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Biomedical subjects

W Baedeker

Publications and source records attributed to W Baedeker.

At least 19 recordsLinked to original sources
PubMed1991

Evaluation of antiarrhythmic drug effects with simultaneous analysis of single ventricular premature contractions, couplets and salvos.

To improve the clinical value of ambulatory Holter electrocardiographic (ECG) monitoring as a tool of antiarrhythmic therapy control, a new statistical model was developed. In a patient group at increased risk of sudden cardiac death, the spontaneous variability of ventricular arrhythmias was assessed, with simultaneous consideration of single ventricular premature complexes, couplets and salvos. The study included 100 patients who suffered from coronary heart disease or idiopathic dilated cardiomyopathy and for whom greater than 30 ventricular premature complexes/h and couplets had been demonstrated on the last Holter ECG before the study. Between 3 and 12 Holter recordings were made for each patient in a drug-free state; the mean follow-up period was 260 days (maximum 1,403). The mean hourly values of the ectopic events (EE) were assessed separately for ventricular premature complexes, couplets and salvos. The spontaneous variability (SV) was calculated for single ventricular premature complexes, couplets and salvos as SV = log (EEday 2 + 0.01/EEday 1 + 0.01) and linked in one, two and three dimensions. Compared with the consideration of only one type of arrhythmia (one-dimensional model), the simultaneous use of two or three types of arrhythmia (two- or three-dimensional model) resulted in considerably lower reduction and aggravation rates as sufficient proof of drug effects. With control intervals up to 1 week, the one-dimensional model yielded reduction rates for ventricular premature complexes, couplets and salvos of -63%, -90% and -95%, respectively. In contrast, with the three-dimensional model, the rates were -28%, -72% and -88%. The corresponding aggravation values were +370, +1,114% and +2,189% versus +38%, +256% and +747%.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMed1991

[Long-term treatment with amiodarone].

The aim of this study was to investigate the efficacy and the side effects of a long-term treatment with amiodarone. We analyzed the data of 41 patients in whom amiodarone therapy had been initiated between 1974 and 1984. Twenty-one patients had dilative cardiomyopathy, 14 patients had chronic myocardial infarction, four patients suffered from WPW syndrome with intermittent atrial fibrillation, one patient had aortic valve surgery, whereas in one patient there was no clinical evidence of a heart disease. All patients had salvos of ventricular extrasystoles, ventricular tachycardia or documented intermittent ventricular fibrillation. There have been seven drop-outs up to the present time. In each patient, the lowest antiarrhythmically effective dose was applied, which was generally higher in patients with low ejection fraction. Effective treatment of the ventricular tachycardia was achieved in 55-92% of patients and did not depend on the duration of treatment. In 10 patients in whom amiodarone therapy had to be stopped for various reasons. Sudden cardiac death was slightly more frequent than in the 24 patients treated with amiodarone, though the difference was not significant. In cases with a history of syncope the prognosis was poor, even with amiodarone therapy. Due to side effects, a dosage reduction or discontinuation of amiodarone treatment became necessary in 14 patients. Amiodarone proved to be an effective drug also for the long-term treatment of ventricular tachycardia, and possibly for the prevention of sudden cardiac death. With the exception of blue skin color, there was no accumulation of side effects, even during long-term treatment of several years.

Adult↗
PubMed1991

[Effect of amiodarone on signal-averaged and long-term ECG].

This prospective study examined the influence of long-term amiodarone therapy on the parameters of the signal-averaged ECG and their relation to simultaneously derived Holter monitoring data. For this purpose, 23 patients with angiographically confirmed dilated cardiomyopathy or coronary heart disease and high-grade ventricular arrhythmias, in whom an average of four class I antiarrhythmic drugs had proven ineffective, were stabilized on amiodarone. Before the beginning of therapy, as well as after 2 months and, subsequently, every 3 months, a resting ECG, a signal-averaged ECG by Simson's method, and Holter monitoring were performed. Compared to the initial measurement, we found a significant increase in the duration of the total filtered QRS complex from an average of 114 +/- 24 ms to 127 +/- 35 ms, while the change in voltage did not reach the significance level. The incidence of late potentials remained largely constant under amiodarone; 10 patients showed a constant late potential, 12 patients had no late potential, and one patient with coronary heart disease developed a new late potential. In the long-term follow-up, we ascertained a relatively high responder rate under amiodarone between 41% and 81%. No relation could be detected between the results of the signal-averaged ECG and those of 24-h Holter monitoring.

Aged↗
PubMed1991

Relation between epicardial electrograms and signal-averaged electrocardiograms after acute myocardial infarction in dogs.

Signal-averaged electrocardiograms allow the non-invasive detection of late potentials which represent locally delayed conduction in the myocardium. To validate this method, it is necessary to compare the signal-averaged data with electrograms recorded directly from the heart. However, the studies performed to date involve only a consecutive collection of the invasively and non-invasively obtained data. To obtain a more direct comparison, we examined this relation at operation by simultaneous epicardial and signal-averaged measurements. Acute infarction in animals was chosen, because the ischemic area is a zone of delayed conduction whose presence can be verified in a signal-averaged electrocardiogram. For this purpose, the left anterior descending artery, proximal of large septal and diagonal branches, was tied off in nine mongrel dogs after thoracotomy. Before infarction, a signal-averaged electrocardiogram was recorded from the body surface. At the same time, epicardial electrograms were performed using bipolar electrodes both from the supply area of the left anterior descending artery and from that of the circumflex artery. Five minutes after coronary ligation, both the epicardial measurements and the signal-averaged electrocardiogram were repeated on the open thorax. Before occlusion of the left anterior descending artery, narrow activation complexes occurred in general in the epicardial electrograms and no late potentials were recorded in any dog by the signal-averaged electrocardiogram. Five minutes after coronary ligation, fractionated and prolonged electrograms occurred in the epicardial recordings from the ischemic zone, while the activation complexes in the uninfarcted supply area of the circumflex artery remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

[Spontaneous variability of ventricular arrhythmias in follow-up of anti-arrhythmia therapy].

The question of the reliability of ambulatory Holter monitoring for assessment of antiarrhythmic treatment has not been adequately resolved. Even though treatment efficacy had been individually assessed with Holter monitoring in the CAST study, during long-term treatment with class IC antiarrhythmic drugs, there were more deaths among patients receiving active drug than in those in the placebo group. Basic biostatistical considerations: Due to the spontaneous variability of frequency and complexity of ventricular arrhythmias, parametric models were developed with the aid of which normal ranges for spontaneous variability of singular ventricular premature complexes (VPC), couplets and salvos can be calculated. We designed a model which enables rapid visual analysis of the results: spontaneous variability = log (EE Day 2 + 0.01/EE Day 1 + 0.01) where EE is the number of ectopic events. For both days, the mean values per hour are applied. The use of parametric models prerequisites normal distribution of the data which can be achieved with logarithmic transformation. A constant is added to all mean values to preclude the mathematically-inadmissible form of log 0. The magnitude of the constant results in some degree of underestimation of the spontaneous variability. We chose the smallest constant, c = 0.01, consistent with a normal distribution of data. Figure 1 shows the normal range of the variability quotients for VPC in patients with cardiac disease and complex ventricular arrhythmias. The contiguous regions above and below the normal range designate active areas indicative of reduction or aggravation. Determinants of spontaneous variability: Frequency of arrhythmias: The number of VPC per unit of time exerts considerable influence on the spontaneous variability. The more infrequent an arrhythmia, the greater is the fluctuation to be anticipated. The differences in the variability of VPC, couplets and salvos are almost exclusively due to their differing frequencies since, in the presence of comparable frequency, they cannot be distinguished statistically from each other (Figure 2). Type and extent of underlying cardiac disease: In our patient population, there were no differences in spontaneous variability of arrhythmias between patients with coronary artery disease and those with dilated cardiomyopathy (Figure 3). Although in patients with coronary artery disease, as compared to those with noncoronary disease, a higher degree of spontaneous variability has been reported for VPC but, due to the inhomogeneity of the latter group, valid comparison is encumbered. The ejection fraction, the left ventricular filling pressure and the end-diastolic volume do not exert meaningful influence on the spontaneous variability (Figures 4 to 6).(ABSTRACT TRUNCATED AT 400 WORDS)

Anti-Arrhythmia Agents↗
PubMed1990

Amiodarone--efficacy and late potentials during long-term therapy.

This prospective study was intended to examine the influence of long-term amiodarone therapy on the parameters of the signal averaged ECG and their relation to simultaneously derived Holter monitoring data. For this purpose 27 patients with angiographically confirmed dilated cardiomyopathy or coronary heart disease and highgrade ventricular arrhythmias, in whom an average of four class I antiarrhythmic drugs had proven ineffective, were stabilized on amiodarone. Before the beginning of therapy, as well as after two months and subsequently every three months if possible, a resting ECG, a signal averaged ECG by the method of Simson and Holter monitoring were performed. Compared to the initial measurement we found a significant increase in the duration of the total filtered QRS complex, while the change in the voltage did not reach the significance level. The incidence of late potentials remained largely constant under amiodarone. In the long-term follow up Holter monitoring showed a relatively high responder rate of between 46 and 81% under amiodarone. No relation could be detected between the results of the signal averaged ECG and those of 24-h Holter monitoring.

Amiodarone↗
PubMed1988

Spontaneous variability of simple and complex ventricular premature contractions during long time intervals in patients with severe organic heart disease.

Calculations of the spontaneous variability of ventricular arrhythmias are usually based upon the results of Holter electrocardiograms recorded either successively or separated by a short time interval. Only recently was it shown that the variability of ventricular premature contractions increases with longer intervals. This study was undertaken to investigate the variability of simple and complex ventricular arrhythmias over long periods to derive efficacy criteria for long-term antiarrhythmic therapy. In a prospective study, the influence of the length of the time interval on spontaneous variability was investigated in 100 patients with coronary artery disease or idiopathic dilated cardiomyopathy and untreated ventricular arrhythmia Lown grade IV. Patient follow-up was carried out for 260 +/- 387 days. In each of the 498 ambulatory Holter tapes, the mean hourly arrhythmia count (AC) of ventricular premature contractions, couplets, and salvos was verified. The variability of arrhythmia counts between two Holter electrocardiograms was defined as the logarithm of the ratio of (ACday 2 + 0.01) to (ACday 1 + 0.01). The 95% intervals for these ratios were calculated as +/- 2 SD, considering the fact that all mean values did not differ significantly from zero. The lower limit of these intervals refers to the reduction that is required for assuming drug efficacy, whereas the upper limit refers to an aggravation. The 95% intervals were calculated for each of four ranges of control intervals (0-6, 7-89, 90-364, and greater than or equal to 365 days). They increased significantly with longer control intervals.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

[Spontaneous variability of complex ventricular extrasystoles over a period of up to 4 years].

In a prospective study, the influence of the length of the time interval on spontaneous variability was investigated in 100 patients with CAD or IDC and untreated ventricular arrhythmia of Lown grade IV. Patient follow-up was carried out over 260 +/- 387 days. In each of the 498 ambulatory Holter tapes, the mean hourly arrhythmia count (AC) of couplets and salvos was verified. The variability of ACs between two Holter ECGs was defined as the logarithm of the quotient AC day 2(n + 0.01)/AC day 1(n + 0.01). The spontaneous distribution of variability quotients (means +/- 2 SD) was defined separately for couplets and salvos and for each of four ranges of control intervals (0-6 days, 7-89 days, 90-364 days, greater than or equal to 365 days). The percentage change in arrhythmia count necessary to establish drug efficacy (R), was calculated according to the formula R(%) = (10(0) - 10(-2SD].100, whereas the percentage change necessary to prove aggravation of arrhythmia (A) was assessed by the formula A(%) = (10(0) + 10(+2SD].100. For couplets, R extended from 90%, 94%, 98% to 99%; A increased from 1114%, 1895%, 6153% to 14032%, respectively. For salvos, R remained almost unchanged at a high level with 95%, 98%, 98%, 99%. The figures of A were 2189%, 4650%, 5698% and 9650%, respectively. It is concluded that the spontaneous variability of complex ventricular arrhythmias is remarkably high with short control intervals and increases further with longer ones.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMed1988

[Spontaneous variability of ventricular arrhythmias in relation to the kind and extent of underlying heart disease].

The influence of the underlying heart disease on the spontaneous variability of ventricular arrhythmias was investigated prospectively in 53 patients (25 CHD, 28 IDC) with frequent and complex ventricular arrhythmias. In each patient, two consecutive ambulatory 24-h Holter ECGs were prepared and in each tape the mean hourly arrhythmia count (AC) was determined separately for singular VPCs, couplets, and salvos. The spontaneous variability between the two long-term ECGs was defined as the logarithm of the ratio (ACday 2 + 0.01)/(ACday 1 + 0.01). The 95% confidence intervals of the stated types of arrhythmias were calculated as +/- 2 SD. The results were analyzed as a function of the underlying etiology, NYHA class, and left ventricular ejection fraction. There were no differences between patients with CHD and IDC. The extent of left ventricular dysfunction did not have any influence either. In patients of NYHA class 3 there was a higher spontaneous variability of VPCs, couplets and salvos than in patients of NYHA class 2, but the differences could not be ensured statistically. We conclude from the results that the validation of an antiarrhythmic treatment can be performed independently from the nature of the underlying heart disease and the left ventricular ejection fraction. However, it remains unclear whether a greater variability must be expected in patients of NYHA class 3 than in patients of NYHA class 2.

Adult↗
PubMed1988

[Follow-up in patients with syncope].

The prognosis of patients with syncopes depends on their age, underlying illness and the available possibilities of treatment. Patients over 70 years and those with syncope caused by cardiovascular disease have a particularly unfavourable prognosis. If the cause of syncope has been clearly diagnosed, 40 to 100% of the patients can be treated effectively. In 40% of all patients with syncope, the cause remains uncertain. In a follow-up period of 2 years, the cause of syncope could be discovered in a further 12% of patients by examinations on an outpatient basis. Of the patients for whom the reason of syncope was unexplained, 75% remained free from syncopes throughout this 2 year observation period, while 8% suffered from further attacks. In some of these patients it is possible to find a probable diagnosis by combining their symptoms.

Follow-Up Studies↗
PubMed1988

[Mitral valve prolapse syndrome and arrhythmias].

In patients with mitral valve prolapse syndrome various disturbances of cardiac rhythm can be observed such as atrial arrhythmias, ventricular tachycardias and conduction disturbances. Of timely interest are the questions of which etiology is at the basis of the arrhythmias, what is their relevance with respect to sudden cardiac death, what are the indications for treatment and which therapeutic results can be anticipated. Cardiac arrhythmias represent the most frequent complication of mitral valve prolapse. Holter ECG monitoring has assumed the central role in detection of all types of arrhythmias. As compared with normal persons, in patients with mitral valve prolapse, both ventricular and supraventricular arrhythmias can be found more frequently. Atrial arrhythmias: Supraventricular arrhythmias can be found less frequently than ventricular arrhythmias (Table 1). Premature atrial contractions can be observed in 35% of those with mitral valve prolapse but also in a similar number of normal individuals such that their presence is not of clinical relevance. There is only a tendency to more frequently incurred supraventricular couplets in mitral valve prolapse. Supraventricular tachycardias can be observed in 10.5 to 32% of which sinus tachycardia (heart rate greater than 120 beats per minute), paroxysmal atrial tachycardia and intermittent atrial fibrillation at about 5 to 6% each are not more common than in control subjects. Atrial fibrillation was seen more frequently in mitral valve prolapse with mitral regurgitation or, conversely, in mitral regurgitation due to mitral valve prolapse more frequently than in mitral regurgitation due to other causes.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMed1988

[Effect of class I anti-arrhythmia agents on the signal-averaged ECG].

This study was designed to determine which parameters in the signal-averaged ECG are subject to the influence of class I antiarrhythmic agents and whether the effects on these parameters differ with respect to the various subgroups of agents within the class I antiarrhythmics. For this purpose, disopyramide was chosen as representative of class Ia, tocainide Ib and flecainide Ic. A total of 23 patients, twelve with coronary artery disease and eleven with dilated cardiomyopathy and high grade ventricular arrhythmics, received randomized and single-blind, placebo-controlled high single oral doses of 300 mg disopyramide, 800 mg tocainide and 300 mg flecainide with a washout period of five half-times of the antecedent drug prior to the subsequent agent. Before and two hours after the respective drugs the signal-averaged ECG was recorded. The position of the electrodes was unchanged throughout the study. A total of 142 recordings were performed. Computerized calculation of the duration and mean voltage of the entire filtered QRS complex and the voltage during the last 40 and 50 ms, respectively, was carried out according to the method of Simson. Additionally, according to a modification by Karbenn, the duration and voltage of late potentials were analyzed. In the baseline signal-averaged ECG, 13 of 23 patients (57%) had late potentials. Of the 18 patients who received disopyramide, ten had late potentials before and after the drug. In seven, late potentials were not present either before or after the drug. In one patient with a negative finding at baseline, late potentials were observed after disopyramide. There was a significant increase in the duration (p less than 0.001) as well as a decrease in the voltage of the entire filtered QRS-complex (p less than 0.01) and the voltage during the last 40 and 50 ms, respectively (p less than 0.05). Late potentials were present before and after tocainide in nine of 18 patients (50%) who received this drug. In the remaining 50%, late potentials were not observed either before or after the drug. Comparison of mean values before and two hours after 800 mg tocainide showed no significant changes for duration or voltage of the entire filtered QRS-complex nor for the voltage during the last 40 and 50 ms, respectively. Before and after flecainide, eight of 17 patients had late potentials (47%).(ABSTRACT TRUNCATED AT 400 WORDS)

Anti-Arrhythmia Agents↗
PubMed1987

[Syncopes of unclear etiology. Diagnosis, follow-up observation and pacemaker therapy].

Clinical findings after syncopal attacks were evaluated in 295 inpatients for examining their clinical significance and the course and prognosis in syncopes of unclear aetiology. This was done after having defined the criteria for "very probable" and "possible" causes of the syncopes. A "typically rhythmogenic" anamnesis had a sensitivity rating of 79%. Long-term ECG proved the most frequent contribution to clarification. Doppler examination of the carotid artery was hardly relevant. Patients with tachycardia usually suffered from cardiac disease (coronary heart disease or cardiomyopathy). Bradycardia predominated in patients with a clinically "healthy" heart, especially in elderly patients. An overall percentage of 37% of the cases could not be clarified despite thorough clinical examination using all available diagnostic tools. Follow-ups over two years and outpatient examinations revealed a favourable prognosis in patients whose syncopes had remained unexplained: No further syncopes had occurred in 75% of these patients over a period of two years. In 12% of the subjects the cause was identified by the follow-up examinations. In 95.5% of the patients subjected to pacemaker treatment no syncopes recurred. A relatively small proportion (19.5%) of the patients with unclarified syncopes continued to suffer from syncopes, the aetiology of which could not be determined during the 2-year follow-up period. This group of patients would require better diagnostic techniques, e.g. long-term ECGs over several days or long-term EEGs.

Adolescent↗
PubMed1987

[Spontaneous variability of ventricular extrasystoles: criteria for validating anti-arrhythmia therapy in relation to the length of the control interval].

Calculations about the variability of PVCs are usually based upon the results of two Holter ECGs, either successive ones or separated by a short interval. No studies are available indicating whether the criteria calculated for short control intervals also holds true when evaluating chronic antiarrhythmic treatment over longer control periods. This study was performed to investigate the influence of the length of the control interval on the spontaneous variability and thus on the reduction of PVCs required to secure an antiarrhythmic effect. In a prospective study, 444 ambulatory ECGs were obtained in 90 patients with CAD or IDC and untreated ventricular arrhythmia of Lown grade IV. Patient follow-up was carried out over an average of 181 +/- 297 days. The degree of arrhythmia was expressed as the mean hourly PVC rate. The variability of PVC counts between two Holter ECGs was defined as the logarithm of the quotient PVCday 2(n + 1)/PVCday 1(n + 1). The spontaneous distribution of variability quotients was defined separately (mean +/- 2 SD) for each of four ranges of control intervals (0-6 days, 7-89 days, 90-364 days, greater than or equal to 365 days). The per cent reduction (R) in PVC frequency necessary to establish drug efficacy, was calculated according to the formula R (%) = 10(0)-10(-2SD) X 100, whereas the percentage change necessary to prove aggravation of arrhythmia (A) was assessed by the formula A (%) = 10(0)+10(+2SD X 100. R increased from 63% (0-6 days), 81% (7-89 days), 93% (90-364 days) to 98% (greater than or equal to 365 days).(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMed1986

[New statistical criteria for validation of the antiarrhythmic effects by acute oral testing].

There are no reliable criteria for the evaluation of acute effects after oral application of a high single dose of an antiarrhythmic agent from the analysis of data of 46 patients with frequent complex VPBs suffering from severe organic heart disease (19 CHD, 27 COCM), we developed a new statistical model. Our calculations were based on nine 10 h Holter ECGs (2 controls, 1 placebo test, 6 class 1 antiarrhythmic agent tests) and two 24 h Holter ECGs (1 control, 1 while on chronic treatment) recorded in each patient. Usually reductions in VPB frequency caused by the medication occurred within 1 hour after application and lasted greater than or equal to 4 hours. The VPB reduction in the course of time was assessed by the parameters r and R (r = VPB reduction of the 4 h interval in comparison to the last hour before application, R = VPB reduction of the 4 h interval in comparison with an analogous interval of a control day). Values of r and R greater than or equal to -50% were never observed simultaneously. In contrast, the majority of all patients developed r and R values greater than or equal to -50% after application of an antiarrhythmic agent, and were classified as responders. As shown at a Holter control after 1 week of chronic treatment, the predictive value of a positive test result was good.

Administration, Oral↗
PubMed1985

Long term efficacy of class I antiarrhythmic agents and amiodarone in patients with malignant ventricular arrhythmias.

The long term efficacy of class I antiarrhythmic drugs and of amiodarone was investigated in 34 patients with severe organic heart disease accompanied by frequent complex ventricular arrhythmias. All patients had undergone cardiac catheterisation which included coronary angiography, and each patient underwent a short and a long term study phase. During the short term study 6 class I antiarrhythmic agents were administered orally in a randomised, single-blind fashion. The drugs investigated were disopyramide, flecainide, mexiletine, prajmalium, propafenon and tocainide. The response was judged to be effective when there was a 90% reduction of couplets and a 100% reduction of salvos. For long term treatment the patient was given one of the agents found to be effective in the short term testing. Holter monitoring was performed after 1 week, and 1, 3 and 6 months. If the drug administered initially was later found to be ineffective, the patient was given another effective class I agent. If during the short term study or the follow-up phase there was no positive response to any class I agent, the patient was given amiodarone. In 78% of the patients, one or more of the class I agents administered short term was effective. The percentage of effectively treated patients after 1 week was 56%, and was 28, 14, and 9% after 1, 3, and 6 months' treatment, respectively. In amiodarone-treated patients there was an effective response rate of 40% after 10 days, 50% after 1 month and 70% after 3 and 6 months.

Amiodarone↗