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Biomedical subjects

M E Josephson

Publications and source records attributed to M E Josephson.

At least 145 records · Page 8Linked to original sources
PubMed1987

Nonsustained ventricular tachycardia in patients with coronary artery disease: role of electrophysiologic study.

Sixty-two consecutive patients with chronic coronary artery disease referred for evaluation of nonsustained ventricular tachycardia (VT) underwent electrophysiologic studies. Sustained VT was induced by one to three ventricular extrastimuli in 28 patients (45%). Therapy was guided by the results of electrophysiologic testing in 44 patients: 19 patients without inducible sustained VT received no antiarrhythmic therapy, and 25 patients with inducible sustained or symptomatic nonsustained VT received therapy guided by the results of electrophysiologic studies. The results of electrophysiologic studies were ignored by physicians for a second group of 18 patients: four had inducible sustained VT but received no antiarrhythmic therapy, and 14 had inducible sustained or nonsustained VT and received antiarrhythmic therapy not guided by results of electrophysiologic testing. After a mean follow-up period of 28 months, 11 patients had died suddenly. Seven of the 11 patients who died suddenly had inducible sustained VT. Three of 44 patients in the group receiving therapy guided by electrophysiologic studies died suddenly versus eight of 18 in the group receiving therapy not guided by electrophysiologic studies (p = .001). Only one of 19 patients without inducible sustained VT who were not treated experienced sudden death. Two of four patients with inducible sustained VT who did not receive antiarrhythmic therapy died suddenly. Multivariate analysis of the relationship of induced arrhythmias, left ventricular ejection fraction, site of myocardial infarction, history of syncope, or type of antiarrhythmic therapy to outcome revealed a greater than twofold increased risk for sudden cardiac death in patients whose therapy was not guided by results of electrophysiologic study.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Prevention of ventricular tachycardia induction during right ventricular programmed stimulation by high current strength pacing at the site of origin.

To determine whether high current strength pacing at the site of origin of ventricular tachycardia (VT) could prevent induction of VT, we studied 11 VTs in 10 patients with chronic coronary artery disease. The left ventricular site of origin of all VT was determined by endocardial catheter mapping. Reproducible VT induction from the right ventricular apex or outflow tract was demonstrated with a pacing current strength equal to twice diastolic threshold (less than or equal to 2.0 mA) with single (two VTs), double (eight VTs), or triple (one VT) extrastimuli following 8 beats of a drive cycle length of 400 to 600 msec. After determination of the baseline VT induction zone (range 10 to 80 msec), repeat induction was attempted while simultaneous pacing was performed during the 8 beat drive train from the left ventricular site of origin with the use of a high current strength (10 mA [two VTs] or 20 mA [nine VTs]) and from the baseline right ventricular site with a current strength equal to twice diastolic threshold. Extrastimuli were introduced only from the right ventricular site over the same range of coupling intervals that resulted in VT initiation during the baseline state. In five of the 11 trials, no VT could be initiated; in one trial, the VT induction zone was decreased from 80 to 10 msec; in three trials, only VT of a different morphology and a distinct (greater than 4 cm distant) site of origin was initiated; and in two trials, VT of the same morphology was initiated. In four of the five trials in which all VT was prevented by simultaneous pacing with a high current strength at the site of origin, simultaneous pacing at a lower current strength (twice diastolic threshold) at the site of origin (three VTs) or with equally increased current strength (10 to 20 mA) at nonsites of origin (two VTs) did not prevent initiation. We conclude that: high current strength pacing at the site of origin during the drive train can inhibit VT induction with extrastimuli and, successful prevention of VT may depend on the pacing site being the site of origin and the current strength used during pacing.

Aged↗
PubMed1987

Early experiences of endocardial catheter mapping of the left ventricle in patients with sustained ventricular tachycardia--efficacy, safety and complications.

In 23 patients with recurrent sustained ventricular tachycardia (VT) which originated from the left ventricle, endocardial catheter mapping has performed. In an additional 14 patients we also stimulated their left ventricle for non-sustained VT. Multiple sites could be mapped for the recording of local electrical activity, for pacing and for the induction of VT. These procedures could be done without complication. A careful, reasonable, and safe method of endocardial mapping will facilitate clinical electrophysiologic study.

Adult↗
PubMed1987

The pharmacokinetic and pharmacodynamic effects of varying the free fraction of disopyramide.

We have evaluated the influence of several factors on the binding of disopyramide to protein in human serum using a new ultrafiltration system and the enzyme multiplied immunoassay technique (EMIT) for disopyramide immunoassay. From these studies and those of other investigators, we conclude that the most significant in vivo factors influencing disopyramide binding in human serum are total disopyramide concentration, the concentration of alpha 1-acid glycoprotein, and the concentration of mono-N-dealkyldisopyramide. Significant variation in binding occurs in patients whose total disopyramide concentration is within the therapeutic range. The proportion of free disopyramide ranged from 16% to 54% in the sera of 50 cardiac patients whose total disopyramide concentration ranged from 0.5 to 5.8 mcg/ml. Since there is so much variation in the proportion of disopyramide that is free, and since it is the unbound form of the drug that is pharmacologically active, it is likely in patients whose arrhythmia responds to disopyramide therapy that unbound drug concentration will be a better indicator of drug efficacy and toxicity than will be total drug concentration. To test this hypothesis, we are investigating the relationship between steady state total and unbound disopyramide plasma levels in patients with supraventricular or ventricular arrhythmias, and pharmacologic response as determined by standard intracardiac electrophysiologic studies.

Blood Proteins↗
PubMed1986

Influence of the site of stimulation on the resetting phenomenon in ventricular tachycardia.

Uniform, sustained ventricular tachycardia (VT) in the setting of prior myocardial infarction is believed to be due to reentry. The ability to reset VT with programmed extrastimuli requires that the premature impulse reach and enter the reentrant circuit. To evaluate the importance of the site of pacing on the ability to reset VT, single ventricular extrastimuli were delivered during 32 morphologically distinct, uniform VTs from both the right ventricular (RV) apex and RV outflow tract. Single ventricular extrastimuli resulted in resetting of VT from the RV apex only in 6 VTs, from the RV outflow tract only in 2, from both sites in 11 VTs and neither site in 13. When VT reset at both RV sites, 1 RV site or neither RV site was compared, a left bundle branch block VT QRS morphologic pattern was found to be more common in VT reset at both sites than at neither site (8 of 11 vs 4 of 13, p less than 0.05). No other differences in VT characteristics analyzed were found between these groups. Multiple ventricular extrastimuli were delivered in 16 VTs; in 6 of these, resetting was shown from at least 1 additional site, as compared to the response with single ventricular extrastimuli. In summary, site of stimulation can influence the ability of premature extrastimuli to reset uniform VT, and site dependence of VT resetting diminishes when multiple extrastimuli are used. This suggests that refractoriness or conduction delay in tissue between the pacing site and tachycardia circuit are important determinants of ability to reset VT from a particular site.

Atrioventricular Node↗
PubMed1986

Usefulness of programmed stimulation in idiopathic dilated cardiomyopathy.

The response to programmed electrical stimulation and the clinical outcome was determined in 47 patients with nonischemic dilated cardiomyopathy (DC). Thirteen patients (group 1) presented with sustained uniform ventricular tachycardia (VT), 14 (group 2) presented with cardiac arrest and 20 (group 3) presented with nonsustained VT. The mean ejection fraction of the study population was 28 +/- 9%. The response to programmed stimulation was related to arrhythmia presentation. In all patients in group 1 sustained, uniform VT was induced, compared with 1 patient in group 2 and 2 patients in group 3 (p less than 0.001). There were 14 sudden cardiac deaths and 1 cardiac arrest during a mean follow-up of 18 +/- 14 months. The only 4 patients who presented with sustained VT or a cardiac arrest in whom sustained arrhythmia induction was suppressed with antiarrhythmic therapy remain alive. Nine of the 23 patients (4 in group 2 and 5 in group 3) in whom no sustained ventricular arrhythmia was induced died suddenly, with 5 of the 9 receiving empiric antiarrhythmic therapy. Three other patients, who had a slower and hemodynamically tolerated VT at the time of arrhythmia induction, died suddenly. Thus, in patients with nonischemic DC, uniform, sustained VT is always and almost solely initiated in patients who present with this arrhythmia; although few patients presenting with sustained VT or cardiac arrest have inducibility of the arrhythmias suppressed with therapy, if it is suppressed the patient appears to have a good prognosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

Abnormalities of endocardial activation pattern in patients with previous healed myocardial infarction and ventricular tachycardia.

Endocardial catheter mapping was performed in 27 patients with anterior wall acute myocardial infarction (AMI) and in 10 patients with inferior wall AMI. All patients had a history of ventricular tachycardia. Left ventricular breakthrough occurred at 10 +/- 4 ms after the QRS complex in inferior AMI and 11 +/- 7 ms after the QRS complex in anterior AMI. Total electrical activity recorded during sinus rhythm was 164 +/- 46 ms in inferior and 144 +/- 28 ms in anterior AMI (p = 0.05). Nine of the 10 patients with inferior AMI had complete activation of the anterior wall within the initial one-half of the QRS complex, compared with only 15 of the 27 patients with anterior AMI (p = 0.05). All 10 patients with inferior AMI had activation of the ventricular septum within the initial half of the QRS complex compared with only 13 of 27 with anterior AMI (p less than 0.005). None of the patients with inferior AMI had activation of the inferoposterior base within the initial one-half of the QRS complex, compared with 21 of 27 patients with anterior AMI (p less than 0.001). Complete activation of the anterior wall occurred at 33 +/- 15 ms in inferior and 58 +/- 30 ms in anterior AMI (p less than 0.005). Complete activation of the septum occurred at 38 +/- 12 ms in inferior and 63 +/- 28 ms in anterior AMI (p less than 0.005). Complete activation of the inferoposterior base occurred at 100 +/- 38 ms in inferior and 50 +/- 21 ms in anterior AMI (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Electrophysiologic sequelae of chronic myocardial infarction: local refractoriness and electrographic characteristics of the left ventricle.

Ventricular tachycardia (VT) has been shown to arise from ischemically damaged left ventricular myocardium, which possesses heterogeneity of refractoriness and activation. Catheter techniques were used to study left ventricular refractoriness using the strength-interval relation and activation by local electrographic characteristics in 8 patients with and 6 patients without previous myocardial infarction (MI). Noninfarcted myocardium in patients with and without previous MI was similar overall with respect to refractoriness and excitability, whereas local electrographic duration in MI patients was longer (66 +/- 2 vs 52 +/- 3 ms, p less than 0.005) and amplitude lower (3.9 +/- 2.1 vs 6.1 +/- 2.0 mV, p less than 0.05). Comparisons of infarcted and noninfarcted regions in MI patients revealed an increased threshold of excitability at infarct sites (e.g., 1.9 +/- 1.0 vs 0.7 +/- 0.4 mA, p less than 0.05) and prolongation of refractory periods (375 +/- 118 vs 275 +/- 13 ms, p less than 0.05) at the lowest level of stimulating current. Shortening of refractory period as a result of change in pacing cycle length was not affected by infarction. The local electrographic duration (95 +/- 17 ms) was significantly longer in infarcted regions than at noninfarcted sites (p less than 0.005), but the electrographic amplitude (3.4 +/- 3.0 mV) differed significantly only in noninfarct patients. It is concluded that considerable electrophysiologic disparity exists between infarcted and noninfarcted myocardium. Whether or not arrhythmogenic tissue possesses unique alterations in electrophysiologic characteristics remains to be established.

Adult↗
PubMed1986

Predictive accuracy of criteria for chronic myocardial infarction in pacing-induced left bundle branch block.

Sensitivity, specificity and predictive accuracy of 5 electrocardiographic criteria for chronic myocardial infarction (MI) in the presence of left bundle branch block (LBBB) were evaluated in 47 patients with known (clinical and electrocardiographic Q wave) MI and 28 patients without MI. Two right ventricular sites were paced (producing LBBB with normal or left axis). The effect of infarct location on these criteria was also evaluated. In patients with LBBB: Cabrera's sign (notching of the upstroke of S wave in V3,4,5) is seen more often with MI than without (anterior more often than inferior), and the left axis increased its sensitivity. Chapman's sign (notching of upstroke of the R wave in I, L or V6) is more common in patients without MI, and its specificity and sensitivity are not altered by axis. Sensitivity of notching in 2, 3, F is too low to be clinically useful. Q 2, 3, F indicates only left axis; predictive accuracy for MI is high (100%) only for normal axis where sensitivity is low (3%). (5) Q 1, L, V6 is no more frequent with MI than without, but if MI is present it is more common in anterior than inferior infarction. Specificity and predictive accuracy are too low to be clinically useful as indicators of MI.

Adolescent↗
PubMed1986

Amiodarone: correlation of early and late electrophysiologic studies with outcome.

Twenty-nine patients with recurrent sustained ventricular tachycardia (VT) or cardiac arrest underwent baseline, early (after 2 weeks of therapy) and late (after 5 months, mean) electrophysiologic studies during oral amiodarone therapy. Inducible sustained VT was present in all patients at baseline study, in 21 of 22 at early and in 26 of 29 at late study. The cycle length of induced VT increased from 263 +/- 60 msec at baseline study to 305 +/- 58 msec at early follow-up study and to 318 +/- 64 msec at late study (p less than .05 = baseline vs late study). The ventricular effective refractory period increased from 237 +/- 22 msec at the baseline study to 253 +/- 26 msec at early and to 268 +/- 24 msec at late study (p less than 0.05 baseline vs early, baseline vs late and early vs late study). Twenty-four patients had no recurrent VT or cardiac arrest on amiodarone (group 1). Five patients had recurrent arrhythmia (group 2). In group 1, the ventricular effective refractory period increased by 39 +/- 19 msec, but in group 2 decreased by 4 +/- 27 from baseline to late follow-up study (p less than 0.05). Similarly, in group 1 the cycle length of induced VT increased by a mean of 75 +/- 56 msec but decreased in group 2 by a mean of 11 +/- 81 msec from baseline to late follow-up study (p less than 0.05). From the above findings we conclude: Chronic electrophysiologic effects of amiodarone are not completely manifest after 2 weeks of oral therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Analysis of the resetting phenomenon in sustained uniform ventricular tachycardia: incidence and relation to termination.

UNLABELLED: Although the phenomenon of resetting has been studied in several experimental and clinical rhythms, it has not been systematically analyzed in ventricular tachycardia. To define the incidence and determinants of resetting as well as its relation to ventricular tachycardia termination, the response to programmed stimulation was prospectively studied during 78 electrically induced episodes of sustained, uniform ventricular tachycardia (mean cycle length 365 +/- 59 ms) in 53 patients. Single and double ventricular extrastimuli were introduced during 78 and 39 episodes of ventricular tachycardia, respectively. Rapid ventricular pacing was performed during 27 episodes. Resetting occurred in response to single ventricular extrastimuli in 43 (55%) of 78 ventricular tachycardias, to double extrastimuli in 31 (79%) of 39 ventricular tachycardias and to rapid pacing in 23 (85%) of 27 ventricular tachycardias. No ventricular tachycardia characteristic distinguished those tachycardias that were reset from those not reset. Termination of ventricular tachycardia occurred in 7 (9%) of 78 episodes with single ventricular extrastimuli, 14 (36%) of 39 episodes with double ventricular extrastimuli and 13 (48%) of 27 episodes with rapid pacing. Termination was less frequent than resetting with both single (9 versus 55%) and double (36 versus 79%) extrastimuli, as well as rapid pacing (48 versus 85%). Resetting preceded termination in 7 of 7 ventricular tachycardias terminated with single ventricular extrastimuli, 12 of 14 terminated with double ventricular extrastimuli and 9 of 13 terminated by rapid pacing. Ventricular tachycardias that were terminated could not be differentiated from those that were reset without termination. IN CONCLUSION: Resetting with programmed extrastimuli is common in hemodynamically stable sustained ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗
PubMed1986

Left ventricular endocardial activation during right ventricular pacing: effect of underlying heart disease.

Endocardial catheter mapping of the left ventricle was performed in 40 patients during right ventricular pacing to determine the effect of underlying myocardial infarction on endocardial activation. Group I comprised 18 patients without infarction, Group II 12 patients with inferior infarction and Group III 10 patients with anteroseptal infarction. Thirty-nine of the 40 patients had only a single left ventricular breakthrough site located on the midseptum in 33 cases, apical septum in 4 cases and basal septum in 2 cases. The earliest left ventricular local activation time during right ventricular pacing was earlier in Group III (40 +/- 11 ms) than in Group I (55 +/- 17 ms) and Group II (60 +/- 15 ms) (p less than 0.01). Total endocardial activation time was significantly longer in Group III (118 +/- 30 ms) than in Group I (76 +/- 14 ms) and Group II (72 +/- 20 ms) (p less than 0.001). The latest left ventricular site of activation during right ventricular pacing was the inferoposterior base in 14 (77%) of the 18 Group I patients, and 10 (83%) of the 12 Group II patients. The latest site of activation in Group III patients was variable. It is concluded that: left ventricular endocardial activation patterns and conduction times are influenced by the site of previous infarction. Longer total endocardial activation in Group III suggests that specialized conducting tissue in the septal and anterior walls may play an important role in left ventricular activation during right ventricular pacing.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗
PubMed1986

Effects of verapamil and diltiazem on human platelet function.

In this study the antiplatelet properties of two calcium channel blockers, verapamil and diltiazem, were evaluated. In 20 random aspirin-abstaining donors, both diltiazem and verapamil (0.01-10 microM) reduced epinephrine-induced aggregation [46 +/- 6% (SE) inhibition] and demonstrated a dose-dependent inhibition of epinephrine-induced [14C]serotonin release (43 +/- 3% reduction). However, at equimolar concentrations, verapamil was twice as effective. Neither drug altered ADP, collagen, thrombin, or calcium ionophore-induced platelet aggregation or platelet granule secretion. Neither drug prevented formation of thromboxane B2 during secondary aggregation. Verapamil, but not diltiazem, increased the Kd of [3H]yohimbine binding from 2.03 to 46.99 nM without altering the calculated number of binding sites per platelet (124 sites/platelet). Supplemental calcium added to citrated platelet-rich plasma reversed both verapamil and diltiazem-induced inhibition of platelet aggregation. We conclude that, at the concentrations tested, both verapamil and diltiazem are specific inhibitors of epinephrine-induced platelet activation. Clearly, both agents may be acting by preventing epinephrine-induced increases in plasma membrane permeability to calcium. However, the greater potency of verapamil compared with diltiazem with only verapamil binding to alpha2-adrenergic receptors suggests that alpha-blockade represents a significant component of verapamil-induced platelet inhibition.

Benzazepines↗
PubMed1986

Electrocardiographic changes after cardioversion of ventricular arrhythmias.

To evaluate rhythm and QRS-T changes after cardioversion of induced ventricular arrhythmias, 56 patients underwent continuous three-lead and serial 12-lead electrocardiographic monitoring for 15 min after 77 cardioversions. Fifty patients were cardioverted externally and nine internally with an implanted automatic cardioverter/defibrillator. Initial energy for external cardioversion was 200 Wsec in 57 of 64 arrhythmia episodes. Two hundred watt-seconds of energy effectively terminated 41 of 44 episodes of ventricular tachycardia and six of 13 episodes of ventricular fibrillation (p less than .001). Early bradycardia (mean cycle length greater than or equal to 1200 msec during the first 5 sec) occurred after 17 of 64 external and two of 13 internal cardioversions (p = NS) in a total of 16 patients. Bradycardia persisted at 10 sec after cardioversion in nine patients. Early bradycardia was associated with the need for multiple cardioversions to terminate the arrhythmia (six of 10 multiple cardioversions vs 13 of 67 single cardioversions, p less than .05) and the presence of inferior myocardial infarction (eight of 16 patients with vs eight of 40 patients without inferior infarction, p less than .05). Supraventricular tachycardia (cycle length less than or equal to 500 msec) occurred after 19 of 64 external and six of 13 internal cardioversions (p = NS). Nonsustained ventricular tachycardia (4 to 40 beats) was observed after seven external cardioversions, with three episodes lasting 3 sec or more.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗