Biomedical subjects
D Andresen
Publications and source records attributed to D Andresen.
Modification of the circadian pattern of ventricular tachyarrhythmias by beta-blocker therapy.
BACKGROUND: Sudden cardiac death exhibits a circadian variation and predominantly occurs during morning hours, Beta-adrenergic antagonists have shown to blunt this morning peak. However, previous reports studying the effects of beta blockers on the circadian variation did not analyze the underlying cause of sudden cardiac death. It thus remains unclear whether ventricular tachyarrhythmias are influenced by beta-blocker therapy. HYPOTHESIS: This study tested the hypothesis that beta-blocking agents blunt the morning peak of life-threatening ventricular tachyarrhythmias. METHODS: In 87 patients who were treated and monitored with an implantable cardioverter defibrillator, the circadian distribution of ventricular tachyarrhythmias terminated by appropriate shocks was analyzed and compared in those receiving beta blockers versus those not receiving beta-blocker therapy. RESULTS: Tachyarrhythmic episodes in the absence of beta-blocker therapy (n = 344) exhibited a circadian variation with a distinct morning peak (16, 38, 28, and 18% of episodes at 0-6, 6-12, 12-18, and 18-24 h, respectively, p < 0.001). In contrast, tachyarrhythmic episodes during beta-blocker therapy (n = 104) were equally distributed over time (22, 27, 24, and 27% of episodes at 0-6, 6-12, 12-18, and 18-24 h, respectively, p = 0.95). The circadian distribution of episodes was significantly different in patients with and those without beta blockade (p < 0.05). CONCLUSION: Beta-adrenergic antagonists influence the circadian distribution of malignant ventricular tachyarrhythmias in patients with an implantable cardioverter defibrillator. The blunted morning peak of tachyarrhythmic events during beta blockade supports the hypothesis that a sympathetic surge is involved in the circadian pattern of malignant arrhythmias.
Risk of ventricular arrhythmias in survivors of myocardial infarction.
The most recent studies have made it clear that the prognosis of asymptomatic post-MI patients has significantly improved in the last two decades. Holter monitoring as well as a low LVEF still is an important method for the risk stratification in the thrombolytic era of patients with post-MI. Patients with normal noninvasive tests do have a good prognosis. The electrophysiological stimulation seems to be the clinically most valuable single method to predict arrhythmic events. However, as an invasive procedure it is not suitable as a screening test for a large cohort. The stepwise risk stratification technique using first noninvasive followed by invasive procedures seem to be most suitable and effective for identifying asymptomatic infarct survivors which incidence of arrhythmic events is as high as the recurrence rate of patients who had been resuscitated from ventricular fibrillation. Consequently, prophylactic implantation of a defibrillator in asymptomatic MI patients, whose positive predictive value is around 30% becomes more and more interesting.
[Implantable defibrillators--current status of guidelines. Recognized and possible indications--prerequisites].
Ten to twenty percent of the patients, who were resuscitated as a result of a persistent ventricular tachycardia or ventricular fibrillation outside of an acute myocardial infarction, die of sudden cardiac death already in the first year after this event. Anti-arrhythmic agents also do not decisively improve this unfavorable prognosis. There is no doubt that the implantable cardioverter/defibrillator (ICD) safely and reliably terminates ventricular tachycardias and ventricular fibrillation and has thus led to an improvement in the care of these high risk patients. Studies have shown that the ICD reduces the risk of sudden cardiac death to 1-2% per year. However, whether the reduction of sudden cardiac death is also accompanied by a reduction in overall mortality has not yet been substantiated. It was, however, been assumed that especially patients with good left ventricular function, whose mortality risk is mainly sudden cardiac death, also profit from the overall prognosis of an ICD. The following presentation and discussion of the indication catalogue for the implantation of defibrillators is based on a guideline paper published by the study group "Interventional Electrophysiology" in the German Society for Cardiology. The statements clearly show how difficult it is to make long-term binding and valid recommendations due to insufficient scientific data and rapid technical development. Identifying patients who should be treated with an ICD requires complete noninvasive and invasive cardiological diagnostics and should ultimately be limited to cardiological centers which possess a large arsenal of diagnostic and therapeutic procedures.
Circadian variation of sustained ventricular tachyarrhythmias terminated by appropriate shocks in patients with an implantable cardioverter defibrillator.
To determine the circadian variation of sustained ventricular tachyarrhythmias, 78 consecutive patients with an implanted cardioverter defibrillator were analyzed with regard to the occurrence of spontaneous shock episodes during a mean follow-up period of 18 +/- 12 months. In 39 patients 207 shock episodes that terminated potentially life-threatening ventricular tachyarrhythmias could be related to an exact time of onset. A circadian variation (p < 0.001) of these events was demonstrated, with a primary morning peak between 7 hours and 11 hours and a secondary, much smaller peak between 16 hours and 20 hours. This finding indicates the relevance of endogeneous or exogeneous triggers in the cause of malignant arrhythmias that potentially lead to sudden cardiac death. Subgroup analyses revealed an association of the circadian pattern to the New York Heart Association functional classification, indicating perhaps a different role of triggers in different patient populations.
Management and prophylaxis of life-threatening arrhythmias--recent achievements.
Patients resuscitated from ventricular fibrillation or haemodynamically compromising ventricular tachycardias have an unfavourable clinical outcome. Moreover, there is no evidence that the prognosis can be improved by empirical use of antiarrhythmic therapy. Therapy guided by electrophysiological stimulation or long-term ECG identifies a subgroup of patients with a better outcome (in whom arrhythmias are suppressed) and a subgroup with a bad prognosis (in whom arrhythmias are not suppressed). However, this does not say that antiarrhythmic drugs actually improve the outcome. It may simply identify patients with an intrinsically good prognosis, regardless of whether they receive drug treatment. Because retrospective trials have reported that empiric administration of amiodarone provides long-term control in two-thirds or more of patients with refractory ventricular tachyarrhythmias, a direct comparison with other drugs guided by electrophysiological testing or long-term ECG was performed (CASCADE-study). Six-years survival was 41% under amiodarone versus 20% with other drugs. Even those conventionally treated patients, whose inducible arrhythmias were suppressed, had a trend toward a worse prognosis compared to those who were inducible and treated empirically with amiodarone. However, the high recurrence rate of arrhythmic events demonstrates the limitation of any antiarrhythmic drug, irrespective of the drug used and irrespective of whether it is given empirically or in a study.
[Cerebral ischemia during implantation of automatic defibrillators].
In order to study the influence of repetitive episodes of ventricular fibrillation (VF) during defibrillator implantation on the electrical activity of the brain, we performed an electroencephalographic (EEG) monitoring during implantation procedure in 18 patients. For defibrillation threshold testing 62 episodes of VF (1-6 episodes per patient) were induced. The mean duration of VF was 20 +/- 12 s; the mean duration of hypotension during an episode (defined as a mean arterial pressure of 50 mm Hg or less) was 33 +/- 16 s. EEG monitoring was performed using the International 10-20 System. The duration of cardiac arrest-related EEG alteration was assessed by an experienced neurologist and could be determined in 41 test-episodes; in 21 episodes analysis was not possible due to poor recordings. Ischemia-related EEG changes started 7.8 +/- 4.6 s after VF induction and lasted 64 +/- 49 s (range, 12-240). The duration of EEG alteration was significantly (p < .001) correlated with the duration of VF episodes (r = .71) and the associated hypotension (r = .82). With regard to patients the duration of ischemia related EEG changes also correlated significantly (p = .001) with the individual cumulative duration of VF (r = .85) and the associated hypotension (r = .88). In females EEG changes lasted longer than in males (p = .03); this finding, however, was only based on 2 women. Other clinical parameters, such as patient age, degree of congestive heart failure, left ventricular ejection fraction, stroke volume and cardiac index, the order of episodes within the testing sequence, and the time interval between episodes did not correlate with the duration of EEG alteration after VF induction. The duration of ischemia-related EEG alteration during VF episodes depends on the duration of cardiac arrest. In females EEG changes tended to last longer than in males, however, this finding has to be confirmed. An association with other clinical parameters has not been observed. Limitation of VF duration appears to be the most important factor to avoid prolonged cerebral ischemia.
Ventricular fibrillation related to coronary spasm in patients without significant coronary or other structural heart disease.
We present three patients without significant coronary or other structural heart disease who were resuscitated after ventricular fibrillation attributed to coronary spasm. Angina pectoris was present in two of the cases and silent myocardial ischemia in the third. All patients were given calcium antagonists at discharge. A defibrillator was also implanted in the patient with silent myocardial ischemia because further episodes of ischemia would probably have occurred without premonitory symptoms. Coronary spasm might be a mechanism of ventricular fibrillation in patients without significant structural heart disease. Diagnostic tests should therefore be performed to confirm or exclude coronary spasm in such cases. The implantation of an automatic defibrillator seems justified in selected patients with documented coronary spasm, silent myocardial ischemia, and associated sustained ventricular tachyarrhythmia, although prospective studies are not yet available.
[Clinical aspects and prognosis of atrial fibrillation].
Atrial fibrillation is alleged to be one of the most frequently occurring arrhythmia. Many patients with atrial fibrillation are asymptomatic. Others, however, complain of palpitations and paroxysmal atrial tachycardias. And especially in patients with preexisting heart failure, atrial fibrillation can lead to a clear worsening of cardiac output. Not only rheumatic but nonrheumatic atrial fibrillation as well are associated with an increased risk of thromboembolic complications. Arterial hypertension, a history of thromboembolism as well as signs of heart failure are clinical parameters which additionally increase the risk of embolism. On the other hand, this increased risk does not hold true for younger patients with idiopathic atrial fibrillation and is also low in patients with only one additional risk factor. Thus, it would indeed be false to anticoagulate every patient with atrial fibrillation. In each case, a careful individual risk stratification including an extensive history and detailed clinical examination should be performed before deciding on antithrombotic therapy.
[Recurrent ST segment elevations in continuous ECG analysis in the acute phase of myocardial infarct treated with thrombolytic therapy].
Early fluctuations of the ST-segment elevation indicating intermittent opening and reocclusion of the infarct artery has been well documented by angiographic monitoring in individual acute myocardial infarction patients undergoing thrombolytic therapy. However, the frequency of such episodes has not been studied in a consecutive patient group. Furthermore, it is not known what impact this finding has on the reinfarction risk during hospitalization and on left ventricular healing. The present investigation included 79 patients with acute myocardial infarction (pain < or = 6 h). Continuous Holter monitoring of the infarct-related ST elevation was initiated before or directly after starting thrombolytic therapy. During the 24-h observation period, 34 patients (43%) showed episodes of recurrent ST elevation after an initial resolution (group 1). Among those without episodes, ST elevation resolved within 4 h in 34 (43%, group 2) and persisted > or = 4 h in 11 (14%, group 3). Episodes of re-elevation were more frequent during the first 4 h (0.25 episodes per hour) than in the late part of the observation period (0.04 episodes per hour). Most episodes were transient and short lasting; only nine patients showed persistent re-elevations longer than 60 min. During hospitalization, group 1 patients had a higher incidence of reinfarctions and severe ischemic events than those without episodes (group 1 12/34 (35%) vs. group 2 4/34 (12%) vs. group 3 1/11 (9%), p = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)
[Reproducibility of symptom-limited oxygen consumption and anaerobic threshold within the scope of spiroergometric studies in patients with heart failure].
A prerequisite for the clinical utility of cardiopulmonary exercise testing is high reproducibility of gas-exchange characteristics. Therefore, we studied reproducibility of peak oxygen uptake and anaerobic threshold during bicycle-exercise stress testing in 34 patients with congestive heart failure in NYHA classes II and III. Additionally, we analyzed interobserver variability with regard to anaerobic threshold measured with the V-slope method. Correlations of results between two exercise stress tests were high concerning peak oxygen uptake and anaerobic threshold (r = 0.871 and r = 0.917, respectively). For both measures, however, 90% percentile of the relative difference between tests was 25% and 22%, respectively. Correlation between two observers with regard to the anaerobic threshold was high (r = 0.985). We conclude that reproducible determination of peak oxygen uptake and anaerobic threshold is possible in heart-failure patients. In individual subjects, however, considerable variation of results may occur during serial exercise testing. Interobserver variability with regard to anaerobic threshold is low.
Prognostic value of ischemia during Holter monitoring and exercise testing after acute myocardial infarction.
Exercise testing is generally accepted for prognostic assessment of patients after infarction, but the prognostic value of transient myocardial ischemia during ambulatory electrocardiographic monitoring remains controversial. Of 281 consecutive postinfarction patients, 173 patients (132 men, 41 women) were prospectively studied with 24-hour Holter monitoring 14 +/- 5 days after acute myocardial infarction, and with submaximal exercise testing after 15 +/- 7 days. Patients with either conduction disturbances or pacemaker rhythm and 71 patients with digitalis medication were excluded. Myocardial ischemia was defined as horizontal or descending ST depressions or transient ST elevations > or = 0.1 mV with or without angina pectoris. The follow-up period was 1 year. Myocardial ischemia was observed in 40 patients (23%) during Holter monitoring, and 96% of the episodes were asymptomatic. Ischemia occurred during exercise testing in 46 patients (27%), two thirds of whom had no symptoms. Ischemia was detected by both methods (group A) in 19 patients (11%), with exercise testing only (group B) in 27 patients (16%), and with Holter monitoring only (group C) in 21 patients (12%). In 106 patients (61%), ischemia could not be ascertained at all. The 4 groups were comparable with regard to sex and age distribution, coronary risk factors, and medication. During follow-up, 50 patients (29%) experienced clinical cardiac events: 6 patients died, 7 had recurrent myocardial infarction, 14 developed unstable angina pectoris and required immediate revascularization, and 23 patients had recurrent but stable angina.(ABSTRACT TRUNCATED AT 250 WORDS)
First- or second-degree atrioventricular block as a risk factor in idiopathic dilated cardiomyopathy.
To evaluate the significance of clinical, hemodynamic and electrocardiographic risk factors in idiopathic dilated cardiomyopathy 94 patients were followed prospectively for 49 +/- 37 months. During follow-up, 30 patients died, 13 died suddenly, 13 died of congestive heart failure and 4 of other causes. Follow-up was completed in 85 patients, and overall cardiac mortality was 31%. Univariate analysis revealed left ventricular ejection fraction among 20 variables as the major indicator of risk of both cardiac death of all causes and sudden cardiac death separately. Multivariate overall analysis determined 3 independent risk factors in the following order for all causes of cardiac death: Ventricular pairs > 40/24 hours (RR 7.2, p < 0.0001), left ventricular ejection fraction < or = 35% (RR 6.5, p < 0.001) and first- or second-degree atrioventricular (AV) block (RR 3.1, p < 0.05). In the subset of patients with ejection fraction < or = 35% ventricular pairs > 40 per 24 hours (RR 10.7, p < 0.001), AV block (RR 3.9, p < 0.05), and the missing administration of vasodilators (RR 3.3, p < 0.05) were the most important. The chief risk factors for sudden cardiac death were age (RR 7.4, p < 0.01) and AV block (RR 4.6, p < 0.05) by adjustment for age, and ejection fraction < or = 35% (RR 7.1, p < 0.01) and AV block (RR 4.2, p < 0.05) if not adjusted for age. A differentiation into 4 risk groups was attempted. The additional independent prognostic importance of AV block was shown, especially in combination with reduced ejection fraction or a high incidence of ventricular pairs.(ABSTRACT TRUNCATED AT 250 WORDS)
Should radiofrequency therapy be performed in every symptomatic patient with supraventricular tachycardia? (Pro drug position).
The indication for treatment of paroxysmal supraventricular tachycardia depends on the frequency and severity of the tachycardia attacks. If the tachycardia attacks are mildly symptomatic and occur only once or twice a year, there is no indication for either continuous drug therapy or radiofrequency ablation. The only therapeutic measure required is termination of each acute event. If symptoms occur frequently, long-term antiarrhythmic drug therapy is then indicated and will be effective for chronic prophylaxis in most individuals with a low risk of proarrhythmic events. Only in patients with severe or life-threatening symptoms or cases refractory to drug therapy would radiofrequency ablation possibly be justified.
[Prevention of sudden (rhythm-induced) cardiac death].
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Prognosis of patients with sustained ventricular tachycardia and of survivors of cardiac arrest not inducible by programmed stimulation.
The aim of this study was to analyze the long-term clinical outcome of 60 prospectively studied patients with documented sustained ventricular tachyarrhythmia that was not inducible during baseline programmed ventricular stimulation: 39 with cardiac arrest due to noninfarction ventricular fibrillation (VF) and 21 with mild hemodynamically compromising sustained ventricular tachycardia (VT). Left ventricular ejection fraction was 55 +/- 14% in the VF group and 50 +/- 13% in the VT group (difference not significant). Patients were discharged without conventional antiarrhythmic drugs and received only empirical beta-blocker therapy. During a mean follow-up period of 21 +/- 16 months (mean +/- SD), 10 of 60 patients (17%) died suddenly. The actuarial incidence of sudden death at 1 and 4 years was similar in both groups (VF group, 10 and 20%; VT group, 16 and 16%) (p = 0.48). The actuarial incidence of sudden cardiac death was significantly higher in patients with left ventricular ejection fraction < or = 40% than in those with > 40% (1-year incidence in VF group, 40 vs 0%; VT group, 50 vs 0%) (p = 0.005 and p = 0.01, respectively). Multivariate regression analysis identified left ventricular ejection fraction < or = 40% and previous myocardial infarction as the only independent predictor of sudden cardiac death. The occurrence of frequent ventricular pairs during Holter monitoring was the only independent predictor of sustained VT recurrences. It is concluded that patients with sustained ventricular tachyarrhythmia in whom arrhythmia was non-inducible during baseline ventricular stimulation and not treated with antiarrhythmic therapy have a favorable outcome if left ventricular ejection fraction is high.(ABSTRACT TRUNCATED AT 250 WORDS)
A comparison of electrophysiologically guided antiarrhythmic drug therapy with beta-blocker therapy in patients with symptomatic, sustained ventricular tachyarrhythmias.
BACKGROUND: Antiarrhythmic drug therapy guided by invasive electrophysiologic testing is now widely used in patients with symptomatic, sustained ventricular tachyarrhythmias. METHODS: We conducted a prospective, randomized trial in 170 patients to investigate whether this approach would improve long-term outcome. Patients whose arrhythmia was inducible by programmed electrical stimulation were assigned to treatment with electrophysiologically guided drug therapy based on serial testing (61 patients) or with metoprolol (54 patients). Electrophysiologically guided therapy consisted of serial testing of antiarrhythmic agents to identify the first one that rendered the arrhythmia noninducible. The 55 patients whose arrhythmia was noninducible during the initial electrophysiologic test were also treated with metoprolol. RESULTS: During a mean (+/- SD) follow-up period of 23 +/- 17 months, recurrent, nonfatal arrhythmia occurred in 44 patients and sudden death due to cardiac factors in 27. The incidence of symptomatic arrhythmia and sudden death combined was virtually the same in the two groups with inducible arrhythmia after two years of observation (electrophysiologically guided therapy vs. metoprolol therapy, 46 percent vs. 48 percent). The outcome was more favorable in the patients with noninducible arrhythmia at base line (75 percent had neither adverse event) than in those with inducible arrhythmia who were assigned to metoprolol therapy (P = 0.009 by log-rank test). Only 6 of the 29 patients (21 percent) with inducible arrhythmia that became noninducible during drug therapy had recurrent arrhythmia or sudden death, as compared with 21 of the 32 patients (66 percent) with arrhythmia that continued to be inducible (P less than 0.001). A multivariate regression analysis identified continued inducibility of the arrhythmia as an independent predictor of recurrent arrhythmia or sudden death (relative risk, 7.3; 95 percent confidence interval, 2.3 to 23.2; P less than 0.001). CONCLUSIONS: As compared with metoprolol therapy, electrophysiologically guided antiarrhythmic drug therapy did not improve the overall outcome of patients with sustained ventricular tachyarrhythmias. However, effective suppression of inducible arrhythmia by antiarrhythmic drugs was associated with a better outcome than was lack of suppression.
Transient ST segment depression during Holter monitoring: how to avoid false positive findings.
To increase the specificity of 24-hour Holter monitoring in detecting transient myocardial ischemia, we separated genuine ST deviations from those dependent on artifacts by adding a detailed shape analysis of real-time printouts to the usual criteria of significant ST segment depression. We screened 116 apparently healthy subjects; 31 had to be excluded, because of pathologic findings in preliminary examinations. The remaining 85 (49 women and 36 men; mean age, 43.1 years) underwent Holter monitoring for assessment of the extent, frequency, and duration of episodes of horizontal and descending ST segment depression of at least 0.1 mV that persisted for at least 60 msec after the J point and that were at least 1 minute apart. On the basis of these criteria, six subjects (7.1%) showed 24 episodes of horizontal or descending ST segment depression with a mean of 0.2 mV (range, 0.15 to 0.25 mV), a frequency of four episodes per 24 hours (one to nine), and a duration of 12.2 minutes (range 3-range 41 minutes). Supplementary criteria--e.g., sudden onset of ST segment depression, identical orientation of PQ and ST segments, or simultaneous increase in R and P wave amplitude--made it possible to identify ST changes caused by artifacts in four volunteers. In only two subjects (2.4%) could true silent ischemia not be differentiated from false positive results. Thus consideration of only the extent, frequency, and duration of episodes does not permit a differentiation between true silent ischemia and false positive results. A supplementary shape analysis increases the specificity of ST segment analysis in detecting transient myocardial ischemia during 24-hour Holter monitoring.