PubMed Health⌕ Search

Biomedical subjects

S H Hohnloser

Publications and source records attributed to S H Hohnloser.

At least 109 records · Page 6Linked to original sources
PubMed1995

[Neurocardiac syncope: pathophysiology, diagnosis, therapy].

The diagnostic work-up and the appropriate therapy of patients with recurrent syncopy represents an often encountered clinical problem. The underlying etiology of a syncopal episode remains not infrequently unknown despite intensive and sometimes costly diagnostic procedures. Particularly in young patients with syncopal attacks, the diagnosis of neurocardiogenic syncope has been established on the basis of normal findings during conventional cardiologic and neurologic work-up. Only since the introduction of the tilt-table test into clinical practice has the clinician had a diagnostic tool to prove the neurocardiogenic etiology of a syncopal episode. It has been demonstrated that this diagnostic method yields a good reproducibility which makes it suitable to assess the efficacy of therapeutic interventions. There have been several therapeutic recommendations according to the multifactorial pathogenesis of neurocardiogenic syncope. Among these, therapy with beta-receptor blocking agents or with theophylline appears to be the most promising treatment modalities. The results obtained in the studies reviewed in the present article have increased our knowledge with respect to the pathogenesis of neurocardiogenic syncope as well as the diagnostic procedures and treatment modalities in patients afflicted with this disorder.

Adrenergic beta-Antagonists↗
PubMed1995

[Sotalol].

Explore the source record for details and available documents.

Arrhythmias, Cardiac↗
PubMed1994

Variability of QT dispersion measurements in the surface electrocardiogram in patients with acute myocardial infarction and in normal subjects.

QT dispersion (defined as maximal QT interval minus minimal QT interval) as assessed on the surface electrocardiogram has been demonstrated to reflect regional inhomogeneity of ventricular repolarization. However, the variability of repeated QT dispersion measurements has not been validated in a prospective study. Thus, the present study is based on the analysis of standard 12-lead surface electrocardiographic (ECG) tracings obtained in 127 persons including 50 subjects without structural heart disease and 77 patients presenting with acute myocardial infarction. RR and QT intervals were measured by means of a digitizer tablet and QT/QTc dispersion was subsequently calculated automatically by PC-based analysis software. Measurements were obtained on 2 separate occasions by the same observer to assess the intraobserver variability. In addition, all tracings were evaluated by a second investigator to determine the interobserver variability. QT dispersion in persons without heart disease averaged 30 +/- 10 ms compared with 56 +/- 24 ms in patients with acute myocardial infarction (p < 0.0001). Patients with infarction who developed ventricular fibrillation within the first 24 hours after admission (11 of 77) had an even larger QT dispersion of 88 +/- 30 ms (p < 0.0001). Repeated measurements of QT dispersion in all 127 subjects revealed a correlation coefficient of 0.91 for both intra- and interobserver variability. Similar results were obtained for repeated determination of QTc dispersion (r = 0.93 and r = 0.90, respectively). When only patients with infarction were considered, correlation coefficients between 0.84 and 0.88 were obtained.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Amiodarone-associated proarrhythmic effects. A review with special reference to torsade de pointes tachycardia.

PURPOSE: To assess the incidence of amiodarone-mediated aggravation of ventricular tachyarrhythmias or the development of new arrhythmias, such as torsade de pointes, in patients with cardiac disease. DATA SOURCES AND STUDY SELECTION: A MEDLINE literature search was done to identify articles published during the last 20 years that presented data on amiodarone-associated proarrhythmic events. The articles were divided into three categories: case reports, uncontrolled retrospective studies, and prospective controlled trials. In addition, articles were identified that examined the effects of amiodarone in patients with previously documented drug-induced torsade de pointes. RESULTS: 65 English-language case reports dealing with torsade de pointes during amiodarone therapy were found in the literature. In many of these cases, other predisposing factors for the development of torsade de pointes were reported. Seventeen studies each reported data from at least 50 patients who were treated with amiodarone for at least 6 months. Of 2878 patients included in these trials, 57 were reported to have a proarrhythmic event while exposed to the drug (an overall incidence of 2%). Torsade de pointes was observed in one third of these patients (an overall incidence of 0.7%). In seven placebo-controlled trials in which the drug was given as monotherapy, amiodarone was not associated with the development of a proarrhythmic event in any patient. Finally, in three reports, 31 patients with previous drug-mediated torsade de pointes were exposed to amiodarone during short- and long-term therapy. In none of these patients did a recurrent episode of torsade de pointes develop, despite the amiodarone-induced prolongation of the QTc interval, which was equivalent to that observed at the time of torsade de pointes during exposure to previous drugs. CONCLUSIONS: Amiodarone appears to be associated with a remarkably low frequency of proarrhythmic events and an incidence of torsade de pointes of less than 1.0%. This low arrhythmogenicity and the negligible negative inotropic effect of the compound constitute properties that make amiodarone particularly useful in treating high-risk patients prone to sudden cardiac death. Its potential to reduce this risk is currently being evaluated in several large prospective trials.

Amiodarone↗
PubMed1994

Sotalol.

Sotalol is a novel antiarrhythmic agent combining beta-adrenergic-antagonist actions with the ability to increase cardiac repolarization and refractoriness. The drug's electrophysiologic and clinical profile is different from that of conventional beta-receptor antagonists. As compared with other antiarrhythmic agents, sotalol prevents recurrences of arrhythmia in a higher proportion of patients, particularly among those presenting with ventricular tachycardia and aborted sudden cardiac death. The net hemodynamic effect of sotalol is the result of a balance between the depressant effects due to beta-receptor blockade and an action that tends to increase contractility. Although initially marketed in the United States for treatment of life-threatening ventricular arrhythmias, sotalol also has demonstrated efficacy in many patients with supraventricular arrhythmias. As with all drugs that prolong the QT interval, the syndrome of torsade de pointes is a serious potential adverse effect.

Action Potentials↗
PubMed1994

Insights into the pathogenesis of sudden cardiac death from analysis of circadian fluctuations of potential triggering factors.

Sudden cardiac death continues to be a poorly understood event in terms of its underlying pathophysiological mechanisms. The observation of a circadian variability in the incidence of this catastrophic event with a prominent peak in the early morning hours provides an opportunity to study triggering factors that may play a causative role in the genesis of sudden cardiac death. As reviewed in this article, there is convincing evidence that transient disturbances in autonomic tone and the resulting consequences may predispose the heart to increased electrical vulnerability. This evidence is based for instance on circadian fluctuations of spontaneous ventricular ectopic activity and transient ischemia, which may serve as trigger factors for the genesis of sustained ventricular tachyarrhythmias. Analysis of heart rate variability provides further evidence of reduced vagal and elevated sympathetic tone during the morning hours particularly in patients with compromised left ventricular function. Diurnal variations in ventricular repolarization as indicated by QT interval changes in the surface ECG also support the concept of triggering factors in the genesis of sudden cardiac death. Therapeutic measures aiming at a reduction in sympathetic input to the heart have been successful in preventing ventricular fibrillation and thus indicate the importance of unbalanced sympathetic tone in patients prone to sudden cardiac death.

Arrhythmias, Cardiac↗
PubMed1994

Indications and limitations of class II and III antiarrhythmic drugs in atrial fibrillation.

In summary, the Class III antiarrhythmic agents amiodarone and sotalol are effective in restoring sinus rhythm in patients with chronic atrial fibrillation with a higher effectiveness of amiodarone. Both agents successfully prevent recurrent episodes of atrial fibrillation after electrical cardioversion and both can control heart rate in persistent atrial fibrillation. Amiodarone appears to be particularly suitable in patients with atrial fibrillation and concomitant congestive heart failure because it lacks clinically relevant negative inotropic activity. Both substances are also effective in controlling ventricular arrhythmias that are frequently present in patients with atrial fibrillation. Finally, both drugs possess antiadrenergic activity, which makes the substances particularly attractive in patients with coronary heart disease as the underlying cause of atrial fibrillation.

Adrenergic beta-Antagonists↗
PubMed1994

Changes in autonomic tone following thrombolytic therapy for acute myocardial infarction: assessment by analysis of heart rate variability.

INTRODUCTION: Little data are available on changes in autonomic tone during the first 24 hours of acute infarction in patients undergoing thrombolytic therapy. Particularly, the association of changes in autonomic tone to reperfusion of the infarct-related artery has not been evaluated in man. Heart rate variability (HRV) is a noninvasive tool to assess cardiac autonomic tone, which carries prognostic information in postinfarction patients. METHODS AND RESULTS: To assess changes in autonomic tone with angiographically assessed success of thrombolysis in patients with acute infarction, the proportion of adjacent RR intervals different by greater than 50 msec (pNN50) was analyzed from 24-hour Holter monitoring initiated before the start of thrombolytic therapy in 103 consecutive patients. Mean heart rate (HR) and pNN50 were available in 95 of 103 patients and were separately analyzed for the first hour after initiation of thrombolysis (reperfusion phase) and the first 24 hours. As assessed by coronary angiography 90 minutes after start of thrombolysis, 74 patients (78%) had successful coronary artery reperfusion. HR averaged 72 +/- 13/min for the first hour in all 95 patients and 74 +/- 13/min for the first 24 hours. The respective values for pNN50 were 11.2% +/- 11.7% for the first hour and 9.7% +/- 9.2% for the first 24 hours. Patients with inferior myocardial infarction (MI) had a lower mean HR of 72 +/- 12/min versus 76 +/- 13/min (P = 0.11) and a higher pNN50 (11.2% +/- 9.8% versus 7.6% +/- 8.3%, P = 0.01) compared to patients with anterior MI. The mean HR correlated weakly with pNN50 (r = -0.33, P < 0.01). For patients with coronary artery patency after 90 minutes, mean HR was 70 +/- 12/min for the first hour compared to 80 +/- 13/min for patients without (P = 0.003). For the first 24 hours, these values were 72 +/- 12/min compared to 80 +/- 14/min (P = 0.02). For the first hour, pNN50 averaged 12.6% +/- 12.4% for patients with successful reperfusion compared to 6.6% +/- 7.3% for patients without (P = 0.024). For the first 24 hours, these values were 9.2% +/- 8.5% compared to 11.5% +/- 11.3% (P = NS). Patients with in-hospital ventricular fibrillation (n = 8) had a higher mean HR throughout the first 24 hours (88 +/- 16/min vs 73 +/- 12/min, P = 0.008) compared to patients with an uneventful course. Additionally, there was a trend toward a lower HRV in patients with ventricular fibrillation. CONCLUSION: Thrombolysis-induced reperfusion of the infarct-related artery results in a higher vagal tone during the early hours of MI as compared to failed reperfusion. This finding is independent from infarct location and associated with a trend toward a lower incidence of ventricular fibrillation during the acute phase of infarction.

Acute Disease↗
PubMed1994

Reflex versus tonic vagal activity as a prognostic parameter in patients with sustained ventricular tachycardia or ventricular fibrillation.

BACKGROUND: The autonomic nervous system has been demonstrated to play a decisive role in the genesis of sudden cardiac death. The loss of protective vagal reflexes, in particular, appears to be associated with an increased incidence of malignant ventricular tachyarrhythmias. Two clinically applicable methods for assessment of cardiac autonomic control have been developed: determination of heart rate variability and evaluation of baroreflex sensitivity. METHODS AND RESULTS: To compare the potential predictive value of both methods, two groups of patients were studied. Group 1 comprised 14 postinfarction patients who had experienced at least one episode of ventricular fibrillation or sustained ventricular tachycardia and who were studied after this event. Group 2 consisted of 14 postinfarction patients without tachyarrhythmic events after their infarct. Both groups were carefully matched with respect to age, sex, infarct location, extent of coronary artery disease, left ventricular ejection fraction, blood pressure, and heart rate at rest. Heart rate variability was assessed from 24-hour Holter recordings, and baroreflex sensitivity was determined by means of the phenylephrine method. Indices of heart rate variability were not significantly different between the two groups (SD of the mean RR interval, 84 +/- 30 milliseconds versus 103 +/- 20 milliseconds; proportion of adjacent RR intervals > 50 milliseconds different, 2.8 +/- 3.2% versus 5.0 +/- 4.1% in group 1 versus 2). Baroreflex sensitivity, however, showed a striking difference: Group 1 patients had a mean value of 1.75 +/- 1.63 ms/mm Hg compared with 9.17 +/- 5.40 ms/mm Hg in group 2 (P = .0002). Eleven of 14 group 1 patients had a baroreflex sensitivity < or = 3.0 ms/mm Hg. By contrast, only 1 of 14 group 2 patients had such a depressed value. CONCLUSIONS: The results of this study indicate that postmyocardial infarction patients who develop life-threatening ventricular tachyarrhythmias, compared with carefully matched postinfarction patients without major arrhythmic episodes, differ strikingly in terms of baroreflex sensitivity but not in terms of heart rate variability. This finding may have implications for the risk stratification of postinfarction patients and may lead to a differential therapeutic strategy based on autonomic testing.

Baroreflex↗
PubMed1994

Coronary atherosclerotic wall thickening and vascular reactivity in humans. Elevated high-density lipoprotein levels ameliorate abnormal vasoconstriction in early atherosclerosis.

BACKGROUND: Abnormal vascular reactivity represents a fundamental disturbance in vascular biology with the development of atherosclerosis. Because endothelial vasodilator function plays a pivotal role in controlling vasomotor tone, we hypothesized that atherosclerotic wall thickening might directly interfere with deficient endothelium-mediated dilation and thereby contribute to the abnormal reactivity of atherosclerotic arteries in vivo. METHODS AND RESULTS: In 26 patients without focal stenoses in the left anterior descending coronary artery, acetylcholine (0.036 to 3.6 micrograms/mL) was infused into the artery to evaluate endothelium-mediated vasodilation. Segmental vasomotor responses to acetylcholine were correlated with the local extent of atherosclerotic wall thickening quantitated by intracoronary ultrasound examination. Seventeen of the patients also underwent cold pressor testing to assess the vasoreactivity to sympathetic activation. The response of coronary artery segments to acetylcholine varied from 35% dilation to 52% constriction and demonstrated a segmental pattern, with dilation and constriction observed in different segments of the same artery. The vasomotor response to acetylcholine was closely correlated with the extent of local atherosclerotic wall thickening (r = -.82, P < .0001). Over the entire range of atherosclerotic wall thickening, segments from patients with elevated high-density lipoprotein (HDL) cholesterol serum levels (> 75th percentile) demonstrated a significantly blunted constrictor response to acetylcholine (P < .01 at the maximal acetylcholine concentration) compared with segments from patients with HDL cholesterol < 75th percentile. The degree of constriction or dilation in response to the acetylcholine infusion correlated with the response to cold pressor testing (r = .75, P < .0001). Again, the cold pressor test-induced constrictor response was significantly (P < .05) blunted in segments from patients with elevated HDL cholesterol serum levels compared with those from patients with HDL cholesterol < 75th percentile despite equal degrees of atherosclerotic wall thickening. CONCLUSIONS: Coronary vasomotor responses to the endothelium-dependent dilator acetylcholine and to sympathetic stimulation by cold pressor test correlate with local atherosclerotic wall thickening. Thus, the degree of abnormal local vascular reactivity is closely related to the extent of atherosclerotic "plaque load" in human epicardial arteries in vivo. Elevated HDL cholesterol serum levels ameliorate abnormal vasoconstriction at any given extent of atherosclerotic wall thickening, suggesting that HDL cholesterol exerts a beneficial effect on abnormal vascular reactivity, a fundamental functional disturbance associated with coronary atherosclerosis.

Acetylcholine↗
PubMed1994

Open infarct artery, late potentials, and other prognostic factors in patients after acute myocardial infarction in the thrombolytic era. A prospective trial.

BACKGROUND: Successful reperfusion of the infarct-related artery in patients with acute myocardial infarction has been shown to reduce in-hospital as well as 1-year mortality. Besides the thrombolysis-induced myocardial salvage, there is increasing evidence that an open infarct-related artery results in increased electrical stability of the heart and that this effect is at least in part responsible for the favorable long-term outcome of these patients. The exact incidence of arrhythmic events during the first year after myocardial infarction and the predictive value of different risk factors for these complications, however, have not been determined in patients in the thrombolytic era. METHODS AND RESULTS: A total of 173 patients with acute myocardial infarction, 51% treated with thrombolysis, were prospectively entered into the study. At the time of hospital discharge, signal-averaged ECG, Holter monitoring, radionuclide angiography, coronary angiography, and levocardiography were performed in all patients. An open infarct-related artery was documented in 136 patients. The overall incidence of late potentials was 24% (41 patients). By multivariate analysis, an occluded infarct-related artery (P = .04) and the presence of regional wall motion abnormalities (P = .02) were the strongest independent predictors for the development of a late potential. Residual ischemia was treated by either percutaneous transluminal coronary angioplasty or surgery in 86 of 173 patients (50%). Seventy percent of the patients received beta-blocker therapy. During a mean follow-up of 12 +/- 5 months, 7 patients died suddenly or had ventricular fibrillation documented, while only 2 developed sustained monomorphic ventricular tachycardia. Overall 1-year mortality was 4.1%. Multivariate analysis revealed only an occluded infarct-related artery as an independent predictor of arrhythmic complications (P = .017). CONCLUSIONS: In patients with acute myocardial infarction treated according to contemporary therapeutic guidelines, with a large proportion of individuals undergoing coronary artery revascularization, a low incidence of arrhythmic events, particularly of ventricular tachycardia, was observed in the first year after the index infarction. The presence or absence of an open infarct-related artery was the strongest independent predictor of these events, whereas other traditional risk factors, such as late potentials, were less helpful in identifying patients prone to sudden death. These findings emphasize the importance of the open artery hypothesis in patients recovering from acute myocardial infarction.

Adult↗
PubMed1994

[Therapy with beta receptor blockers in myocardial infarct].

During the last 10-15 years, a total of 49 prospective, randomized, controlled studies have been performed to evaluate the efficacy and safety of early administered beta-receptor antagonists in patients with acute myocardial infarction. Those trials in which beta-receptor antagonists were administered intravenously followed by oral medication within 72 h after the onset of symptoms reported a significant reduction in early mortality (on average 13%; 95% confidence interval -2% to -25%). The efficacy of beta-receptor antagonists in reducing mortality was particularly obvious in patients at higher risk (i.e., older patients, previous infarction) with the maximal efficacy observed during the first 3-4 days of therapy. Similarly, there was a reduction in the incidence of reinfarction which averaged 19% for the patients treated with beta-receptor antagonists. The metaanalysis also showed a significant reduction in the incidence of nonfatal cardiac arrest due to primary ventricular fibrillation for the group receiving beta-receptor antagonists (average risk reduction 16%; 95% confidence interval -2% to -30%). As calculated on the basis of the ISIS-1 data, treatment with beta-receptor antagonists in approximately 200 patients with acute myocardial infarction would lead to the avoidance of one death, one reinfarction, and one episode of ventricular fibrillation. Based on these data, it is recommended that administration of beta-receptor antagonists should be an important adjunctive therapeutic modality in patients with acute myocardial infarction and no contraindications for this form of treatment.

Administration, Oral↗
PubMed1994

[Amiodarone therapy after sotalol-induced torsade de pointes: prolonged QT interval and QT dispersion in differentiation of pro-arrhythmic effects].

In a 70-year-old patient with sotalol-induced torsade de pointes, QT-dispersion in the 12-lead surface ECG was determined in an attempt to evaluate the role of this method in determining risk factors for the development of proarrhythmic effects. After recovery from torsade, the patient was successfully treated with amiodarone over a 3-month follow-up period. Whereas the degree of QT prolongation was comparable during amiodarone therapy to that observed with sotalol, QT dispersion was markedly less (47 ms) than during previous treatment with sotalol (77 ms). During drug-free control, QT dispersion was 43 ms. This case-report indicates that determination of QT dispersion can provide information with respect to identification of patients prone to class III antiarrhythmic drug-induced proarrhythmic effects.

Aged↗
PubMed1994

[Atrial fibrillation and the autonomic nervous system].

The autonomic nervous system plays an important role in the genesis of various cardiac rhythm disorders. Experimental studies have indicated that in atrial fibrillation particularly vagal activity may have a decisive influence on the electrophysiologic properties of atrial myocardium. In patients with paroxysmal atrial fibrillation, a carefully taken history and electrocardiographic findings obtained during Holter monitoring can help to distinguish vagally mediated from adrenergically mediated atrial fibrillation. The former is considered to represent a form of lone atrial fibrillation affecting particularly males aged 40 to 50 years. The arrhythmic episodes manifest themselves most often during the night lasting from minutes to hours. There is a lack of tendency towards the development of permanent atrial fibrillation. Digitalis glycosides or beta-receptor antagonists are not helpful in the therapy of this form of atrial fibrillation whereas class I antiarrhythmic drugs have been shown to be more effective. Adrenergically mediated atrial fibrillation is in general less frequently observed than the vagally-induced form. In patients with episodes of atrial fibrillation provoked by emotional or physical stress, the diagnosis of adrenergically mediated atrial fibrillation should be suspected. The episodes of atrial fibrillation occur mostly during daytime. beta-receptor antagonists play a major role in the treatment of this form of atrial fibrillation.

Adult↗
PubMed1994

[Effect of sotalol on heart rate variability in patients with symptomatic, complex ventricular arrhythmias].

Heart rate variability (HRV) as determined from 24-h Holter recordings is being recognized as a measure of cardiac autonomic control. In patients surviving myocardial infarction HRV has been established as a useful tool for risk-stratification. The effects of antiarrhythmic agents on HRV, however, have not been extensively studied. The present study therefore examined time- and frequency-domain measures of HRV in 28 patients (10 females, 18 males at a mean age of 59 +/- 15 years) with symptomatic complex ventricular arrhythmias (> 30 VPB/h plus repetitive arrhythmias) before and during treatment with sotalol, a beta-receptor blocking agent with class-III antiarrhythmic activity. Heart rate variability before treatment was independent of the density of spontaneous arrhythmias. Therapy with sotalol resulted in a significant improvement in indices of vagal tone compared to baseline (SDNN 113 +/- 45 vs. 99 +/- 43 ms (p = .05); rMSSD 39 +/- 23 vs. 30 +/- 17 ms (p = .009); pNN50 11.4 +/- 12.5 vs. 6.8 +/- 9.5% (p = .005); HF 13 +/- 7 vs. 11 +/- 7 (p = .048). This improvement was particularly evident in patients with reduced left ventricular function (LVEF < 40%) and was independent of therapy-induced changes in mean heart rate (pNN50 vs. Mean NN r = 0.37; n.s.) or suppression of ventricular arrhythmias (pNN50 vs. In VES/24 h r = 0.41; n.s.). These effects on heart rate variability and thus on cardiac autonomic tone may contribute significantly to the antifibrillatory efficacy profile of sotalol.

Adult↗
PubMed1993

Effect of sotalol on heart rate variability assessed by Holter monitoring in patients with ventricular arrhythmias.

Reduced vagal activity has been demonstrated to be associated with an increased risk of sudden death. Assessing the heart rate variability as a measure of the autonomic control of the heart has been established as a useful tool for the risk stratification of patients after myocardial infarction. In the current study, heart rate variability assessed by time- and frequency-domain measures was determined from Holter recordings before and during treatment with sotalol in 28 patients with chronic ventricular arrhythmias. The heart rate variability at baseline was independent of the presence or absence of spontaneous arrhythmias and of left ventricular function. Therapy with sotalol produced a significant improvement over control values in indices of parasympathetic tone (root mean square of the difference in successive RR intervals, proportion of adjacent RR intervals different by > 50 msec, high-frequency power spectrum). This improvement was not related to drug-induced changes in the mean heart rate or the suppression of ventricular ectopic activity. These effects on heart rate variability may contribute significantly to the overall efficacy profile of sotalol.

Adult↗
PubMed1993

Usefulness of CKMB and troponin T determinations in patients with acute myocardial infarction complicated by ventricular fibrillation.

The usefulness of creatine kinase (CK) time activity curves for diagnosis of acute myocardial infarction in patients who have been defibrillated for ventricular fibrillation is limited due to the release of the enzyme as a result of the countershock. The present study of four patients with acute infarction complicated by primary ventricular fibrillation indicates that analysis of CKMB and even more so of troponin T, a specific cardiac antigen, permits reliable diagnosis of acute myocardial infarction in this particular setting. Furthermore, the data indicate that noninvasive assessment of coronary artery patency may be also possible in these patients by means of these two serum markers.

Acute Disease↗