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Biomedical subjects

M E Josephson

Publications and source records attributed to M E Josephson.

At least 163 records · Page 9Linked to original sources
PubMed1986

Endocardial catheter mapping in patients in sinus rhythm: relationship to underlying heart disease and ventricular arrhythmias.

Catheter mapping during sinus rhythm was performed in 132 patients with coronary artery disease and 26 patients with congestive noncoronary cardiomyopathy. Each of the patients had a clinical history of one of the following: no ventricular arrhythmia, nonsustained ventricular tachycardia, cardiac arrest, or sustained ventricular tachycardia. The characteristics of the endocardial electrogram and other measured indexes of slow endocardial conduction were compared between patients with different types of disease and in different arrhythmia groups to determine if differences existed. The cardiomyopathic group had a higher percent of normal endocardial electrograms than the coronary artery disease group, with no evidence of slow endocardial conduction. The sustained ventricular tachycardia group exhibited a greater percent of abnormal endocardial electrograms and more evidence of slow endocardial conduction, distinguishing this group from the three other arrhythmia groups. We conclude the following: The underlying electrophysiologic substrate varies in patients with different ventricular arrhythmias. It is therefore inappropriate to analyze all patients with ventricular arrhythmias as a single group. Patients with congestive noncoronary cardiomyopathy, regardless of the type of their arrhythmia, have a relatively normal endocardium. Those patients with serious ventricular arrhythmias should not be considered candidates for surgery directed at removing abnormal endocardium.

Aged↗
PubMed1986

Resetting response patterns during sustained ventricular tachycardia: relationship to the excitable gap.

We analyzed the resetting response (a noncompensatory pause after electrical stimulation) during 37 hemodynamically tolerated ventricular tachycardias (VTs) induced by programmed electrical stimulation in 32 patients with chronic coronary artery disease. The mean cycle length of VT was 369 +/- 59 msec. Single extrastimuli were delivered at the right ventricular apex during all 37 VTs, and double extrastimuli were delivered at the same site during 23 VTs. The resetting response pattern was considered increasing, decreasing, or flat if the return cycle increased, decreased, or remained constant in response to progressively shorter coupling intervals of the extrastimuli. Ten VTs had an increasing pattern and nine a flat pattern. In 11 VTs the pattern was mixed (flat at longer coupling intervals and increasing at shorter ones), and in the remaining seven the pattern could not be defined. No VT had a decreasing pattern. The mean duration of the resetting interval (range of coupling intervals resulting in resetting) was 66 +/- 45 msec, or 17% of the cycle length of VT. VT with a mixed pattern had longer resetting intervals than VT with an increasing pattern (102 +/- 34 vs 64 +/- 40 msec; p less than .035); however, cycle lengths of VT were similar (370 +/- 58 vs 386 +/- 86, p = NS). An excellent correlation was observed between the shortest return cycles in response to single and double extrastimuli (r = .99), with a mean difference of 5 msec. The cycle length of VT exceeded the return cycle (measured to the QRS onset) during 15 VTs (41%).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗
PubMed1986

Amiodarone versus amiodarone and a type IA agent for treatment of patients with rapid ventricular tachycardia.

Induction of rapid ventricular tachycardia or fibrillation during therapy with amiodarone is associated with an increased risk of sudden death. To determine whether the addition of a type IA antiarrhythmic agent to therapy would improve outcome, 37 patients in whom ventricular tachyarrhythmia of a cycle length less than 350 msec was induced after 14 +/- 2 days of amiodarone were randomly assigned to therapy with amiodarone alone (group 1, 20 patients) or amiodarone plus type IA agent (group 2, 17 patients). Type IA therapy consisted of procainamide in 13 patients and quinidine in four procainamide-intolerant patients. To assess the short-term effects of a type IA agent on inducibility of ventricular tachyarrhythmia, cycle length, and hemodynamic tolerance, 16 of 20 patients in group 1 and all patients in group 2 underwent repeat programmed stimulation after the intravenous administration of procainamide during amiodarone therapy (mean procainamide serum concentration 7.2 +/- 2.0 micrograms/ml). Procainamide prevented induction of sustained arrhythmia in only two of 33 patients. Procainamide increased the cycle length of induced ventricular tachycardia from 283 +/- 30 to 352 +/- 46 msec (p less than .001). After the addition of procainamide, 16 of 31 patients vs 10 of 37 patients on amiodarone alone had an induced arrhythmia that was tolerated hemodynamically (p less than .05). There were no differences between groups 1 and 2 with respect to patient or arrhythmia characteristics, response to short-term procainamide, or duration of follow-up. The mean follow-up for all patients was 14 +/- 10 months.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Amiodarone hepatotoxicity. A clinicopathologic study of five patients.

Five patients had amiodarone hepatotoxicity detected on routine biochemical monitoring. Symptoms attributable to hepatotoxicity were minimal or absent; reversible hepatomegaly was seen in two patients, whereas three patients had signs of nonhepatic amiodarone toxicity before or with hepatotoxicity. Serum aminotransferase levels were elevated in all patients and alkaline phosphatase levels in four; no patient had hyperbilirubinemia or prolongation of the prothrombin time. Light microscopy showed steatosis, cellular degeneration, and cellular necrosis in the biopsy samples of four patients, whereas the fifth patient's sample had a granulomatous injury pattern. Electron microscopic study of liver tissue done in two patients showed phospholipid-laden lysosomal lamellar bodies. These findings suggest that both toxic and hypersensitivity liver injury can occur in response to amiodarone. The presence of phospholipid-laden lysosomal lamellar bodies may help differentiate amiodarone hepatotoxicity from alcoholic liver disease or other causes of hepatic steatosis.

Aged↗
PubMed1986

The automatic implantable cardioverter-defibrillator: efficacy, complications, and device failures.

Twenty-six patients with refractory ventricular arrhythmias received the automatic implantable cardioverter-defibrillator. A patch lead only was placed during arrhythmia surgery in 7 other patients. During 13 +/- 6 (SD) months, the device discharged in 10 patients because of a sustained ventricular arrhythmia. No sudden deaths occurred. There were 31 complications in 17 patients, including postoperative refractory heart failure, coronary artery erosion, subclavian vein thrombosis, postoperative stroke after conversion of atrial fibrillation, atelectasis with pneumonia, symptomatic pleural effusions, and infection at the generator site. The cardioverter-defibrillator discharged in 9 asymptomatic patients, failed to terminate ventricular fibrillation during postoperative testing in 3 patients, and had premature battery failure in 4 patients. Tachycardia slowing during chronic amiodarone therapy and unipolar ventricular pacing during ventricular fibrillation precluded or delayed arrhythmia sensing. Thus, the cardioverter-defibrillator can be life saving, but its potential complications and interactions with antiarrhythmic drugs and pacemakers must be considered at patient selection.

Adolescent↗
PubMed1986

Improved results in the operative management of ventricular tachycardia related to inferior wall infarction. Importance of the annular isthmus.

Ventricular tachycardia associated with inferior wall myocardial infarction has had a lower surgical cure rate with localized subendocardial resection than ventricular tachycardia related to anterior infarction. Some investigators have advocated visually directed extensive subendocardial resection, including resection of the papillary muscles and mitral valve replacement, even without documenting the origin of ventricular tachycardia at these sites. We have operated on 46 patients (43 men and three women) for ventricular tachycardia associated with inferior wall myocardial infarction. Thirty-one consecutive patients (Group I) had standard localized subendocardial resection. Two patients in this group had mitral valve replacement for mitral insufficiency. Fifteen consecutive recent patients (Group II) underwent subendocardial resection plus focal endocardial cryoablation (3 minutes at -70 degrees C) of the annular isthmus. The annular isthmus is defined as the ventricular muscle between the basal end of the ventriculotomy and the mitral valve anulus. In Group I there were four operative deaths (13%). Ventricular tachycardia was noninducible in 15 of 27 operative survivors (56%) at postoperative electrophysiologic studies. In Group II there was one operative death (7%) and 13 of 14 survivors (93%) had no inducible ventricular tachycardia at postoperative electrophysiologic studies (p less than 0.01 versus Group I). No Group II patient required mitral valve replacement. Six operative survivors in Group II had intraoperative activation maps consistent with macroreentry incorporating the annular isthmus. Group I and Group II were indistinguishable in terms of preoperative hemodynamics, number of coronary arteries diseased, or the presence of left ventricular aneurysm. These results suggest that subendocardial resection with additional cryoablation of the annular isthmus results in improved control of ventricular tachycardia in patients with ventricular tachycardia associated with inferior wall myocardial infarction. Mitral valve replacement is not required unless intrinsic mitral valve disease is present. These data also suggest that the annular isthmus is a critical component of the reentrant circuit in these tachycardias.

Adult↗
PubMed1985

Entrainment of ventricular tachycardia by atrial depolarizations.

Four patients in whom rapid atrial pacing resulted in transient entrainment of a sustained ventricular tachycardia (VT) are reported. Ventricular fusion was seen in 3 of the 4. The following new observations were made: (1) A single atrial depolarization resulted in ventricular fusion and resetting of a VT, while atrial pacing at a faster rate entrained the same VT but without detectable fusion. This suggests that fusion during entrainment may be a rate-dependent phenomenon. (2) The interval between the last paced beat and the first nonpaced VT beat was different from the pacing cycle length in 3 patients. Two mechanisms accounted for this: the initial forces of each entrained QRS occurring as a result of the pacing wavefront, with fusion taking place only during the terminal forces, and the last entrained cycle exceeding the pacing cycle length by an amount related to the nonfused portion of the QRS, and delay in the presumed reentrant circuit responsible for the tachycardia. One VT was entrained with atrial pacing while ventricular pacing at the same rate resulted in termination, suggesting "site specificity" for termination. It is concluded that entrainment can occur without the criteria previously described as characteristic of it and that additional phenomena may be observed after stimulation that further support reentry as the mechanism of VT.

Adult↗
PubMed1985

Electrical alternans in wide complex tachycardias.

The occurrence of electrical alternation of 0.1 mV or greater of the QRS or T wave was analyzed in 156 electrocardiograms that showed wide QRS complex tachycardias from 91 patients. One hundred thirty-six ventricular tachycardias (VT) were recorded from 74 patients and 20 supraventricular tachycardias (SVT) from 17 patients. Alternans was present in 42 tracings (27%) from 35 patients (38%) and was equally frequent in the patients with VT (39%) and those with SVT (35%). Alternans occurred in 36 VTs (27%) and 6 SVTs (30%). Tachycardias with alternans had a shorter mean cycle length than tachycardias without alternans (339 +/- 53 vs 368 +/- 85 ms, p less than 0.05), but were not associated with a particular QRS morphology or axis. Alternans was most frequent in leads V2 and V3 and was seen in more leads during SVT than VT (7.2 +/- 2.6 vs 3.7 +/- 2.5, p less than 0.005). All SVTs with alternans incorporated an atrioventricular bypass tract. Electrical alternans occurs frequently in wide QRS tachycardias. Alone, it does not help differentiate VT from SVT. SVTs utilizing bypass tracts frequently show alternans even if the QRS is wide, and this finding may be useful in determining the mechanism of SVTs with aberrant intraventricular conduction.

Bundle-Branch Block↗
PubMed1985

Anatomic and hemodynamic effects of catheter-delivered ablation energies in the ventricle.

Twenty dogs were studied to characterize the anatomic, hemodynamic and pathologic effects of catheter-delivered cardioversion (CDCV) in the left ventricle. Five dogs each received 1 CDCV of either 50, 100, 200 or 300 J at the left ventricular apex. The injury occurred at the posteroinferior apex. Structural integrity of the ventricle remained intact. Energy doses of 50 and 100 J resulted in focal subendomyocardial injury. Higher energy levels resulted in localized transmural injury. There was a linear dose-related correlation between the volume of injury and delivered energy. Electrocardiographic changes were seen immediately in all dogs. Fifteen dogs had acute, transient ventricular arrhythmias. One dog died with refractory arrhythmias. Minimal hemodynamic changes were associated with the CDCV. Unique histopathologic changes were observed. Thus, local tissue destruction can be produced with CDCV. The extent of injury is dose-related and is associated with minimum hemodynamic changes. The lesion may be acutely arrhythmogenic.

Animals↗
PubMed1985

Ventricular activation in normal sinus rhythm: abnormalities with recurrent sustained tachycardia and a history of myocardial infarction.

Left ventricular activation was studied in 21 patients: 7 with normal electrocardiograms (group I), 7 with prior transmural myocardial infarction (group II) and 7 with prior transmural myocardial infarction (MI) and recurrent sustained ventricular tachycardia (VT) (group III). Fragmented electrograms were defined as those less than 3 mV in amplitude and longer than 60 ms in duration. Such electrograms were found in no group I patients, 6 of 7 group II patients and all 7 group III patients. An average of 2 of the 12 sites mapped in each patient displayed fragmented electrograms in group II; an average of 6 of the 12 sites displayed fragmented electrograms in group III (p less than 0.01). Twelve of the 84 total sites mapped in group II displayed fragmented electrograms, whereas 39 of the 84 sites mapped in group III patients did (p less than 0.01). The longest fragmented electrogram found in the 6 group II patients in whom such electrograms were found was shorter in duration than the longest electrogram found in each of the 7 group III patients with fragmented electrograms (76 ms vs 135 ms, p less than 0.005). The duration of endocardial activation was longer in group II patients (79 +/- 7 ms) than in group I patients (39 +/- 4 ms, p less than 0.001). Duration of activation was also longer in group III patients (151 +/- 12 ms) than in either of the other groups (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Electrocardiography↗
PubMed1985

Subendocardial resection for sustained ventricular tachycardia in the early period after acute myocardial infarction.

One hundred nineteen patients with drug-refractory ventricular tachycardia (VT) underwent mapping-guided subendocardial resection for control of their arrhythmias from 3 weeks to 10 years after acute myocardial infarction (AMI). Patients were separated into 2 groups: those treated early (within 4 months, group I) and those treated later (after 1 year, group II) after AMI. There were 32 patients in group I and 72 patients in group II. Both groups of patients had similar clinical, angiographic and hemodynamic characteristics. Patients in group I had VT with a shorter mean cycle length than patients in group II (322 +/- 71 vs 349 +/- 88 ms, p less than 0.05). The groups did not differ with respect to operative mortality (12% vs 7%), late mortality (31% vs 33%, mean follow-up 23 months), or frequency with which subendocardial resection without any adjunctive therapy prevented postoperative spontaneous or inducible VT (21% vs 34%). Group I was further separated into patients who underwent subendocardial resection within 1 month of AMI (n = 7) and those who underwent subendocardial resection with 2 months of AMI (n = 14). Although patients in group I were characterized by having more spontaneous morphologically distinct tachycardias, their operative mortality, total mortality and surgical success rates were comparable to those of patients in group II.(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗
PubMed1985

Relation of late potentials to site of origin of ventricular tachycardia associated with coronary heart disease.

Signal-averaged electrocardiograms and endocardial catheter mapping were performed in 41 patients with coronary artery disease and sustained ventricular tachycardia (VT) to determine the relation between signal-averaged late potentials (SA-LPs) and catheter-mapped late activity (CM-LA) to the site of origin of VT. The 41 patients had 79 morphologically distinct VTs. Either CM-LA or SA-LP was present during sinus rhythm in 37 of 41 patients (90%). Twenty-two out of 30 patients (73%) had CM-LA corresponding to SA-LP during normal sinus rhythm. Patients with SA-LP had a significantly greater number of sites of CM-LA, which were later and longer in duration than patients without SA-LP present during sinus rhythm. In a select group of patients, those with both SA-LP and CM-LA, the site of origin of VT was located at or adjacent to a site of CM-LA during sinus rhythm in 38 of 44 (86%); however, 36 of 78 sites (46%) of CM-LA were clearly distant from the site of origin of VT. In conclusion, CM-LA corresponding to SA-LP in patients with VT is sensitive but not specific for the site of origin of VT.

Adult↗
PubMed1985

Electrophysiologic evaluation and follow-up characteristics of patients with recurrent unexplained syncope and presyncope.

One hundred nineteen patients with unexplained syncope (82%) or presyncope (18%) underwent complete electrophysiologic study (EPS). Symptoms were recurrent in 72% of the patients. Fifty-two percent of the patients had structural heart disease. Forty-one patients had normal EPS results and 78 had electrophysiologic abnormalities (ventricular tachycardia in 31, induced atrial flutter/fibrillation in 17, vasovagal syncope in 8, hypersensitive carotid sinus syndrome in 7, supraventricular tachycardia in 6, heart block in 5 and sick sinus syndrome in 4). The presence of structural heart disease (p = 0.0033) and previous myocardial infarction (p = 0.05) were the only clinical or electrocardiographic predictors of a positive EPS response. Therapy was guided by EPS and patients were followed for 27 +/- 20 months (mean +/- standard deviation). In the patients with negative EPS results, 76 +/- 11% (mean +/- standard error) were symptom-free at follow-up, compared to 68 +/- 10% in the group with positive EPS responses. No clinical variables helped to predict remission in the absence of therapy. One patient in the negative EPS response group and 2 patients in the EPS positive group died suddenly (cumulative survival 94 +/- 4%). Total cardiovascular mortality was 13% in the positive EPS response group, and 4% in the negative EPS response group. Thus, certain clinical characteristics are helpful in selecting patients for study. Electrophysiologically guided therapy is associated with a recurrence and sudden death rate similar to an untreated control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Value of Holter monitoring in identifying risk for sustained ventricular arrhythmia recurrence on amiodarone.

Seventy-four patients with sustained ventricular tachyarrhythmias had 22 +/- 3 hours of Holter monitoring before and after 11 +/- 6 days of amiodarone treatment. On control Holter recordings, 55 patients (group I) had frequent (more than 10 extrasystoles per hour) and/or complex (at least couplets) ventricular ectopic activity (VEA), and 19 patients (group II) had infrequent and simple VEA. A positive Holter monitor response to amiodarone was defined as a decrease in VEA by more than 85% and abolition of all complex VEA. In group I, 34 patients (62%) had a positive Holter monitor response. In group II, 16 patients (84%) had persistent, infrequent and simple VEA and 3 had frequent and/or complex VEA. During a mean follow-up of 13 +/- 12 months, 22 patients (30%) had ventricular tachycardia (VT) or sudden death. In group I, VT or sudden death occurred in 6 of 34 (18%) patients with a positive Holter monitor response and 11 of 21 (52%) with a negative Holter monitor response (p less than 0.01), and in group II, VT or sudden death occurred in 5 of 16 patients (31%) with persistent, infrequent and simple VEA. All episodes of VT or sudden death occurred after at least 2 weeks of amiodarone therapy (mean 5 +/- 6 months). The predictive accuracy of a positive Holter monitor response as an indicator for subsequent prevention of sustained ventricular tachyarrhythmias and sudden cardiac death was 82% and for a negative Holter monitor response as an indicator of tachyarrhythmia or sudden death recurrence on therapy it was 52%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Catheter mapping during sinus rhythm: relation of local electrogram duration to ventricular tachycardia cycle length.

Catheter mapping was performed during sinus rhythm in 52 patients with 102 morphologically distinct ventricular tachycardias (VT). Twenty patients had a single VT morphologic pattern. The cycle length of VT was correlated with the duration of all electrograms and various electrogram subgroups, including abnormal, fractionated, late, and longest electrograms, as well as the electrogram recorded at the site of origin of VT and at sites other than the site of origin using linear regression analysis. No correlation was found between local electrogram duration of any of these groups and VT cycle length. There was no relation regardless of whether the patient had a single or multiple morphologic patterns. Thus, the local electrogram duration measured with catheter mapping during sinus rhythm does not correlate with VT cycle length. This finding provides additional support that catheter mapping during sinus rhythm does not give sufficient information to guide localized endocardial resection for VT surgery.

Electrocardiography↗