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M Zehender

Publications and source records attributed to M Zehender.

At least 73 records · Page 4Linked to original sources
PubMed1991

[Arrhythmia and anti-arrhythmia therapy as prognostic risks].

The incidence of sudden death is estimated to be 0.25%/year in the industrialized world. 30 to 40% of patients are known to be at major risk before they succumb sudden death. Etiology is usually coronary heart disease (75%), dilated and hypertensive cardiomyopathy as well as valvular disease. 75% of patients dying suddenly die from ventricular fibrillation. The most common mechanism of sudden cardiac death in heart failure is sustained ventricular tachycardia deteriorating into ventricular fibrillation, the initiating factors being single ventricular beats, ventricular pairs or nonsustained ventricular tachycardia (trigger mechanism). At least 50% of patients dying during Holter monitoring have been on antiarrhythmic treatment during the time of sudden death and this percentage is increased to 70% in patients dying from torsade de pointes ventricular tachycardia. The question that has arisen is whether suppression of such arrhythmias by antiarrhythmic agents will reduce the incidence of sudden cardiac death. Unfortunately, the patient group at highest risk - low ventricular ejection fraction and high incidence of nonsustained ventricular tachycardia episodes during 24 hour-monitoring and thus, the group most in need of arrhythmia suppression - has the lowest responder rate as well as the highest incidence of serious toxicity. Until the suppression of those arrhythmias by antiarrhythmic agents is demonstrated to improve prognosis in this patient group, routine use of antiarrhythmic agents cannot be recommended in this patient population.

Anti-Arrhythmia Agents↗
PubMed1990

Lidocaine in the early phase of acute myocardial infarction: the controversy over prophylactic or selective use.

In acute myocardial infarction, lidocaine is considered the drug of choice for the treatment of malignant ventricular arrhythmias. While initially a so-called "selective" treatment strategy prevailed, in which lidocaine was administered only after the onset of certain "warning arrhythmias," the prophylactic use of lidocaine in acute myocardial infarction has been gaining wider usage in intravenous and intramuscular application in recent years. Both therapeutic applications have been found to be problematic of late, which has led to increasingly restrictive use of lidocaine. While in selective treatment forms, the definition and prompt recognition of the so-called warning arrhythmias created especially acute problems, the prophylactic therapeutic use is problematic due to the occurrence of sometimes serious side effects, which is to be expected as the size of the collective being treated increases. Both treatment forms also appear limited by the narrow preventive efficacy of lidocaine against malignant ventricular arrhythmias, especially against ventricular fibrillation. The current therapeutic recommendation for lidocaine in acute myocardial infarction should be limited to patients presenting with very frequent and complex ventricular arrhythmias, especially when these are elicited by an R-on-T phenomenon. Side effects and other therapeutic problems encountered when the therapeutic modality is switched or adjusted can be greatly reduced by careful dosing and selection of the optimal combination substances.

Acute Disease↗
PubMed1990

ECG variants and cardiac arrhythmias in athletes: clinical relevance and prognostic importance.

These findings permit the following conclusions on cardiac changes induced by high-performance sports and high levels of training. Sinus bradycardia and AV block can frequently be observed in athletes, but they do not require attention as long as they are asymptomatic or do not produce pauses exceeding 4 seconds. Persistent rather than transient second-degree AV block or Mobitz second- or third-degree AV block is an extremely unusual finding even in athletes and should be considered a sign of organic lesions until proved otherwise. Supraventricular and AV node ectopic beats are not more frequent in athletes than in the general population except for atrial fibrillation. WPW syndrome is of particular importance, since rapid conduction to the ventricle via the accessory AV pathway is possible, especially if there is a tendency toward atrial fibrillation. Likewise caution is required in athletes with hypertrophic cardiomyopathy. Here hemodynamic deterioration must be anticipated with the occurrence of supraventricular tachycardia. Simple ventricular arrhythmias occur among athletes with the same frequency as in the general population, but they usually disappear with exercise. The occurrence of complex ventricular forms of arrhythmia should always prompt cardiologic examination in search of underlying cardiac disease, particularly hypertrophic or dilated cardiomyopathy. The presence of ventricular arrhythmias without evidence of underlying heart disease does not indicate a special or increased risk of sudden cardiac death. A higher incidence of right and/or left ventricular hypertrophy, exercise-reversible ST elevation, and exercise-reversible changes in T waves (T negativity, sharp and/or excessive T waves) can be considered physiologic changes in the ECGs of athletes. These changes correlate closely with the type of sports activity and degree of training and are reversible when the activity is stopped. Horizontal ST segment depression are by contrast very rare in athletes and should always be clarified by cardiologic examination. Exercise-induced sudden cardiac death in athletes is unusual without preexisting heart disease. The cause of sudden cardiac death among athletes less than 40 years of age can be predominantely ascribed to congenital heart diseases (such as hypertrophic cardiomyopathy or coronary anomalies). In athletes more than 40 years of age and with increasing age, coronary heart disease is the most frequent autopsy finding. A corresponding risk stratification should take these partial dangers into account.

Arrhythmias, Cardiac↗
PubMed1990

Beta-blocking agents vs. antiarrhythmic interventions in heart failure complicated by arrhythmias.

Approximately 40-50% of the patients with end-stage cardiac failure (either ischemic or nonischemic) die suddenly and unexpectedly, most probably from ventricular fibrillation. It is unclear whether the complex ventricular arrhythmias observed in large numbers of these patients were related to the mode of death. Theoretically, it seems quite reasonable to attempt to suppress the development of life-threatening ventricular arrhythmias (e.g., sustained ventricular tachycardia or ventricular fibrillation) in those patients. If antiarrhythmic drug therapy is ineffective, alternative antiarrhythmic interventions (antiarrhythmic surgery or implantation of an automatic implantable cardioverter defibrillator) should be considered. In patients with so-called potentially malignant ventricular arrhythmias (e.g., nonsustained ventricular tachycardia), antiarrhythmic drug therapy remains controversial as presently there is no definitive proof that this therapy prolongs life or reduces the incidence of sudden cardiac death. In patients with end-stage cardiac failure, beta-blockade can result in a decrease in resting tachycardia, improvement in clinical heart failure symptoms, and increase in work load capacity. It remains controversial whether treatment with these agents can also improve prognosis and prevent sudden cardiac death. Therefore, at this time, only patients in the earlier stages of this clinical syndrome and with clinical signs of markedly increased sympathetic tone can be treated with low doses of beta-blockers.

Adrenergic beta-Antagonists↗
PubMed1990

Incidence and clinical relevance of QT prolongation caused by the new selective serotonin antagonist ketanserin. Multicenter Ketanserin Research Group.

Efficacy and safety of ketanserin was studied prospectively in a randomized and double-blind trial involving 221 patients treated for hypertension and/or coronary artery disease. Since ketanserin has been suggested to cause QTc prolongation, we investigated the incidence and severity of this effect, as well as its influence on the incidence of malignant ventricular arrhythmias during Holter monitoring. After a 1-week run-in-period, all patients were examined, measuring blood pressure, electrocardiogram (ECG) and 24-hour Holter ECG. Two thirds of the patients (n = 147) were then randomized to ketanserin, 1 week 20 mg b.i.d. followed by 3 weeks 40 mg b.i.d.; one third of the patients (n = 74) received placebo b.i.d. for 4 weeks. After 4 weeks of treatment, blood pressure, ECG and 24-hour Holter ECG were performed. In hypertensive patients, ketanserin resulted in a significant reduction of systolic (mean reduction: -17 +/- 2 mm Hg; p less than 0.0001) and diastolic blood pressure (-12 +/- 1 mm Hg; p less than 0.0001) as compared to baseline, and to the placebo group (p less than 0.005 for systolic and diastolic blood pressure). The QTc interval was prolonged with ketanserin (mean value: 400 to 418 ms; p less than 0.01) but not with placebo (399 vs. 402 ms). In the ketanserin group 30% of patients and in the placebo group 8% of patients had QTc prolongation greater than 30 ms (p less than 0.01). QTc was not prolonged to greater than 500 ms in any patient. During Holter monitoring 128/147 patients (ketanserin group) and 61/74 patients (placebo group) had ventricular premature beats; in 42 (ketanserin group) and 13 patients (placebo group) ventricular pairs and tachycardia were documented. Incidence and severity of the ventricular arrhythmias after 4 weeks of treatment were not different between the ketanserin and placebo groups. No sustained ventricular tachycardia occurred in any patient after ketanserin treatment. Thus, though ketanserin prolonged QTc in one third of the patients, the drug was not arrhythmogenic or antiarrhythmic.

Aged↗
PubMed1990

[How are tachycardic cardiac arrhythmias modified by therapy of congestive heart failure?].

Previous studies have demonstrated the high prevalence of frequent and complex ventricular arrhythmias in patients with severe congestive heart failure. It has been claimed that these arrhythmias are independent risk factors of prognosis. Moreover in severely depressed left ventricular function frequent and repetitive arrhythmias may deteriorate the hemodynamic situation. Recent clinical studies have drawn increasing attention to the possibility that the desired therapeutic effect of Class I antiarrhythmic agents may be complicated by their ability to aggravate the arrhythmia or to provoke new arrhythmias. These "proarrhythmical effects" were more frequent in patients with life-threatening arrhythmias and in those with severely depressed left ventricular function. Prevention trials with Class I antiarrhythmic agents have failed to show beneficial effects on the arrhythmia profile and on the prognosis of those patients. On the other hand, it is now well recognized that the incidence of cardiac death can be reduced by the use of ACE-inhibitors in this patient population. Accordingly, there is evidence of a reduced incidence of complex ventricular arrhythmias during treatment with these drugs in some of the patients with congestive heart failure. The influence of digitalis on the arrhythmia profile and the cardiac mortality in these patients is still a matter of debate. On the other hand, there is evidence that newer positive inotropic agents such as phosphodiesterase-inhibitors rather increase the number of arrhythmias and the prevalence of sudden cardiac death in this patient population.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1990

[Predictive value of programmed electrostimulation in patients with spontaneous idiopathic ventricular tachycardia].

In contrast to patients with organic heart disease, there are only few data available on the incidence and type of inducible arrhythmias during programmed electrical stimulation (PES) in patients with spontaneous ventricular tachycardia (VT) but without evidence of underlying heart disease. Additionally, no consensus has been achieved in these patients on the most appropriate stimulation protocol required to reproduce the clinical arrhythmia. In a prospective study we analyzed in 40 patients without idiopathic VT, incidence and type of inducible VT, as well as the mode of initiation during a right ventricular PES protocol with 1-2 (part I) and three extrastimuli (part II). Twelve patients had spontaneous sustained monomorphic VT (group A), 28 patients were studied with spontaneous non-sustained VT (group B). During PES, a non-sustained polymorphic VT was induced in 3/12 patients (group A, 25%) and in 10/28 patients (group B, 36%); a non-sustained monomorphic VT was induced in 5/12 patients (group A, 41%) and in 4/28 patients (group B, 14%). In all 7/12 patients (59%) of group A with inducible sustained monomorphic VT, the arrhythmia was initiated with 1-2 extrastimuli. In group B, only 2/28 patients (7%) were induced to a sustained monomorphic VT. When the clinical arrhythmia was exercise-related, 5/6 patients (83%) in group A and 7/13 patients (54%) in group B were induced to a VT, while 2/6 patients (33%) in group A and 1/13 (8%) patients in group B were induced to a sustained monomorphic VT. Isoprenaline was not effective to increase the incidence of sustained monomorphic VT.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

Incidence and clinical relevance of QT prolongation caused by the new selective serotonin antagonist ketanserin.

Efficacy and safety of ketanserin were studied prospectively in a randomized, double-blind trial involving 221 patients treated for hypertension or coronary artery disease, or both. Since ketanserin has been suggested to cause QTc prolongation, the incidence and severity of this effect were investigated, as was the incidence of malignant ventricular arrhythmias during Holter monitoring. After a 1-week run-in period, all patients were examined: blood pressure was measured and electrocardiograms and 24-hour Holter electrocardiograms were obtained. Two thirds of the patients (n = 147) were then randomized to receive ketanserin for 1 week (20 mg twice daily) followed by 3 weeks of 40 mg twice daily; one third of the patients (n = 74) received placebo (twice daily) for 4 weeks. After 4 weeks of treatment, blood pressure, electrocardiograms and 24-hour Holter electrocardiograms were repeated. In hypertensive patients, ketanserin significantly reduced systolic (mean reduction 17 +/- 2 mm Hg, p less than 0.0001) and diastolic blood pressure (12 +/- 1 mm Hg, p less than 0.0001) compared to baseline, and to the placebo group (p less than 0.005 for systolic and diastolic blood pressure). The QTc interval was prolonged with ketanserin (mean 400 to 418 ms, p less than 0.01) but not with placebo (399 vs 402 ms). In the ketanserin group 30% of patients and in the placebo group 8% of patients had QTc prolongation greater than 30 ms (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

Comparison of twice daily with thrice daily administered encainide for benign or potentially lethal ventricular arrhythmias.

The antiarrhythmic efficacy of encainide administered 2 (group A) or 3 times daily (group B) was evaluated in a randomized, placebo-controlled trial involving 101 patients with benign or potentially malignant ventricular arrhythmias. In group A, encainide was titrated at dosages of 35, 50 and 75 mg twice daily and in group B at dosages of 25, 35 and 50 mg 3 times daily. Drug efficacy, as judged by repeated ambulatory monitoring, was defined as greater than 75% reduction in ventricular premature complexes combined with a greater than 90% abolition of pairs and runs of nonsustained ventricular tachycardia. In group A, 27 of 52 patients (52%) had their arrhythmia suppressed by the drug compared with 34 of 49 (69%) in group B (difference not significant). There was a trend toward better arrhythmia control in group B if a total daily dose of greater than 100 mg was necessary for arrhythmia suppression. Side effects were frequent in both groups (24 vs 28%, difference not significant). Thus, encainide administered twice daily effectively suppresses ventricular arrhythmias in this patient population.

Adult↗
PubMed1989

Antiarrhythmic efficacy and tolerance of oral propafenone in patients with frequent ventricular arrhythmias: experience of a multicentre study.

In a multicentre study efficacy and safety of propafenone 450 mg day-1 and 750 mg day-1 was studied in 97 patients with frequent ventricular premature beats (VPB greater than 30 h-1). 70 patients suffered from organic heart disease, in 27 patients no organic heart disease was present during an initial work-up. After a 1-week washout period, all patients underwent 24 h Holter monitoring. Patients were then treated by propafenone 450 mg day-1 and controlled for 24 h Holter, ECG, blood pressure, blood chemistry and side-effects after 1 week of treatment. At this time, 35 patients were responders (reduction of VPB greater than 84%, of ventricular pairs greater than 90% and of ventricular tachycardia 100%). The mean reduction of VPB in all patients was 60%, of ventricular pairs 88% and of ventricular tachycardia 100%. When treatment was continued for 3 weeks 20/35 patients (56%) were still responders. The mean reduction of VPB was 83%. In 42 non-responders to 450 mg day-1 the dose was increased to 750 mg day-1. Of these patients, 17 (41%) became responders after 3 weeks of treatment; the mean reduction of VPB increased from 17% (first week, 450 mg day-1) to 63% (750 mg day-1). Ventricular pairs were reduced by 80%, ventricular tachycardia by 100%. Side-effects occurred in 11/97 patients and limited therapy in six patients. The most frequent complaints were dryness of the mouth, nausea, tiredness, headache and gastrointestinal upset. In conclusion, propafenone in a dose of 450-750 mg day-1 seems to be an effective and safe antiarrhythmic agent in the majority of patients.

Administration, Oral↗
PubMed1989

[Validation of a discontinuously recording, digital long-term ECG system (Siemens-Sirecust 802/850) using a single beat analysis].

Using beat-to-beat analysis we studied the annotation of 44 data-bases of the Massachusetts Institute of Technology (MIT) in comparison to the classification performed by a new microprocessor of a 24-h-ambulatory electrocardiographic device, which is based on real-time analysis and a solid-state ECG documentation. QRS detection was performed with an accuracy of 99%. Sensitivity and positive predictive accuracy were 70% and 87% for supraventricular ectopy. Using a fixed prematurity index of 80%, ventricular ectopy with a total of 7,845 beats was identified with a sensitivity of 64% and a positive predictive accuracy of 97%. With the additional consideration of late premature ventricular beats (PVB) sensitivity increased to 91% with a positive predictive accuracy of 96%. A sensitivity of more than 80% for singular PVB was achieved in 28/33 databases (85%), a similar positive accuracy was achieved in 27/33 databases (82%). Altogether, ventricular pairs and ventricular tachycardia resulted in a sensitivity of 83% and 76%, respectively, and in a positive predictive accuracy of 87% and 73%, respectively. Sensitivity exceeded 80% for ventricular pairs in 11/15 databases (77%) and for ventricular tachycardia in 10/14 databases (71%); similar results were observed for the positive predictive accuracy with 11/15 (73%) and 9/14 (64%) databases. In 42/44 databases and in all databases for arrhythmias of Lown class IVA and IVB, Lown classification was determined correctly. The Sirecust-Holter-ECG-system, a new device with real-time analysis and solid-state memory results in an accuracy for singular and complex ventricular arrhythmias, comparable to some of the presently available Holter systems.

Arrhythmias, Cardiac↗
PubMed1989

Electrophysiologic effects of enoximone in patients with congestive heart failure.

The electrophysiologic effects of enoximone were evaluated in 12 patients with idiopathic dilated cardiomyopathy undergoing routine programmed electrical stimulation (PES). Enoximone (1.5 mg/kg for 20 min followed by 0.75 mg/kg for 20 min) significantly shortened the spontaneous sinus cycle length as well as the atrial and ventricular refractory period. Neither during control PES nor during enoximone infusion were sustained ventricular arrhythmias provoked. However, in 5 of 12 patients, there was an increase in the number of repetitive ventricular responses induced by PES during enoximone administration. The observed electrophysiologic changes may be indicators for increased electrical instability of the myocardium in selected patients.

Adult↗
PubMed1989

[Ventricular arrhythmia in silent myocardial ischemia--diagnosis and clinical relevance].

Silent myocardial ischemia and ventricular arrhythmias were known to be independent risk factors in patients with coronary artery disease. This has become more important since the technique of Holter monitoring has been improved and has demonstrated a high incidence of silent myocardial ischemia in the majority of patients with coronary artery disease, as well as a close relation to the occurrence of sudden cardiac death. Unfortunately, prospective data on the interaction of both risk factors are missing. We therefore studied patients undergoing exercise-testing, percutaneous transluminal angioplasty and 24-h-Holter-monitoring to assess such an interaction. During exercise testing the total incidence of ventricular arryhthmias in patients with asymptomatic ST segment depression was 42%; 6% of patients had frequent ventricular arrhythmias, 6% had ventricular pairs, and 1% had ventricular tachycardia. The incidence was similar to patients with symptomatic ST depression, but was 3.2-times higher as compared to patients without ST segment depression. During 103 attempts of percutaneous transluminal angioplasty, in 26 patients ventricular arrhythmias occurred, the incidence of ventricular tachycardia was 1-3%. No difference was observed for symptomatic and asymptomatic attempts. In 36 patients with severe coronary stenosis (greater than 90%) 24-h-Holter-monitoring showed 145 episodes of myocardial ischemia with a total duration of 967 min; two-thirds of episodes were asymptomatic. The incidence was similar in patients with symptomatic and asymptomatic episodes of myocardial ischemia, but 30 to 50-times higher as compared to the interval with ischemia. In summary, episodes of myocardial ischemia have a higher risk of ventricular arrhythmias, however, there is no difference between symptomatic and asymptomatic myocardial ischemia.

Arrhythmias, Cardiac↗
PubMed1988

Mode of death in idiopathic dilated cardiomyopathy: a multivariate analysis of prognostic determinants.

A total of 110 patients with idiopathic dilated cardiomyopathy were followed prospectively for 53 +/- 8 (range 41 to 69) months to determine prognostic factors identifying patients at risk for sudden death or death from congestive heart failure. During the follow-up period 39 patients died, 14 of congestive heart failure and 25 suddenly. The incidence of cardiac death after 1 year was 18%, after 2 years 35%, and after 4 years 39%. Multivariate logistic regression analysis identified four independent prognostic factors: left ventricular ejection fraction, cardiac index, number of ventricular pairs/24 hours, and atrial rhythm (sinus rhythm or atrial fibrillation). With the final model of logistic regression 77 of 88 patients (88%) could be classified correctly as being at risk for death from chronic heart failure or sudden cardiac death. Patients who were likely to die of congestive heart failure were characterized by a markedly impaired left ventricular function (measured in terms of left ventricular ejection fraction, cardiac index, or both) and a low number of pairs/24 hours. The association between frequent complex ventricular arrhythmias and depressed left ventricular function identifies patients who are at risk for sudden death. The presence of atrial fibrillation significantly increases the risk of sudden death and death from congestive heart failure.

Adult↗
PubMed1988

Changes in cycle length at the onset of sustained tachycardias--importance for antitachycardiac pacing.

We analyzed changes in the spontaneous cycle length of sustained tachycardia during the first 100 beats after electrophysiologic initiation of sustained monomorphic ventricular tachycardia (VT), atrioventricular nodal tachycardia (AVNT), and circus movement tachycardia incorporating an accessory pathway (CMT). The mean cycle length of VT was 288 +/- 75 msec, for AVNT this value was 388 +/- 63 msec, and for CMT this value was 348 +/- 76 msec. After initiation, in all three types of tachycardia changes in cycle length of up to +/- 15% to 25% were observed. The changes in cycle length ranged from +12% to -18% in patients with VT, from +17% to -15% in patients with AVNT, and from +17% to -15% in patients with CMT. The mean percentage of changes during the first 100 beats of tachycardia was 7.0 +/- 4.7% (VT), 9.5 +/- 5.4% (AVNT) and 8.3 +/- 5.4% (CMT). Patients with VT and AVNT showed both a constant increase or decrease or alteration of the rate of tachycardia. In no patient with CMT was there a constant decrease in cycle length after initiation. The mean time to achieve the maximal increase or decrease in cycle length was 13 +/- 6 and 11 +/- 9 seconds in patients with VT and 16 +/- 3 and 20 +/- 7 seconds in patients with AVNT. In patients with CMT, the mean time to achieve the maximal increase (10 +/- 7 seconds) or decrease (20 +/- 9 seconds) varied markedly.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗