Search PubMed⌕ Search

Biomedical subjects

M Zehender

Publications and source records attributed to M Zehender.

At least 37 records · Page 2Linked to original sources
PubMed1996

Calcium antagonist drugs in hypertensive patients with angina pectoris.

Arterial hypertension frequently occurs in association with myocardial ischaemia and is an independent and significant risk factor for the development of coronary artery disease (CAD), as is left ventricular hypertrophy due to arterial hypertension. The prevalence of CAD in patients with hypertension is high, while hypertension occurs in approximately 60% of patients with CAD. Myocardial ischaemia occurs both in the presence and absence of CAD, probably as the result of limitation of coronary vasodilator capacity and reduction in coronary flow. This may occur in hypertension due to increased transmural coronary artery resistance, alterations in the vascular wall and endothelial dysfunction. Furthermore, left ventricular hypertrophy itself predisposes the heart towards ischaemia due to an increased diffusion distance between capillaries. When myocardial ischaemia occurs in hypertensive patients, 90% of all episodes are aysmptomatic. The highest incidence of ischaemic episodes appears to occur in treated elderly hypertensive men with inadequate blood pressure control (40%). Calcium antagonists exert a range of beneficial effects in hypertensive patients, including reduction of blood pressure, improvement in myocardial blood flow, regression of left ventricular hypertrophy and cardioprotection in reperfused organs. However, while vasoprotective effects have been demonstrated in animal models, beneficial effects in man are uncertain. Thus, in established coronary atherosclerosis, calcium antagonist treatment has produced only a mild reduction in the appearance of new atherosclerotic lesions.

Angina Pectoris↗
PubMed1996

Adenosine in treating cardiac arrhythmias.

1. Adenosine is an endogenous nucleoside which causes a brief blockade of the AV nodal conduction pathway following intravenous administration. 2. Such a brief AV block can be used therapeutically for reliable termination of AV nodal re-entry tachycardia and WPW re-entry tachycardia. It can also be used for demasking atrial activity in rapid suspected supraventricular tachycardia with a broad QRS complex or a Delta wave, not present during sinus rhythm with normal AV node conduction, indicating the presence of a hidden WPW syndrome. 3. Side effects after adenosine application are frequent, but very transient rarely serious (1-3% of cases, e.g. status asthmaticus, ventricular fibrillation) and therefore require a certain degree of experience with this drug on the part of the treating physician.

Adenosine↗
PubMed1996

Three-year experience with a stylet for lead extraction: a multicenter study.

INTRODUCTION: The extraction of chronically implanted and infected pacemaker and defibrillator leads is an important issue. This article describes the experience gathered between 1990 and 1994 by seven European centers regarding a locking stylet that is uniformly applicable for a wide variety of internal pacing coil diameters. This interventional locking stylet for lead extraction has an outer diameter of 0.4 mm (0.016 inches). The stylet consists of a hollow shaft in which an inner traction wire is embedded. At the tip of the inner traction wire an anchoring mechanism, which can be opened by retraction, is applied. Removal attempts were made for 150 leads, 110 in ventricular and 40 in atrial positions. RESULTS: Complete removal was possible in 122 cases (81%). Partial removal was possible in 18 cases (12%). Failure to remove the lead with the extraction stylet was experienced in 10 cases (7%). In seven patients, the leads were removed by cardiothoracic surgery; 3 defective leads were left in place. There were no serious complications associated with the procedure. None of the patients died. CONCLUSION: The experience with this extraction stylet for lead removal has shown good results. Despite a low complication rate thus far, each case for lead removal should be judged on the individual basis of benefit-to-risk ratio.

Aged↗
PubMed1996

[Magnesium as an anti-arrhythmic therapy principle in supraventricular and ventricular cardiac arrhythmias].

The use of magnesium as an antiarrhythmic agent in ventricular and supraventricular arrhythmias is a matter of an increasing but still controversial discussion during recent years. With regard to the well established importance of magnesium in experimental studies for preserving electrical stability and function of myocardial cells and tissue, the use of magnesium for treating one or the other arrhythmia seems to be a valid concept. In addition, magnesium application represents a physiologic approach, and by this, is simple, cost-effective and safe for the patient. However, when one reviews the available data from controlled studies on the antiarrhythmic effects of magnesium, there are only a few types of cardiac arrhythmias, such as torsade de pointes, digitalis-induced ventricular arrhythmias and ventricular arrhythmias occurring in the presence of heart failure or during the perioperative state, in which the antiarrhythmic benefit of magnesium has been shown and/or established. Particularly in patients with one of these types of cardiac arrhythmias, however, it should be realized that preventing the patient from a magnesium deficit is the first, and the application of magnesium the second best strategy to keep the patient free from cardiac arrhythmias.

Animals↗
PubMed1996

[Value of beta-blocker therapy in treatment of coronary heart disease and sudden cardiac death with special reference to carvedilol].

Beta-blocking agents are well established in the treatment of patients with coronary artery disease. Synergistic effects on mortality, myocardial ischemia, the risk for myocardial (re-)infarction and, as most recently shown, on sudden cardiac death form the basis for the convincing prognostic impact of these agents. The present paper is directed to summarize the clinical evidence for the therapeutic benefit of beta-blocking agents in post-infarction patients, to characterize subgroups of patients who will benefit most from such a therapeutic intervention and to discuss the present impact of newer beta-blocking agents, such as carvedilol which beside its effects on beta-1 and beta-2 receptors exerts potent vasodilating properties via an alpha-1 receptor blockade.

Adrenergic beta-Antagonists↗
PubMed1995

Prevalence, characteristics, and risk stratification of electrocardiographic and symptomatic silence of myocardial ischemia despite scintigraphically evidenced ischemia in symptomatic patients presenting with severe coronary artery stenosis.

Symptoms of angina pectoris and transient ST-segment depression are most commonly used to evidence acute myocardial ischemia during exercise testing. However, the diagnostic accuracy of either or both criteria in relation to clinical characteristics and the patient's exercise response has been a subject of controversy. The prevalence and severity of symptoms of angina pectoris and/or ST-segment depression were studied prospectively in 147 consecutive patients with a history of daily angina pectoris, scintigraphic evidence of exercise-induced myocardial ischemia, and coronary artery stenosis > 75%. Logistic regression analysis was applied to determine absence of any or both criteria by the clinical characteristics or exercise response of the patient. During exercise testing, ST-segment response failed to prove scintigraphically evidenced myocardial ischemia in 14/147 patients (10%) and 35/147 patients (24%) when ST-segment depression > or = 0.1 in either > or = 1 or > or = 2 ECG leads was chosen. Symptoms of angina pectoris were found to be absent in 69/147 patients (47%). Only 58 patients (40%) suffered from angina and met the ECG criterion at the time of scintigraphic myocardial ischemia. Absence of ST-segment depression was best predicted by clinical variables such as large myocardial infarction (increase: 2.6 times, p = 0.007), number of stenoses < or = 2 (2.0 times, p = 0.023), and presence of diabetes mellitus (4.3 times, p = 0.035). Painless myocardial ischemia was determined by blood response to exercising. Thus, a double product > 23 increased the risk of painless myocardial ischemia by 1.5 times (p = 0.017).(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗
PubMed1995

Ventricular tachyarrhythmias, myocardial ischemia, and sudden cardiac death in patients with hypertensive heart disease.

Hypertensive heart disease is increasingly considered to be a strong and independent risk factor for sudden cardiac death. Ventricular tachyarrhythmias in these patients are common and mainly the result of electrophysiologic abnormalities and increased electrical vulnerability of the hypertrophic myocardium. However, proarrhythmia in the hypertrophic heart often is facilitated and aggravated by electrolyte disturbances, the sympathoadrenergic tone, transient blood pressure crisis, and especially by the occurrence of myocardial ischemia. Myocardial ischemia in the setting of hypertensive heart disease may result from stenotic lesions in large and/or small coronary artery vessels and, in the absence of both, will result from the altered cellular oxygen supply and consumption in the hypertrophic myocardium. Recent studies have shown that acute and transient myocardial ischemia are common in many hypertensives, often fail to be symptomatic, and that the dynamic interaction of left ventricular hypertrophy, transient myocardial ischemia, and ventricular tachyarrhythmias may provide a crucial link for the high incidence of sudden cardiac death in patients with hypertensive heart disease.

Antihypertensive Agents↗
PubMed1995

Clinical evidence for the fatal interaction of ventricular tachyarrhythmias, myocardial ischemia and sudden cardiac death.

During recent years, experimental data have collected convincing evidence for the fatal interaction of myocardial ischemia, ventricular tachyarrhythmias, and sudden cardiac death. In the clinical setting, data reporting on the daily relevance of such a fatal interaction lacked until recently. However, there is now increasing evidence from autoptic studies, from the evaluation of patients who survived one episode of sudden cardiac death, from the follow-up of these patients when treated or not by revascularization therapy and/or an implantable cardioverter-defibrillator and, most recently, from studies in patients with stable and especially unstable angina pectoris suffering from Holter-documented ischemic proarrhythmia, that acute and transient myocardial ischemia play an important role for the initiation as well as the aggravation of ventricular tachyarrhythmias and out-of-hospital sudden cardiac death. The present work is directed to summarize our clinical knowledge on this topic and to indicate that preventive strategies for myocardial ischemia are the "antiarrhythmic" of choice in patients with severe coronary artery disease and evidence for ischemic proarrhythmia.

Coronary Disease↗
PubMed1994

[Acute right ventricular myocardial infarct. New diagnostic and therapeutic approaches in a prognostically unfavorable disease picture].

BACKGROUND: Acute inferior myocardial infarction frequently involves the right ventricle (RV). However, very little is known on the prognostic impact of RV involvement in the in-hospital and longterm course, as well as on reliable diagnostic strategies to identify RV infarction early after admission. PATIENTS AND METHODS: In 200 consecutive patients with acute inferior myocardial infarction, we assessed on admission the prevalence and diagnostic accuracy of ST elevation in lead V4R to determine RV involvement, as well as its prognostic implications for in-hospital complications, early and late mortality and the benefit of thrombolytic therapy. Follow-up period was one to six years (mean +/- SD, 37 +/- 12 months). RESULTS: In-hospital mortality after inferior myocardial infarction was 19%, major complications occurred in 47% of patients. Presence of ST-segment elevation in V4R in 107 patients (54%) was highly predictive of RV infarction (sensitivity: 88%, specificity: 78%, diagnostic efficiency: 83%) and increased the in-hospital mortality rate from 6% to 31% (p < 0.0001) and major in-hospital complications from 28% to 64% (p < 0.0001). Cox regression analysis showed ST elevation in V4R to be independent of and superior to all other clinical variables available at the time of admission (additional risk for in-hospital mortality: 7.7; for major complications: 4.7). Thrombolysis was associated with a reduced mortality (3.7 times, p < 0.0005) and complication rate (2.4 times, p < 0.0001) only in patients with RV infarction. Post-hospital course was similar in patients with and without RV infarction. CONCLUSIONS: RV involvement during acute inferior myocardial infarction, accurately diagnosed by ST-segment elevation in V4R, is a strong, independent parameter for mortality and major in-hospital complications and may help to identify patients who will benefit most from thrombolytic therapy. Electrocardiographic assessment of RV infarction should be routinely performed in all patients admitted with acute inferior myocardial infarction.

Aged↗
PubMed1994

Torsade de pointes complicating drug treatment of low-malignant forms of arrhythmia: four cases reports.

In patients with malignant ventricular arrhythmias, antiarrhythmic therapy is known to carry a substantial risk of proarrhythmia. This risk is usually considered to be low when supraventricular arrhythmias or benign ventricular arrhythmias are considered. We were able to collect data on four patients without a history of life-threatening arrhythmias, in whom antiarrhythmic therapy was used and resulted in documented ventricular fibrillation or torsade de pointes. In Cases No. 1 and 2, atrial fibrillation was treated with either quinidine or quinidine and sotalol in combination. In both patients Holter monitoring, 4-12 h after conversion to sinus rhythm, documented the spontaneous occurrence of torsade de pointes degenerating into ventricular fibrillation and requiring DC shock for termination. In Case No. 3, atrial fibrillation was treated with sotalol and amiodarone for 2 months when incessant episodes of torsade de pointes were documented. In Case No. 4, frequent but unsustained ventricular arrhythmias were treated with amiodarone in a patient suffering dilative cardiomyopathy. After 6 days of treatment at a heart rate of 54 beats/min, a marked QT increase was associated with the occurrence of repetitive episodes of polymorphic ventricular tachycardia degenerating into ventricular fibrillation. None of the patients presented significant electrolyte abnormalities in the laboratory. A pathologic increase of the QTc-time was documented in Cases No. 1, 3, and 4. In all patients antiarrhythmic therapy was withdrawn after the proarrhythmic event and the patient became free of malignant tachyarrhythmias. Antiarrhythmic therapy also carries a considerable risk of proarrhythmia when "benign" cardiac arrhythmias are treated. The risk seems to be lower than in patients with malignant arrhythmias, however it includes the occurrence of lethal tachyarrhythmias. Special attention should be paid to the selection of antiarrhythmic agents when used in combination.

Aged↗
PubMed1994

Continuous monitoring of acute myocardial ischemia by the implantable cardioverter defibrillator.

The present generation of implantable cardioverter defibrillators (ICDs) provides a very effective device for monitoring and treating life-threatening ventricular tachyarrhythmia. Patients at risk of sudden cardiac death who are directed to this form of treatment usually have severe coronary artery disease, previous myocardial infarction, and low ejection fraction. Progression of the underlying heart disease predisposes these patients to subsequent ischemic events, including symptomatic and asymptomatic myocardial ischemia and reinfarction, which carry a substantial risk of fatal ventricular proarrhythmia. Multipolar lead configurations presently available in the ICD appear to be effective in assessing acute myocardial ischemia as induced by exercise testing or transient coronary artery occlusion. Continuous monitoring of myocardial ischemia (COMONI) by a sophisticated, multimodal ICD appears to be feasible, may offer the means to closely supervise progression and various complications of the underlying heart disease, and may help to guide automatic or interactive antiischemic treatment.

Algorithms↗
PubMed1994

Eligibility for and benefit of thrombolytic therapy in inferior myocardial infarction: focus on the prognostic importance of right ventricular infarction.

OBJECTIVES: This study was undertaken to determine eligibility for and benefit of thrombolytic therapy in patients with acute inferior myocardial infarction with or without right ventricular involvement. BACKGROUND: Right ventricular involvement commonly complicates acute inferior myocardial infarction and is considered to have prognostic relevance. We hypothesized that the presence of right ventricular infarction, diagnosed early by ST segment elevation in the right precordial lead (V4R), may be of clinical importance in identifying patients who will benefit most from thrombolytic therapy. METHODS: We studied 200 consecutive patients with acute inferior myocardial infarction to assess the prognostic impact of right ventricular infarction in those considered eligible or ineligible for reperfusion therapy. Prognostic analyses were based on the in-hospital period and a 1- to 6-year follow-up (mean [+/- SD] 37 +/- 12 months). RESULTS: ST segment elevation in lead V4R was a reliable marker of right ventricular infarction (sensitivity 88%, specificity 78%, diagnostic efficiency 83%) in 107 patients (54%) with inferior myocardial infarction. Seventy-one eligible patients (36%) received thrombolytic therapy and had a lower mortality (8% [6 of 71]) and complication (31% [22 of 71]) rate than ineligible patients (mortality rate 25% [32 of 129], p < 0.01; complication rate 56% [72 of 129], p < 0.01). However, the overall benefit of thrombolysis was restricted to patients with right ventricular infarction complicating acute inferior myocardial infarction (with vs. without thrombolysis, respectively: mortality rate 10% vs. 42%, p < 0.005; complication rate 34% vs. 54%, p < 0.05). In the absence of right ventricular infarction, no difference was observed in the mortality (7% vs. 6%, p = NS) and major in-hospital complication (27% vs. 29%, p = NS) rates, whether or not the patient underwent thrombolytic therapy. Posthospital course over 37 +/- 12 months was not different in patients with and without right ventricular infarction but was best in all patients considered for reperfusion therapy. CONCLUSIONS: During acute inferior myocardial infarction, the right precordial electrocardiogram is a simple but promising variable to identify a subgroup of patients with an unfavorable course who will benefit most from thrombolytic therapy.

Aged↗
PubMed1994

Comparison of diagnostic accuracy, time dependency, and prognostic impact of abnormal Q waves, combined electrocardiographic criteria, and ST segment abnormalities in right ventricular infarction.

OBJECTIVE: To determine the diagnostic and prognostic impact of abnormal Q waves in comparison to or in combination with ST segment abnormalities in the right precordial and inferior leads as indicators of right ventricular infarction during the acute phase of inferior myocardial infarction. DESIGN: Prospective study of a consecutive series of 200 patients with acute inferior myocardial infarction with and without right ventricular infarction. SETTING: Department of internal medicine, university clinic. RESULTS: Right ventricular infarction was diagnosed in 106 (57%) out of 187 patients from the results of coronary angiography, technetium pyrophosphate scanning, and measurement of haemodynamic variables or at necropsy, or both. In the acute phase of inferior infarction ST segment elevation > or = 0.1 mV in any of the right precordial leads V4-6R was the most reliable criterion for right ventricular infarction (sensitivity, 89%; specificity, 83%). Abnormal Q waves in the right precordial leads, the most specific criterion (91%) for right ventricular infarction, were superior to ST segment elevation in patients admitted > 12 hours after the onset of symptoms. Both ST segment elevation in leads V4-6R (increase in in hospital mortality, 6.2-times; P < 0.001; major complications, 2.3-times; P < 0.01) and abnormal Q waves (2.3-times, P < 0.05; 1.8-times, P < 0.05) on admission were highly predictive of a worse outcome during the in hospital period. In the presence of inferior myocardial infarction previously proposed combined electrocardiographic criteria were not better diagnostically or prognostically than ST segment abnormalities and abnormal Q waves alone. CONCLUSIONS: During the first 24 hours of inferior myocardial infarction ST segment elevation and abnormal Q waves derived from the right precordial leads are complementary rather than competitive criteria for reliably diagnosing right ventricular infarction, both indicating a worse in hospital course for the patient. In this they are better than any other previously proposed combined electrocardiographic criteria in diagnosing right ventricular infarction. Right precordial leads should be routinely monitored in acute inferior myocardial infarction.

Aged↗
PubMed1994

Drug-induced torsade de pointes. Incidence, management and prevention.

Torsade de pointes is a particular form of polymorphic ventricular tachycardia causing few haemodynamic symptoms, but carries a poor prognosis because of recurrence and sudden death in up to 31% of patients. A wide range of agents have been shown to aggravate and even to cause torsade de pointes by prolonging the QT interval or increasing QT dispersion. For the majority of substances the incidence of torsade de pointes remains unclear, but is of the order of 3 to 15% for a wide range of agents. Elicitation of proarrhythmia by drug-induced QT prolongation is mainly based on increased cellular excitability and/or abnormal dispersion of ventricular repolarisation. Torsade de pointes has been shown to be related to bradycardia-dependent early after-depolarisations and/or increased dispersion of repolarisation. Clinically, patients with predisposing factors prior to medication should be considered at risk of drug-mediated proarrhythmia. Typically, torsade de pointes occurs during the first days of antiarrhythmic therapy. During this phase, QT interval measurement and assessment of the QTc time should be performed frequently. Phases of bradycardia or occurrence of ventricular extra beats with a long coupling interval may be of help to identify patients at high risk of proarrhythmic events. As a first attempt in managing this arrhythmia, magnesium sulphate has been shown to be effective in many patients. In case of recurrence of torsade de pointes, the use of a temporary pacemaker with pacing at about 100 to 120 beats/min is the therapy of choice until the causative agent has been completely eliminated.

Anti-Arrhythmia Agents↗
PubMed1994

[Amiodarone and verapamil/quinidine in treatment of patients with chronic atrial fibrillation].

Rapid, reliable and safe reestablishment of sinus rhythm is the major aim of pharmacologic treatment in patients with chronic atrial fibrillation. The mainstay of therapy in this arrhythmia has been quinidine. More recently, amiodarone was shown in noncomparitive studies to be superior to class IA agents under certain conditions. In 40 patients with atrial fibrillation persisting for 4 weeks up to 2 years, the efficacy and safety of either quinidine and verapamil (days 1 to 3, quinidine 1,500 mg/day; days 4 to 6, quinidine 1,500 mg+verapamil 240 mg/day) or amiodarone therapy (days 1 to 3, amiodarone 1,200 mg/day intravenously; days 4 to 14, amiodarone 800 mg/day orally) were randomly examined. Responders continued on their effective medication for 3 months. Thereafter, all patients were treated with a fixed regimen of quinidine (480 mg/day) plus verapamil (240 mg/day) for up to 2 years. During atrial fibrillation, quinidine reduced mean ventricular cycle length by 40 ms (-5%), quinidine and verapamil increased mean cycle length by 57 ms (8%) and amiodarone by 192 ms (28%, p < 0.01). In addition, quinidine and verapamil had a characteristic "rate-smoothing" effect on atrioventricular conduction during atrial fibrillation. The rhythm was converted to sinus rhythm after quinidine in 5 (25%) of 20 patients and after the combination of quinidine and verapamil in 11 (55%) of 20 patients. Amiodarone restored sinus rhythm in 12 (60%) of 20 patients. Overall, a shorter duration of atrial fibrillation (p < 0.05) and a smaller left atrial size (p < 0.01) were predictive of successful conversion of the arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗