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Biomedical subjects

M Zehender

Publications and source records attributed to M Zehender.

At least 91 records · Page 5Linked to original sources
PubMed1988

Prediction of efficacy and tolerance of oral mexiletine by intravenous lidocaine application.

In a controlled crossover trial, 15 patients with frequent ventricular arrhythmias were treated with lidocaine to predict efficacy and safety of oral mexiletine. After an initial control period, patients received intravenous lidocaine (bolus infusion of 200 mg/20 min followed by 3.6 gm/24 hr and for 7 days oral mexiletine (200 mg four times a day). Efficacy was controlled by 24-hour Holter monitoring (responders = suppression of single premature ventricular beats [PVB] greater than 84% and of complex PVB greater than 90%). After lidocaine, 10 of 15 patients (67%) were responders (mean PVB reduction: 97%). After mexiletine, five of 15 patients (33%) were responders (mean PVB reduction: 81%); efficacy was closely related to the plasma concentration. When efficacy of both agents was compared, lidocaine infusion had a positive predictive value of only 50%; however, the negative predictive value was 100%. Thus in nonresponders to lidocaine, mexiletine is very likely to fail in the suppression of ventricular ectopy.

Administration, Oral↗
PubMed1988

[Diprafenone--comparative study of anti-arrhythmia therapy with propafenone].

Diprafenone is a new antiarrhythmic agent with a dominant local anesthetic action and additional beta-sympathicolytic activity. In a randomized study, we analyzed the antiarrhythmic efficacy and tolerance of diprafenone (450-600 mg/day) in comparison to that of propafenone (450-500 mg/day) in ten patients with frequent and complex ventricular premature beats. After an initial control period, all patients received either diprafenone 450 mg/day or propafenone 450 mg/day for 5 days. In the case of a drug response (VPB suppression greater than 84%, suppression of ventricular pairs greater than 90%, suppression of ventricular tachycardia greater than 100%), after a wash-out period of 7 days patients were treated with the second antiarrhythmic medication for 5 days. In the case of nonresponsiveness, the dose of diprafenone and propafenone was increased to 600 mg/day and treatment continued for a second 5-day period. During the control period and at every drug administration, 24-h-Holter monitoring and ECG were performed, and plasma concentration and side effects were checked. After individual dose titration, 7/10 cases were effectively treated with diprafenone (mean dose: 471 mg; mean VPB suppression: 92%) and 5/10 cases with propafenone (mean dose: 540 mg; mean VPB suppression: 80%). Altogether four patients reported side effects, mainly gastrointestinal, which limited therapy in one patient in each group. Compared to propafenone, diprafenone had a strong effect on AV-nodal and ventricular conduction intervals; however, in no patient was therapy limited by these changes. Thus, also in comparison to propafenone, diprafenone is effective in the treatment of ventricular arrhythmias.

Aged↗
PubMed1988

[Bepridil--electrophysiologic properties of a new calcium antagonist with an anti-arrhythmia effect].

In 12 patients with recurrent pre-syncope or syncope and suspected sick sinus syndrome, the electrophysiologic properties of bepridil were tested using 1-2 extrastimuli during four basic pacing rates. Bepridil was given in a dose of 5 mg/kg body weight over 10 min. It caused no significant changes in sinus cycle length (+5%) and corrected sinus node recovery time during pacing of 100/min (-6%), 120/min (+8%) and 140/min (+4%). The conduction times PQ- (+10%) and QRS-interval (+6%) increased significantly, AH- (+8%) and HV-interval (+5%) were slightly prolonged. Antegrade Wenckebach point increased from 460 to 508 ms (p less than 0.05). The effective refractory period was prolonged in the atrium (+11%, p less than 0.05), the AV-node (+14%, p less than 0.05) and the right ventricle (6-11% at pacing rates 100-140/min, p less than 0.05 for each cycle length). In relation to the pacing rate, QTc-interval increased highly significantly (p less than 0.01) by 16% (sinus rhythm), 12% (100/min), 20% (120/min) and 19% (140/min). After a mean of 5 min after the start of infusion a doubled T-wave was observed in 11/12 patients, persisting during Holter monitoring for several hours without evidence of increased incidence of spontaneous ventricular arrhythmias. During programmed electrical stimulation with 1-2 extrastimuli, no increase in vulnerability of the right ventricle was obvious in any patient.

Adolescent↗
PubMed1987

Programmed electrical stimulation in healed myocardial infarction using a standardized ventricular stimulation protocol.

The diagnostic accuracy of programmed electrical stimulation was prospectively assessed in 111 patients with myocardial infarction (MI) with or without a history of spontaneous ventricular arrhythmias. In 29 patients neither ventricular tachycardia (VT) nor episodes of 10 premature ventricular depolarizations per hour was documented. Fifty patients had documented nonsustained VT and 32 had sustained monomorphic VT. One and 2 extrastimuli (twice diastolic threshold, 2 ms in duration) were given during sinus rhythm and ventricular pacing at 100, 120 and 140 beats/min in the right ventricular apex (part I). When this protocol failed to induce a sustained monomorphic VT, a third extrastimulus was introduced (part II). Repetitive ventricular responses were induced in all patients, and in 15 (14%) polymorphic ventricular arrhythmias requiring DC shock were induced. Incidence of initiation of sustained monomorphic VT and polymorphic ventricular arrhythmias requiring DC shock was related to the clinical arrhythmia and the stimulation protocol. In patients with documented sustained monomorphic VT, a third extrastimulus only increased the incidence of sustained monomorphic VT (68% to 94%), whereas in patients with documented nonsustained VT and without VT the incidence of both polymorphic and monomorphic arrhythmias increased by 7 to 12%. Sustained monomorphic VTs induced in patients without such a history were faster (p less than 0.01), depended on site of MI (p less than 0.05) and were more often preceded by nonsustained polymorphic VT (p less than 0.01) than in patients with documented sustained monomorphic VT.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

[Relation between spontaneous and electrically inducible ventricular arrhythmias in patients with coronary heart disease].

In a prospective study, 267 patients with invasively diagnosed coronary artery disease were studied by programmed electrical stimulation (PES) and induced ventricular arrhythmias were compared to spontaneous arrhythmias occurring during 24 h Holter registration. In 89 patients (33%) no evidence of myocardial infarction was present, 61 patients (23%) were studied for 6 weeks to 3 months, 36 patients (13%) for 3-6 months and 81 patients (31%) for more than 6 months after myocardial infarction. PES was performed in the right ventricular apex with 1 and 2 extrastimuli during pacing with 100, 120 and 140 beats/min. Endpoint of the study was defined by the induction of 4 repetitive ventricular responses (RVR). Within 72 hours after PES a 24 h Holter registration was performed in all patients. During PES, 15 patients (6%) were not inducible for any RVR. Single RVR (1-2) were induced in 146 patients (55%) and 3-5 RVR in 68 patients (25%). Ventricular tachycardia and ventricular fibrillation were induced in 38 patients (14%); 6 patients showed a sustained, monomorphic tachycardia. Altogether, the incidence of RVR was higher when a history of myocardial infarction was present. With increasing time after infarction the incidence of inducible 3-5 RVR remained stable; however, the number of greater than 6 RVR decreased. During Holter registration, 54/255 patients (21%) showed no spontaneous ventricular arrhythmias, 70 patients (28%) had arrhythmias of Lown-class I/II, 84 patients (33%) of Lown-class III. Complex arrhythmias were observed in 47 patients (18%) (Lown-class IVA: 33 patients, IVB: 14 patients).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1987

[Anti-arrhythmia effectiveness and tolerance of retard in comparison with standard mexiletine].

In a controlled randomized cross-over trial, 21 patients with coronary artery disease and frequent ventricular arrhythmias were studied to test the efficacy and tolerance of mexiletine 200 mg t.i.d. in comparison to a released application form of mexiletine perlongettes 360 mg b.i.d. During 24-hour Holter monitoring, all patients but one showed more than 30 ventricular premature beats/h; additionally, in 16 patients, complex ventricular arrhythmias (Lown class IV) were documented. In all patients each medication was given for 5 days. Before treatment and during both medication periods, a 4 days' wash-out period was interposed. Mexiletine and mexiletine perlongettes each resulted in a suppression of ventricular ectopy of more than 84% in 10/21 patients (47%); in two patients the response was different. The mean reduction rate in all patients was 68% for mexiletine and 64% for mexiletine perlongettes. In the responder group, the mean reduction rate amounted to 95% under both medications. Ventricular pairs and tachycardia were reduced by more than 90%. Plasma concentration under mexiletine perlongettes was slightly higher, as compared to the standard form of mexiletine; however, under mexiletine, significant changes of plasma concentration were observed during the day only when the standard form was used. Side effects were observed in 8/21 patients (38% for mexiletine) and in 5/21 patients (24% for mexiletine perlongettes). These were mainly gastrointestinal or neurological, but were mild in all patients and did not necessitate discontinuation of the medication in any patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

[Relation between hemodynamics and ventricular arrhythmia in patients with heart valve diseases].

The incidence and severity of ventricular arrhythmias were compared with hemodynamic findings of cardiac catheterization, in 160 patients with mitral and aortic valve disease. All patients underwent right and left heart catheterization, as well as M-mode and 2D-echocardiography, and 24-hour ambulatory electrocardiographic monitoring. Out of 160 patients, 68 had mitral valve disease and 92 had aortic valve disease. In mitral regurgitation the degree and frequency of ventricular arrhythmias showed a positive correlation to the degree of regurgitation (rs = 0.44, rs = 0.56, respectively) and a negative correlation to left ventricular ejection fraction (rs = -0.49, rs = -0.57) and to cardiac index (rs = 0.48, rs = 0.53). In aortic valve disease the incidence and severity of ventricular arrhythmias were not related to the type of valve lesion, to the transvalvular pressure gradient nor to the degree of regurgitation. In aortic stenosis, the degree of arrhythmia showed a negative correlation to left ventricular ejection fraction (rs = 0.55) and a positive correlation to left ventricular endsystolic volume index (rs = 0.40) and to peak systolic left ventricular wall stress (rs = 0.59). In aortic regurgitation the number of ventricular arrhythmias showed a negative correlation to left ventricular ejection fraction (rs = -0.43) and a positive correlation to left ventricular endsystolic volume index (rs = 0.43) and to peak systolic left ventricular wall stress (rs = 0.37). These data demonstrate that the incidence and severity of ventricular arrhythmias, in patients with aortic valve disease and mitral regurgitation, are strongly associated with the impairment of left ventricular function.

Adult↗
PubMed1986

Electrophysiologic characteristics of ventricular tachycardia or fibrillation in relation to age of myocardial infarction.

Evaluation of ventricular myocardium after the onset of acute myocardial infarction (AMI) suggests that the substrate for ventricular arrhythmias changes as the substrate for ventricular arrhythmias changes as the AMI heals. To determine if the ability of programmed stimulation to initiate ventricular tachycardia (VT) varies according to the interval between AMI and electrophysiologic testing, the clinical and electrophysiologic data of 42 patients with spontaneous sustained VT and 12 patients with ventricular fibrillation (VF) more than 3 days after a single AMI were analyzed. For patients with VT, there were no significant differences in the incidence of initiation of sustained monomorphic VT among those evaluated 1 to 3 weeks (100%), 3 to 8 weeks (75%), 2 to 6 months (100%), 6 to 18 months (80%) or more than 18 months (81%) after AMI, and the mean number of extrastimuli required for initiation did not differ among the groups. Patients evaluated more than 4 weeks after the initial episode of VT had a lower incidence of inducible VT than those studied earlier (14 of 21 [71%] vs 21 of 21 [100%], p less than 0.05), although this appeared to be a result of earlier termination of the stimulation protocol owing to initiation of polymorphic arrhythmias in those studied later. The 14 patients evaluated within 8 weeks of AMI had significantly faster VT rates (mean cycle length 269 +/- 45 ms) than the 28 patients studied later (320 +/- 75 ms, p less than 0.01), possibly because of more out-of-hospital presentations of VT in patients studied later.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1986

Dysrhythmias after direct-current cardioversion.

The success rate of direct-current (DC) countershocks and postshock arrhythmias are of concern for the design of automatic devices. Results of 112 DC shocks for induced ventricular tachycardia/fibrillation (VT/VF) (n = 99) or atrial fibrillation (AF) were analyzed. Clinical and arrhythmia characteristics were related to the success rate of DC shocks as well as postshock arrhythmias. Sixty-one patients were men and 14 were women; mean age was 52 +/- 15 years. Coronary artery disease was present in 56 patients and cardiomyopathy in 4. The other patients had no apparent structural heart disease. The success rate of transchest DC shocks for VT and VF were identical. The first DC shock interrupted 80% of VT and VF episodes. All episodes were terminated by 4 or fewer DC shocks. A single DC shock changed morphologic pattern or rate of 4 episodes of VT. Asystole after VT/VF (1,900 +/- 960 ms) was longer than after atrial fibrillation (1,150 +/- 470 ms, p less than 0.01). VT/VF recurred (within 3 minutes) after 26 of 99 initially successful DC shocks, requiring repeat shocks in 2 cases. Sinus bradycardia (n = 18) or high degree atrioventricular block (n = 11) necessitated rate support pacing in 10 patients. Antiarrhythmic drugs did not prevent postshock tachycardias, but facilitated the development of bradycardias. In conclusion, reliable and continuous analysis of cardiac rhythm after discharge is mandatory to enable automatic devices to correct unsuccessful discharges or recurring VT/VF. In addition, demand pacing capability is desirable to prevent severe bradycardia after DC shocks in patients receiving antiarrhythmic drugs.

Adult↗
PubMed1986

Importance of modes of electrical termination of ventricular tachycardia for the selection of implantable antitachycardia devices.

Different implantable systems for electrical treatment of ventricular arrhythmias are available. Information about mode of termination of ventricular tachycardia (VT) helps to select the most appropriate electrical treatment for drug-resistant VT. During 158 electrophysiologic studies, the mode of termination of 215 episodes of VT was analyzed in 2 groups of patients. Group 1 consisted of 54 patients with documented monomorphic VT and group 2 of 46 patients with other documented or suspected ventricular arrhythmias. Eighty-two patients had coronary heart disease, 8 had other structural heart disease and 10 had idiopathic VT. Termination of VT was attempted using extrastimuli and overdrive pacing; direct-current (DC) shocks were given in case of syncopal VT. During 33 of 96 studies (34%) in group 1, DC shock was required to interrupt VT, compared with 45 of 62 studies (73%) in group 2 (p less than 0.001). This difference was a result of less frequent induction of immediately syncopal VT in group 1 (14 of 129 VTs, vs 40 of 86 in group 2, p less than 0.001). Non-syncopal VT could reliably and safely be terminated by pacing in 61%, irrespective of the clinical arrhythmia. Pacing-induced acceleration of VT occurred in 6% (single extrastimuli) to 36% (over-drive pacing) (mean 26%) of attempts. Subsequent DC shock was required in half of these cases. Immediate collapse after induction of VT was not related to the presence of heart disease, but was related to a combination of VT cycle length (shorter than 260 ms) and left ventricular ejection fraction (less than 40%). Antiarrhythmic drugs reduced the need for DC shock.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

Can potentially significant polymorphic ventricular arrhythmias initiated by programmed stimulation be distinguished from those that are nonspecific?

Polymorphic ventricular arrhythmias (PVAs) initiated by programmed electrical stimulation may be a nonspecific response or evidence of ventricular electrical instability. To determine if PVAs initiated in patients with spontaneous sustained ventricular tachycardia or fibrillation differ from those which are clearly a nonspecific response in structurally normal hearts, the initiation, characteristics, and relationship to ventricular repolarization of PVAs greater than five beats in duration were evaluated in 32 patients without structural heart disease and in 36 patients with spontaneous sustained ventricular arrhythmias more than 9 days after myocardial infarction. Patients received one to four extrastimuli during sinus rhythm and right ventricular pacing. In a comparison with patients who completed the same steps (defined by the basic drive cycle length and number of extrastimuli) in the stimulation protocol, there was no difference in the cumulative risk of initiation of a PVA between the patients with and those without heart disease at any step. This risk was 51% vs 38% for patients who received two or fewer extrastimuli at four basic cycle lengths (p = NS). PVAs were initiated by the same mean number of extrastimuli (2.3 +/- 0.5 vs 2.6 +/- 0.9 p NS) with the same degree of prematurity in both groups. Forty-four percent of the PVAs in the myocardial infarction group had a cycle length greater than 250 msec or a coupling interval of the first tachycardia beat to its initiating stimulus greater than 320 msec as opposed to only one (6%) in the group without heart disease (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Effects of early reperfusion in acute myocardial infarction on arrhythmias induced by programmed stimulation: a prospective, randomized study.

This study compares inducibility of ventricular tachyarrhythmias by programmed electrical stimulation of the heart in patients with myocardial infarction with and without reperfusion after streptokinase therapy. Sixty-two consecutive patients admitted with an acute myocardial infarction were randomized to either combined intravenous and intracoronary streptokinase (streptokinase group) or to standard coronary care unit treatment (control group). Thirty-six of the 62 patients (21 patients from the streptokinase and 15 from the control group) with a first myocardial infarction were studied by programmed ventricular stimulation after a mean of 26 +/- 14 days. No patient had a history of antiarrhythmic drug use or documentation of a ventricular arrhythmia before the initial admission. A sustained ventricular arrhythmia was induced in 10 (48%) of the 21 patients randomized to streptokinase therapy and in all 15 (100%) control patients (p less than 0.001). Sustained monomorphic ventricular tachycardia was induced in 6 (29%) and 10 (67%) patients, respectively (p less than 0.05). To terminate an induced arrhythmia, direct current countershock was required in 33% of patients in the streptokinase group and 73% of patients in the control group (p less than 0.02). Seventeen of the 21 patients treated with streptokinase and no control patient had evidence of early reperfusion 200 +/- 70 minutes after the onset of pain. In comparison with patients without early reperfusion, patients in the reperfused group had a lower maximal serum creatine kinase value (p less than 0.01), a shorter time to peak creatine kinase value (p less than 0.001) and a higher angiographic left ventricular ejection fraction (62 versus 45%, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1986

Ventricular arrhythmias initiated by programmed stimulation in four groups of patients with healed myocardial infarction.

Programmed electrical stimulation of the heart was prospectively used in 160 patients with healed myocardial infarction to study the incidence and characteristics of ventricular arrhythmias induced. Thirty-five patients had neither documented nor suspected ventricular arrhythmias (Group A); 37 patients had documented nonsustained ventricular tachycardia (Group B); 31 patients had been resuscitated from ventricular fibrillation (Group C); and 57 patients had documented sustained monomorphic ventricular tachycardia (Group D). No electrophysiologic differences were found between patients in Group A and Group B, but patients in both groups differed significantly from patients in Group C and Group D. In the last two groups, sustained monomorphic ventricular tachycardia was more frequently induced, the cycle length of the induced ventricular tachycardia was slower and a lesser number of premature stimuli was required for induction. No differences were found in the incidence, rate or mode of induction of nonsustained monomorphic ventricular tachycardia, but nonsustained polymorphic ventricular tachycardia and ventricular fibrillation were more frequently induced in Groups A and B. It is concluded that the substrate for sustained ventricular arrhythmia is present in at least 42% of patients after myocardial infarction. The electrophysiologic characteristics of the substrate for ventricular tachycardia seem to be the major determinant of the clinical occurrence of sustained ventricular arrhythmia. Changes in the electrophysiologic properties of the substrate of ventricular tachycardia, either spontaneously with time or induced by ischemia or antiarrhythmic drugs, can contribute to the clinical occurrence of sustained ventricular arrhythmias in patients with an old myocardial infarction.

Anti-Arrhythmia Agents↗
PubMed1986

Role of programmed electrical stimulation of the heart in the selection and design of implantable units for the treatment of recurrent tachycardia.

The introduction of programmed electrical stimulation of the heart opened up new ways for the diagnosis and treatment of recurrent tachycardias. Programmed stimulation not only allows study of the site of origin and mechanisms of arrhythmias, but also the evaluation of the modes of reproducible initiation and termination of tachycardia and the study of effects of drugs on the tachycardia mechanisms. By analyzing results of invasive and non-invasive programmed stimulation, the most successful pacing modality to reproducibly terminate tachycardia can be identified, but complications of pacing can also be recognized (such as the initiation of other arrhythmias). Careful consideration of the results of programmed electrical stimulation is necessary to select the best implantable unit for a particular patient, and to design or redesign new or already implanted antitachycardia units.

Arrhythmias, Cardiac↗
PubMed1985

Determinants of prognosis in idiopathic dilated cardiomyopathy as determined by programmed electrical stimulation.

The incidence and prognostic significance of electrically induced ventricular arrhythmias were prospectively assessed in 42 patients with idiopathic dilated cardiomyopathy. All patients underwent 24-hour, long-term electrocardiographic (Holter) monitoring and 30 were analyzed by a signal-averaging vectorcardiographic procedure at entry into the study. Their response to programmed electrical stimulation during basic right ventricular pacing was investigated using 1 and 2 ventricular extrastimuli. A monomorphic tachycardia was not induced in any patient. In 36 patients (86%) polymorphic ventricular arrhythmias were initiated. Three or more induced consecutive ventricular premature complexes occurred in 9 patients (21%), nonsustained polymorphic ventricular tachycardia in 2 (4.8%) and ventricular fibrillation in 1 patient (2.4%). There was no association between electrically induced polymorphic ventricular arrhythmias and the degree of impairment of left ventricular function. Furthermore, the incidence of induced ventricular arrhythmias was not related to the Lown grade or to the total number of ventricular premature complexes during Holter monitoring. A late potential was detected by the averaged vectorcardiogram in only 1 of the 30 patients. During follow-up (mean 16 +/- 7 months) 7 patients died, 5 from chronic congestive heart failure and 2 from sudden cardiac death. No patient had an electrically induced arrhythmia of 3 or more ventricular premature complexes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1985

Arrhythmias induced during termination of supraventricular tachycardia.

Pacing is being used frequently for the treatment of drug-resistant, paroxysmal supraventricular tachycardias (SVT). SVT can usually be terminated by pacing, but arrhythmias may be induced which interfere with the safety of antitachycardia pacing. To quantify these pacing-induced arrhythmias, 453 attempts to terminate SVT in 111 patients were analyzed. The patients were 6 to 73 years old (mean 41); 62 were male. Seventy-six patients had SVT using an accessory atrioventricular bypass, and 35 patients had intranodal SVT. Single and then, if required, multiple ventricular and atrial premature beats and overdrive pacing were delivered from the atrium and ventricle. A pacing-induced arrhythmia occurred in 9% of all attempts (34% of patients). Atrial flutter or fibrillation (AF) was the most frequent arrhythmia (in 8% of all attempts and sustained in 75%). Atrial vs ventricular pacing resulted in a 12% vs 2% incidence of AF. AF was unrelated to age, sex, atrial size and SVT type, and was predominantly induced by multiple premature beats. In 6 patients a different SVT and in 2 patients a nonsustained ventricular tachycardia was induced. In 6 patients SVT could only be terminated by initiating another arrhythmia. Thus, AF is frequently induced during attempted pacing termination of SVT. To limit the risk of AF, a single premature beat should preferentially be used to terminate SVT. In 6% of patients, SVT can only be terminated by inducing another arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗