[Effect of heart rate on ST segment analysis in long-term ECG].
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Biomedical subjects
Publications and source records attributed to D Andresen.
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Ambulatory ECG monitoring has been suggested as a method for the detection of transient myocardial ischemia. But it is still unclear how accurately ST-segment alterations can be detected with the different systems. Measurement of amplitude and phase response is a valid method to estimate the fidelity of reproduction of an ECG-signal. We investigated the direct-recording long-term ECG systems CardioData Mk4 with recorder PR3, CardioData Mk4 with Spacelabs recorder, DMI Eclipse with DMI Recorder, Reynolds Pathfinder II with Oxford replay PB2 and recorder MR-10 and Reynolds Pathfinder III with tracker in comparison to a standard ECG recorder Picker Schwarzer C6800. Amplitude vs frequency response curves were derived from input sinus waves ranging from 0.01 to 500 Hz. The phase response was measured with a phase-sensitive waveform at a frequency range from 0.05 to 10 Hz. To determine the distortion of the ST-segment on the actual ECG, we produced a standard PQRST-signal that was modified to provide flat ST-segment depressions from 0 to 0.5 mV at 0.05 mV increments. The low and high frequency cut-off of the amplitude response was found at 0.09 and 220 Hz with the standard ECG recorder. A phase shift of -30 degrees was detected at 0.07 Hz. ST-segment depressions of the test-ECG were reflected to the same extent. For the CardioData-System, both cassette recorders yielded lower and upper cut-off frequencies of 0.06 and 0.07, and 20 and 16 Hz, respectively. A phase shift of -30 degrees was found at 0.35 and 0.31 Hz, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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The accuracy of ST-segment analysis with a direct-recording long-term ECG system (CardioData Mk 4) with a good low-frequency response was compared to that obtained by a standard ECG-recorder. Twenty-two patients with coronary heart disease and a positive exercise test were submitted to a second bicycle exercise test with concomitant long-term ECG registration. Application of a special switch device made it possible to record not only extremity and chest leads but also the two bipolar long-term ECG leads simultaneously on both the standard-ECG (leads ECG 1 and 2), and the long-term ECG (leads LEG 1 and 2). We determined the time of the beginning, end, maximum, and the magnitude of the ST-segment depression in bipolar leads LEG 1/2 and ECG 1/2, as well as in the unipolar leads V5/V6 of the exercise ECG. The long-term ECG was just as accurate as the standard ECG: the time intervals between the different leads showed good agreement. The degree of maximum ST-segment depression in ECG 1 (MW +/- SD = 2.2 +/- 1.1 mm) was identical to that in LEG 1 (2.2 +/- 1.3 mm). The maximum extent of ST-segment depression was lower in ECG 2 and LEG 2 but also comparable (ECG 2: 1.4 +/- 1.4 mm, LEG 2: 1.5 +/- 1.7 mm). Comparison of the unipolar leads V5/V6 of standard ECG with the bipolar lead LEG 1 of the long-term ECG yielded nearly identical results: V5/V6 2.0 +/- 0.7 mm; LEG 1: 2.2 +/- 1.3 mm.(ABSTRACT TRUNCATED AT 250 WORDS)
Digitoxin is considered a risk factor for ventricular arrhythmias in hemodialysis patients. In a randomized, crossover controlled study, 55 hemodialysis outpatients with sinus rhythm were prospectively investigated in two 48-h periods of electrocardiographic monitoring, one on and one off digitoxin or vice versa. The frequency of ventricular ectopic beats (mean +/- SD) which were found in 31 of 55 patients (56%), was slightly higher on hemodialysis (10 +/- 28 beats/h) than in the following 20 h (5.4 +/- 10 beats/h) and the next day off hemodialysis (3.6 +/- 6.6 beats/h); however, no difference was seen in patients on digitoxin during hemodialysis (10 +/- 29 beats/h), in the following 20 h (4.8 +/- 15 beats/h) and on the next day off hemodialysis (1.2 +/- 6.6 beats/h). The frequency of ventricular bigemini, polymorphous ectopies, couplets, more than 30 ectopies/h, salvos and tachycardias (10 vs 9 patients) on and off digitoxin was about the same (n.s., Fisher test). Supraventricular bigemini, salvos, tachycardias, and atrial fibrillation, however, occurred in significantly fewer patients on digitoxin (3 vs 13) than in those off digitoxin (P = 0.01, Fisher test). It is concluded that digitoxin does not increase the risk of ventricular arrhythmias in hemodialysis patients. Digitoxin, however, may have a beneficial effect on the supraventricular arrhythmias frequently observed in these patients.
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In an open randomized therapeutic study, 20 patients known to have frequent ventricular premature beats (VPB) and/or ventricular pairs (VP) were treated with both 2 X 200 mg flecainide (F) and 4 X 20 mg prajmalium-bitartrate (P) for 3 months each. There was a drug-free interval of one week between the two therapy phases. 24-hour long-term ECG-registrations were carried out before the start of the therapy phases as well as 1 week, 1 month, 2 months and 3 months after the initiation of antiarrhythmic therapy. After one week, the group as a whole evidenced a VPB reduction of 94% under F and only 57% under P (p less than or equal to 0.05). The percentage of individual patients in whom there was a statistically significant VPB reduction was also higher under F than under P (65% vs. 40%). In the group as a whole, there was a VP reduction of 99% under F and 88% under P (p less than or equal to 0.05) after one week. Of the 13 individuals with frequent VP (over 16 VP/24 h), a significant reduction was seen in 77% under F and only 38% under P. The difference between the two antiarrhythmic agents registered after one week was also observed in the further course of therapy but could no longer be statistically confirmed for the ventricular pairs. An aggravation of ventricular arrhythmias was observed in 2 patients under F and in 3 under P.(ABSTRACT TRUNCATED AT 250 WORDS)
UNLABELLED: The results of serial electrophysiologic testing in patients with sustained ventricular tachycardia or ventricular fibrillation indicate that if the arrhythmia is suppressible with antiarrhythmic drugs, the prognosis is better than when arrhythmias continue to be inducible despite antiarrhythmic drug treatment. Whether electrophysiologically guided antiarrhythmic drug therapy improves outcome or merely selects groups of patients with good and bad prognosis, is not known. To answer this question, a prospective randomized trial was conducted with 166 patients (sustained ventricular tachycardia n = 84; primary ventricular fibrillation n = 46; syncope n = 36). When the arrhythmia was inducible by programmed stimulation during control, patients were allocated to receive either electrophysiologically guided antiarrhythmic drug therapy (group I), or metoprolol (daily dose up to 200 mg) without invasive testing (group II). Patients with non-inducible arrhythmias were also treated with metoprolol (group III). RESULTS: During a follow-up of 10 +/- 8 (SD) months, there were arrhythmia recurrences in 30 patients, and sudden cardiac death in 17. Follow-up did not differ between group I (n = 59) and group II (n = 53). There was a tendency for the outcome to be better in patients of group III (n = 54) than in those of group II (Log-rank test p = 0.057). In group I, patients whose arrhythmias became suppressed did much better during follow-up than those with still inducible arrhythmias (p less than 0.0001). Thus, while invasive testing is a good predictor of outcome, electrophysiologically guided antiarrhythmic drug therapy is not better than a beta blocker in patients with sustained ventricular tachyarrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)
In 736 patients, 24 hour electrocardiographic recordings were performed 14 to 36 days after acute myocardial infarction before the start of randomized treatment with 320 mg of slow release oxprenolol (n = 358) or placebo (n = 378). Follow-up 24 hour electrocardiographic recordings were obtained 5 to 12 days (median 10) and 3, 6 and 12 months after the first administration of the study medication. Oxprenolol-treated patients had a significantly lower daytime heart rate as compared with the placebo group, whereas no difference was found at night. At baseline, 22.1% of the patients allocated to oxprenolol treatment and 29.6% of the placebo group had more than 30 ventricular extrasystoles in 1 hour at least once during 24 hour monitoring; multiform ventricular extrasystoles were present in 58.4 and 62.7%, ventricular couplets in 29.6 and 33.9% and ventricular tachycardia (3 or more consecutive ventricular extrasystoles) in 21.5 and 20.9% of the oxprenolol-treated and placebo-treated patients, respectively. During the 1 year follow-up period, the prevalence of these arrhythmias did not change significantly in either treatment group. There was a trend toward a reduction in the daytime frequency of ventricular couplets in the oxprenolol group. After 3 and 6 months, only multiform ventricular extrasystoles were significantly less frequent in the oxprenolol group than in the placebo group (47.4 and 42.7% versus 59.7 and 57.9%, respectively). Twelve months after the acute event, however, multiform ventricular extrasystole frequency was the same in both groups of patients (52.1 versus 51.0%, respectively). Thus, oxprenolol had a weak suppressant effect on ventricular tachyarrhythmias in survivors of myocardial infarction.
The effect of a standardized psychological stress test on frequency and severity of ventricular extrasystoles was compared in 42 patients with the results of 24-hour ECG monitoring and of an exercise ECG test. Frequent ventricular extrasystoles (greater than 1/min) occurred in the 24-hour-ECG in 22, in the psychological stress test in 24 and on physical exercise in 22 patients. 24-hour monitoring gave the only positive finding in ten, the psychological stress test in six, the exercise test in four. Complex arrhythmias (coupled or runs of ventricular extrasystoles) occurred in the 24-hour ECG in 30, with the psychological stress test in 16 and the exercise test in 12 patients. The 24-hour ECG was alone positive in 16, the psychological test in two, the exercise test in one. Thus in an individual patient the psychological stress test may provoke additional arrhythmias which are not recorded in either the 24-hour ECG or after exercise. The findings point to an independent significance of the psychological stress test in the diagnosis of simple and complex ventricular arrhythmias.
The incidence and prognostic significance of ventricular arrhythmias identified by 24-hour ambulatory electrocardiography (Holter) was prospectively assessed in 74 patients with idiopathic dilated cardiomyopathy (IDC). The criteria for diagnosis of IDC were based on clinical and cardiac catheterization findings. Holter monitoring was performed at the time of entry into the study. Patients were followed for 2 to 21 months (mean 11 +/- 3). Frequent ventricular premature complexes (VPCs) (greater than 1,000/24 hours) were seen in 35%, and complex VPCs (Lown grade III and IV) in 87% of the patients. Forty-nine percent of the patients had nonsustained ventricular tachycardia (VT) consisting of 3 to 32 beats with rates from 110 to 230 beats/min, and 20% had ventricular pairs. No correlation was found between clinical symptoms or the degree of left ventricular (LV) impairment and the number of ventricular pairs or episodes of VT. During follow-up, 19 patients died, 7 from congestive heart failure (CHF) and 12 suddenly. Patients who died suddenly had significantly more episodes of VT, ventricular pairs or total VPCs (p less than 0.01 each) compared with survivors and those who died from CHF. No significant differences were found between patients who died from CHF or suddenly with respect to LV end-diastolic pressure, LV end-diastolic volume index, LV ejection fraction (EF) and cardiac index. A linear stepwise discriminant function analysis using hemodynamic (LVEF and cardiac index) and arrhythmic (number of VT episodes and ventricular pairs) variables resulted in a meaningful separation between survivors and patients who died from CHF or suddenly.(ABSTRACT TRUNCATED AT 250 WORDS)
The aim of this study was to develop standards to define both antiarrhythmic drug efficacy and a drug-induced arrhytmogenic effect. In 45 patients with frequent and complex ventricular tachyarrhythmias 3 continuous 24-hour Holter recordings were performed. The spontaneous variability of ventricular premature beats and ventricular pairs was calculated using a new statistical method (transformation model). If two 24-hour Holter monitoring periods, one period before and the other with antiarrhythmic therapy, are compared, at least 75% reduction of ventricular premature beats and 90% reduction of ventricular pairs is necessary to be reasonably certain that one is measuring a drug response rather than spontaneous arrhythmia reduction (p less than or equal to 0.05). On the other hand, drug-induced aggravation can be assumed if ventricular premature beats and ventricular pairs have increased by more than 144% and 227%, respectively (p less than or equal to 0.05).
Continuous long-term ECG monitoring over three 24-hour periods was undertaken in 42 patients with complex ventricular tachy-arrhythmias. The arrhythmias were divided by degree of severity. The lowest degree was assigned to frequent ventricular extrasystoles (more than 20 per hour). The next degree was assigned to ventricular bigeminal rhythm, while runs of extrasystoles were assigned the highest degree. In 30 patients the highest arrhythmia level was reached within the first 24-hours, in nine after a further 24 hours, in three during the third 24-hour period. Comparing the three periods of registration there were differences between the various arrhythmias, not of kind but of frequency of the arrhythmia. Simple VES and the complex forms differed in their occurrence: although of 33 patients with frequent VES (more than 20/h) 30 also had runs of VES, in six patients with runs of VES the frequency of extrasystoles was low (less than 20/h). In 70% of cases 24-hour monitoring was sufficient to record the highest level of ventricular tachy-arrhythmia. If, however, no severe arrhythmias have been recorded during this period, increasing the duration of monitoring to 48-hours can be useful. A third period or more is of little further value.
42 patients with complex ventricular arrhythmias were subjected to continuous long-term ECGs for three 24-hour periods. In 21 patients, the occurrence and frequency of simple ventricular premature beats (VPB) did not depend on whether it was day or night. The other 21 patients showed a regular reproducible day-and-night rhythm during all three registration periods. 14 (33%) of them had the highest VPB-frequency during day and 7 (17%) at night.--16 patients showed paired VPB. Again, only 50% (8 patients) showed a regular reproducible day-and-night rhythm during all three registration periods. 6 of them had the highest frequency of paired VPB during day and 2 at night. 23 patients showed a clearly recognizable relationship between VPB-frequency and heart rate during all three periods. In 18, the VPB-frequency ran parallel to the heart rate, but in 5 patients the VPB-frequency ran contrary to the heart rate. In 16 patients, the VPB-frequency showed a constant relationship to both heart rate and time of day, 5 patients only evidenced a relationship to time of day and 7 only to heart rate. The distinct dependence of VPB-frequency upon heart rate and/or time of day in numerous patients could be of differential therapeutic significance.
27 of 101 patients with complex ventricular ectopy (ventricular bigeminy, couplets, ventricular salvo and ventricular tachycardia) during 24-hour Holter monitoring died during a mean follow-up of 12 months. Mortality was 28% when ventricular salvos had been detected, and 43% in patients with ventricular tachycardia. Detection of ventricular bigeminy had no, registration of ventricular couplets little prognostic significance. Prognosis was altered by presence of cerebral symptoms (dizziness and/or syncope) only for patients with ventricular tachycardia: additional bradyarrhythmia (asystole longer than 1.5 sec due to sinus-atrial or atrioventricular block) did not effect the prognosis, which was significantly worse for patients with a history of myocardial infarction, although patients in the first year after acute myocardial infarction were not included in this study. Prognosis of complex ventricular ectopy significantly worsens with age, it seems of little prognostic significance for patients under the age of 60.
Within 6 hours after the onset of acute myocardial infarction, 93 patients received a brief high-dose intravenous infusion of streptokinase, 49 patients received 500,000 IU within 30 min and 44 patients received 1,500,000 IU within 60 min. 26 patients had angiography in the acute phase, after 24 hours, and in the 4th week; 52 patients had angiography in the 4th week only; and 15 had no angiography. 7 patients died in hospital and 6 suffered a nonfatal reinfarction. There were no complications with bleeding. In 52% of cases, reopening of an occluded infarct vessel was achieved within 1 hour of the beginning of treatment. During the 4th week after infarction a patent infarct vessel was found in 84%, and 58% had a residual stenosis less than 70%. In contrast, in a control group that received no streptokinase treatment, 25% had a patent infarct vessel and 4% had a residual stenosis less than 70%. Indicative for salvage of ischemic myocardium are a significant improvement in local contraction disorders between the acute phase and the 4th week and a significant correlation between infarct size in the 4th week and beginning of treatment after onset of symptoms. 1. It may be concluded that: brief intravenous infusion of streptokinase results in restoration of blood flow in an infarcted coronary artery in a high percentage of cases; the shorter thrombus-lysis time with intracoronary streptokinase infusion could be made up for by the earlier initiation of intravenous streptokinase treatment; and a conclusive randomized trial is needed to ascertain the true impact of a brief high-dose intravenous infusion of streptokinase on mortality and morbidity following acute myocardial infarction.
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