia was initiated by a late coupled VPD (RR':QT ratio greater than 1.0). The VPD was often morphologically similar to the ensuing ventricular tachycardia (eight of 11 episodes that began after a single VPD). No correlation was found between the modes of initiation of spontaneous and induced ventricular tachycardia. We hypothesize that concealed decremental slow conduction, reflected in the long coupling intervals of VPDs initiating ventricular tachycardia, is of critical importance in initiating ventricular tachycardia. We conclude that major differences exist in the timing and number of VPDs associated with the onsets of spontaneous and induced sustained ventricular tachycardia.

Adult↗

Nonuniform recovery of excitability in the left ventricle.

The purpose of this study was to determine left ventricular activation, dispersion of refractoriness, and total recovery time in patients with coronary artery disease and ventricular tachycardia and in patients with the long QT syndrome and to compare these patients with a group of normal patients. Left ventricular endocardial catheter mapping and left ventricular refractory period determination were performed in 18 patients. Group 1 consisted of seven patients with no heart disease and no arrhythmia; group 2 consisted of six patients with previous infarction and sustained ventricular tachycardia; and group 3 consisted of five patients with prolonged QT interval and previous cardiac arrest. Total left ventricular endocardial activation was significantly longer in group 2 (75 +/- 23 msec, mean +/- SD) compared with group 1 (34 +/- 9 msec, p less than 0.01) and group 3 (42 +/- 5 msec, p less than 0.05). Dispersion of refractoriness was significantly greater in group 3 (87 +/- 27 msec) than in group 1 (40 +/- 14 msec, p less than 0.01) and group 2 (53 +/- 14 msec, p less than 0.05). Dispersion of total recovery time was significantly greater in group 2 (90 +/- 30 msec) than in group 1 (52 +/- 14 msec, p less than 0.05) as well as group 3 (114 +/- 43 msec) compared with group 1 (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Nonpharmacologic therapy of ventricular tachycardia.

Nonpharmacologic therapies for patients with sustained ventricular tachycardia have been necessitated by the low frequency of drug-responsive patients. These nonpharmacologic therapies include antitachycardia pacemakers, low-energy cardioverters, defibrillators, surgery and, for the present, catheter ablation. Antitachycardia pacing alone should never be used because of the known incidence of acceleration of ventricular tachycardia to ventricular fibrillation. Thus, all electrical devices must include a back-up defibrillator at the very least. The current automatic implantable cardioverter-defibrillator, which has been implanted in over 1000 patients, has been shown to prevent sudden death. Surgery has offered the only method to cure the arrhythmia by removing the arrhythmogenic substrate. Improved surgical techniques with electrophysiologic guidance have an acceptable mortality and a clinical success rate in 80-90% range. Catheter ablation, which is an experimental procedure at this time, offers the promise of a nonsurgical technique to extirpate the ventricular tachycardia substrate.

Electric Countershock↗

Electrophysiology of Ethmozine (moricizine HCl) for ventricular tachycardia.

Moricizine HCl, an antiarrhythmic phenothiazine drug, was investigated for its efficacy against ventricular tachycardia (VT) in a group of 60 patients from 8 institutions using electrophysiologic testing before and after oral administration. Moricizine HCl significantly prolonged PR, QRS, AH and HV intervals and cycle length for atrioventricular nodal block, but had minimal or no effect on repolarization or cardiac refractory periods. Induction of sustained VT (in 33 patients) and nonsustained VT (in 14 patients) occurred at baseline. During moricizine HCl therapy, sustained VT was induced in 31 patients and nonsustained VT in 7 patients. In individual patients, suppression of VT induction was obtained in 18% of patients with sustained VT and in 27% of patients with nonsustained VT. Cycle length of induced VT was significantly prolonged by moricizine HCl therapy. During prospective follow-up of 37 patients, electrophysiologic study predicted recurrence of nonrecurrence of VT with a sensitivity value of 82% and specificity of 65%.

Adult↗

The resetting response of ventricular tachycardia to single and double extrastimuli: implications for an excitable gap.

UNLABELLED: To evaluate the influence of local tissue refractoriness and delay in intervening tissue on the ability of single ventricular extrastimuli to reset and characterize a resetting response pattern in ventricular tachycardia (VT), single ventricular extrastimuli were delivered during 81 VTs and double ventricular extrastimuli in 45 of the 81 VTs. Resetting of VT was recognized as a less than fully compensatory pause after stimulation and was seen in 43 of 81 VTs (53%) with single ventricular extrastimuli and 35 of 45 (78%) with double ventricular extrastimuli. Double ventricular extrastimuli reset 16 VTs not reset by single ventricular extrastimuli. The return cycle, the interval from the extrastimulus to the first VT beat after extrastimuli, has 1 of 3 distinct response patterns: flat, increasing, and flat plus increasing. In 19 VTs, resetting was seen with both single ventricular extrastimuli and double ventricular extrastimuli; 4 flat responses with single ventricular extrastimuli became flat plus increasing with double ventricular extrastimuli. All other patterns were unchanged. In the 19 VTs reset by both single and double ventricular extrastimuli, the estimate of both the total reset zone (94 +/- 36 vs 56 +/- 32 ms) and the flat portion of the reset zone (52 +/- 42 vs 42 +/- 28 ms) was significantly longer with double ventricular extrastimuli (p less than 0.001 and p less than 0.02, respectively). IN CONCLUSION: (1) when single ventricular extrastimuli failed to reset a VT, double ventricular extrastimuli from the same site may reset the VT.

Cardiac Pacing, Artificial↗

Results of signal-averaged electrocardiography and electrophysiologic study in patients with nonsustained ventricular tachycardia after healing of acute myocardial infarction.

Programmed stimulation and signal-averaged electrocardiography were performed in 43 consecutive patients with nonsustained ventricular tachycardia (VT) after healing of inferior (29 patients) or anterior wall (14 patients) acute myocardial infarction. Twenty-two patients had inducible sustained VT. Patients with inferior infarction and inducible sustained VT had significantly longer filtered QRS durations (125 +/- 19 vs 112 +/- 15 ms, p less than 0.01) and significantly lower voltage in the last 40 ms of the filtered QRS complex (19 +/- 5 vs 30 +/- 14 microV, p less than 0.05) than those without inducible sustained VT. In contrast, the signal-averaged electrocardiographic measurements in patients with anterior infarction and inducible sustained VT did not differ significantly from those without inducible sustained VT. The results of these studies were compared with those of 2 control groups: 45 patients without ventricular arrhythmias after myocardial infarction and 95 patients with spontaneous and inducible sustained VT after myocardial infarction. The signal-averaged electrocardiographic measurements in patients with spontaneous nonsustained VT after inferior infarction were intermediate between the control group without arrhythmias and the control group with sustained VT. The signal-averaged electrocardiograms in patients with nonsustained VT after anterior infarction were not significantly different from those in patients without ventricular arrhythmias. The study shows that the site of infarction influences the signal-averaged electrocardiogram in patients with VT after myocardial infarction. The signal-averaged electrocardiogram may be useful in identifying patients with nonsustained VT after a remote inferior myocardial infarction who have inducible sustained VT.

Cardiac Pacing, Artificial↗

Hazards of intravenous verapamil for sustained ventricular tachycardia.

In 11 of 25 patients (44%) with sustained ventricular tachycardia (VT) who received intravenous verapamil (5 to 10 mg), acute severe hypotension or loss of consciousness developed, necessitating immediate cardioversion. Comparison of these 11 patients with the 14 who did not have adverse effects after verapamil revealed no significant difference in age, heart disease, ejection fraction, blood pressure before verapamil administration, other oral or intravenous drugs use, verapamil dose or VT characteristics (rate and morphologic pattern). Although most patients with severe adverse effects after verapamil had prior myocardial infarction, deterioration also occurred in patients without coronary disease and in patients with a normal left ventricular ejection fraction. VT terminated after verapamil infusion in 6 patients. No single electrocardiographic morphologic pattern characterized these patients. A control group of 25 patients presenting with hemodynamically stable VT who received other antiarrhythmic agents was examined. Hypotension developed in only 1 patient during acute therapy and did not require emergency cardioversion. Thus, although verapamil may terminate VT, severe adverse effects occur much more often. Use of verapamil to differentiate supraventricular tachycardia with aberrant conduction from ventricular tachycardia is hazardous.

Adult↗

Relationship of steady-state serum concentrations of amiodarone and desethylamiodarone to therapeutic efficacy and adverse effects.

The relationship of steady-state serum levels of amiodarone and its major metabolite, desethylamiodarone, to therapeutic and toxic effects was evaluated in 111 patients treated for supraventricular and ventricular arrhythmias. All patients were treated for more than two months (mean 10 +/- 7), and repeated serum levels determined at least two months apart were within 0.5 mg/liter of each other. Effective control of arrhythmias during steady-state therapy was achieved in 91 patients (82 percent of the study populations); recurrent arrhythmias or sudden death did not correlate with levels. An adverse drug effect necessitating cessation of therapy and/or concomitant medical therapy for the adverse effect occurred in 12 patients (11 percent); an additional 33 patients (30 percent) had an adverse effect that did not require change in therapy. The mean serum concentrations of amiodarone and desethylamiodarone associated with adverse drug effects were higher (2.6 +/- 1.2 mg/liter and 2.0 +/- 0.8 mg/liter) than those in patients without adverse effects (2.1 +/- 1.0 mg/liter and 1.5 +/- 0.7 mg/liter), p less than 0.05. An amiodarone serum concentration of 2.5 mg/liter or more had a positive predictive value of 76 percent for identifying patients with an adverse effect. The level of desethyl metabolite of amiodarone correlated directly with the serum amiodarone concentration (r = 0.82). Measurement of desethylamiodarone did not increase the sensitivity or specificity of the amiodarone level alone in the identification of patients at risk for adverse drug effects.

Adult↗

Usefulness of electrophysiologic study to determine the clinical tolerance of arrhythmia recurrences during amiodarone therapy.

The relation of clinical and electrophysiologic variables to outcome was evaluated in 121 patients treated with amiodarone for sustained ventricular tachyarrhythmias. Electrophysiologic study was performed in all patients a mean of 14 days after beginning amiodarone therapy. Forty-six patients who were given oral amiodarone therapy experienced arrhythmia recurrence. Multivariate analysis was performed using 16 clinical and electrophysiologic variables to determine which factors were associated with 1) arrhythmia recurrence and 2) a poorly tolerated arrhythmia recurrence (that is, cardiac arrest or sudden cardiac death) during oral amiodarone therapy. No variable predicted arrhythmia recurrence. Five variables correlated significantly with a poorly tolerated arrhythmia recurrence. Hemodynamic stability of the arrhythmia induced on electrophysiologic testing during amiodarone therapy had the best predictive value (p less than 0.001). Younger age, lower ejection fraction, a poorly tolerated rhythm at clinical presentation and absence of left ventricular aneurysm were also associated with a poorly tolerated arrhythmia recurrence. Only 3 of 57 patients who had a well tolerated arrhythmia induced on electrophysiologic testing during amiodarone therapy had recurrence of a poorly tolerated arrhythmia versus 19 of 47 who had hemodynamically unstable arrhythmias induced during amiodarone therapy (p less than 0.001). Thus, electrophysiologic testing during amiodarone therapy appears useful in identifying patients who are prone to have catastrophic arrhythmia recurrences and could allow for the institution of additional or alternative modes of therapy.

Amiodarone↗

Inducible polymorphic ventricular tachycardia and ventricular fibrillation in a subgroup of patients with hypertrophic cardiomyopathy at high risk for sudden death.

This investigation was undertaken to elucidate the underlying electrophysiologic substrate in hypertrophic cardiomyopathy and to identify possible predictors of sudden death in this patient population. Programmed stimulation was performed in 18 patients aged 14 to 64 years (mean 36) believed to be at high risk for sudden death on the basis of prior cardiac arrest or syncope, nonsustained ventricular tachycardia on Holter ambulatory electrocardiographic (ECG) monitoring or a family history of frequent sudden death. Polymorphic ventricular tachycardia that deteriorated to ventricular fibrillation was reproducibly induced in 8 (44%) of the 18 patients (Group A). This rhythm was induced in all three patients with a history of cardiac arrest. No sustained monomorphic ventricular tachycardia was induced. Group B comprised the 10 patients in whom a sustained arrhythmia could not be reproducibly initiated. The electrophysiologic substrate was distinctly different in patients with, than in those without, inducible sustained arrhythmia. The refractory period was shorter at the right ventricular outflow tract (232 +/- 22 ms) compared with the apex (264 +/- 12 ms) in Group A (p less than 0.005) whereas there was no difference in Group B (271 +/- 25 ms versus 271 +/- 13 ms). The local ventricular electrogram of most patients in both groups was prolonged and markedly multiphasic. However, 5 of the 8 Group A patients exhibited a double electrogram (V-V') with premature stimulation compared with 1 of the 10 patients in Group B (p less than 0.02). A positive R wave in lead aVR of the scalar ECG and poor R wave progression in the precordial leads were more common in Group A than in Group B (p less than 0.001 and p less than 0.001, respectively). The reason for the distinctly different electrophysiologic substrate and the high prevalence of inducible polymorphic arrhythmia is unclear. It may relate to the underlying myocardial architecture in these patients, characterized by myocardial cellular disarray and fibrosis.

Adolescent↗

Atrioventricular nodal reentrant tachycardia: studies on upper and lower 'common pathways'.

Electrophysiologic studies were performed in 28 patients with documented atrioventricular (AV) nodal reentrant supraventricular tachycardia (SVT) to investigate the presence of AV nodal tissue situated between the tachycardia circuit and both the atrium (upper common pathway, UCP) and the His bundle (lower common pathway, LCP). All patients demonstrated a 1:1 AV relationship during SVT. The study protocol consisted of atrial then ventricular pacing at the SVT cycle length. UCPs were manifested in eight of 28 (29%) patients by either antegrade AV Wenckebach (six patients) or a paced atrium-His (AH) interval exceeding the AH in SVT (two patients, differences 5 and 9 msec). LCPs were manifested in 21 of 28 (75%) patients by either retrograde Wenckebach periodicity (two patients) or a paced HA interval exceeding the HA in SVT (19 patients, mean difference 25 +/- 20 msec). By these criteria, eight patients (29%) had evidence for both UCPs and LCPs. UCPs were more likely than LCPs to be manifested by Wenckebach criteria (p less than .05). Thus the AV nodal reentrant SVT circuit appears to be intranodal and is frequently surrounded by AV nodal tissue (UCP and LCP), antegrade and retrograde conduction properties of these common pathways are discordant in some cases, and conduction properties of UCP tissue differ from those of LCP tissue. These findings may have relevance in that the UCP or LCP may limit the ability of premature extrastimuli to penetrate the circuit to initiate or terminate AV nodal SVT.

Cardiac Pacing, Artificial↗