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P Barthel

Publications and source records attributed to P Barthel.

At least 19 recordsLinked to original sources
PubMed2001

Value of programmed ventricular stimulation for prophylactic internal cardioverter-defibrillator implantation in postinfarction patients preselected by noninvasive risk stratifiers.

OBJECTIVES: The aim of this prospective study was to evaluate the role of programmed ventricular stimulation (PVS) after noninvasive risk stratification to identify a subgroup of acute myocardial infarction (AMI) survivors considered at risk for ventricular arrhythmias and whether these patients could benefit from internal cardioverter-defibrillators (ICDs). BACKGROUND: The predictive value of noninvasive and invasive risk stratifiers after AMI has been questioned. The question of whether the group of patients with inducible monomorphic ventricular tachycardia (VT) after AMI could profit from ICD implantation is unanswered. METHODS: A consecutive series of 1,436 AMI survivors was screened noninvasively by Holter monitoring, heart rate variability, ventricular late potentials, and ejection fraction. A subgroup of 248 patients (17.3%) were identified as high-risk patients and scheduled for PVS. Due to the study design, 54 patients >75 years were excluded; thus, 194 patients were eligible for PVS. Triple extrastimuli at two paced cycle lengths (600 ms and 400 ms) were applied. RESULTS: In a subgroup of 98 (51%) high-risk patients, PVS was performed; 21 patients had an abnormal response, and in 20 patients an ICD was implanted. During a mean follow-up of 607 days the arrhythmic event rate (sudden cardiac death, symptomatic VT, cardiac arrest) was 33% with a positive electrophysiological test versus 2.6% (p < 0.0001) with a negative electrophysiological test. A subgroup of 96 high-risk patients declined electrophysiological study. In this nonconsent group, cardiac mortality (combined sudden and nonsudden) was significantly higher (log-rank chi-square 9.38, p = 0.0022, relative risk 4.7, 1.6 to 13.9) compared to the group guided by electrophysiological testing and consecutive ICD implantation. CONCLUSIONS: After a two-step risk stratification, PVS is helpful in selecting a subgroup of AMI survivors without spontaneous ventricular arrhythmias who benefit from prophylactic ICD implantation.

Defibrillators, Implantable↗
PubMed2000

Extent of cardiac sympathetic neuronal damage is determined by the area of ischemia in patients with acute coronary syndromes.

BACKGROUND: Prior studies have demonstrated that acute ischemic injury causes sympathetic neuronal damage exceeding the area of necrosis. The aim of this study was to test the hypothesis that sympathetic neuronal damage measured by (123)I-metaiodobenzylguanidine (MIBG) imaging would be determined by the area of ischemia as reflected by area at risk in patients undergoing reperfusion therapy for acute coronary syndromes. METHODS AND RESULTS: In 12 patients, the myocardium at risk was assessed by (99m)Tc-sestamibi SPECT before reperfusion, and infarct size was measured by follow-up (99m)Tc-sestamibi SPECT 1 week later. All patients also underwent (123)I-MIBG SPECT within a mean of 11 days after onset. The SPECT image analysis was based on a semiquantitative polar map approach. Defect size on the (123)I-MIBG or (99m)Tc-sestamibi SPECT was measured for the left ventricle (LV) with the use of a threshold of -2.5 SD from the mean value of a normal database and was expressed as %LV. The (123)I-MIBG defect size (47+/-18%LV) was larger than the infarct size (27+/-23%LV, P<0. 001) but was similar to the risk area (49+/-18%LV, P=NS). Furthermore, the (123)I-MIBG defect size was closely correlated with the risk area (r=0.905, P<0.001). CONCLUSIONS: Sympathetic neuronal damage measured by (123)I-MIBG SPECT is larger than infarct size and is closely related to risk area, suggesting high sensitivity of neuronal structures to ischemia compared with myocardial cells.

Adult↗
PubMed1999

Heart-rate turbulence after ventricular premature beats as a predictor of mortality after acute myocardial infarction.

BACKGROUND: Identification of high-risk patients after acute myocardial infarction is essential for successful prophylactic therapy. The predictive accuracy of currently used risk predictors is modest even when several factors are combined. Thus, establishment of a new powerful method for risk prediction independent of the available stratifiers is of considerable practical value. METHODS: The study investigated fluctuations of sinus-rhythm cycle length after a single ventricular premature beat recorded in Holter electrocardiograms, and characterised the fluctuations (termed heart-rate turbulence) by two numerical parameters, termed turbulence onset and slope. The method was developed on a population of 100 patients with coronary heart disease and blindly applied to the population of the Multicentre Post-Infarction Program (MPIP; 577 survivors of acute infarction, 75 deaths during a median follow-up of 22 months) and to the placebo population of the European Myocardial Amiodarone Trial (EMIAT; 614 survivors of acute myocardial infarction, 87 deaths during median follow-up of 21 months). Multivariate risk stratification was done with the new parameters and conventional risk factors. FINDINGS: One of the new parameters (turbulence slope) was the most powerful stratifier of follow-up mortality in EMIAT and the second most powerful stratifier in MPIP: MPIP risk ratio 3.5 (95% CI 2.2-5.5, p<0.0001), EMIAT risk ratio 2.7 (1.8-4.2, p<0.0001). In the multivariate analysis, low left-ventricular ejection fraction and turbulence slope were the only independent variables for mortality prediction in MPIP (p<0.001), whereas in EMIAT, five variables were independent mortality predictors: abnormal turbulence onset, abnormal turbulence slope, history of previous infarction, low left-ventricular ejection fraction, and high mean heart rate (p<0.001). In both MPIP and EMIAT, the combination of abnormal onset and slope was the most powerful multivariate risk stratifier: MPIP risk ratio 3.2 (1.7-6.0, p<0.0001), EMIAT risk ratio 3.2 (1.8-5.6, p<0.0001). INTERPRETATION: The absence of the heart rate turbulence after ventricular premature beats is a very potent postinfarction risk stratifier that is independent of other known risk factors and which is stronger than other presently available risk predictors.

Aged↗
PubMed1999

Kinetics of 123I-MIBG after acute myocardial infarction and reperfusion therapy.

UNLABELLED: Metaiodobenzylguanidine (MIBG) washout from the myocardium has been thought to reflect sympathetic nerve tone. After acute myocardial infarction, however, little is known about this parameter. The aim of this study was to determine the significance of cardiac washout after myocardial infarction and early reperfusion by investigating MIBG kinetics and correlating those kinetics to clinical parameters. METHODS: Sixty patients with acute myocardial infarction underwent planar MIBG and thallium imaging within 14 d of early reperfusion therapy. Global uptake and washout in myocardium, lungs and liver were calculated from early and delayed images. A regional analysis of myocardial kinetics in normal and infarcted myocardium and in an infarct border zone was also performed. Scintigraphic data were correlated with heart-rate variability as an electrophysiologic marker for autonomic tone and prevalence of arrhythmia in 52 patients. Heart-rate variability was described by time-domain indices from long-term electrocardiogram recordings. An age-matched normal control group for MIBG consisted of 10 individuals without heart disease. RESULTS: The infarct patients had preserved left-ventricular ejection fraction (LVEF) (56% +/- 17%). Although late myocardial uptake was expectedly lower in infarct patients compared with healthy volunteers (2.36 +/- 0.66 versus 2.80 +/- 0.55; P = 0.04), global myocardial MIBG washout was faster (11.6% +/- 7.9% versus 0.2% +/- 10.2%, respectively; P = 0.002). Lung and liver kinetics did not differ in patients and healthy volunteers. Global MIBG washout showed a weak but significant positive correlation with the baseline heart rate (r = 0.28, P = 0.03) and an inverse correlation with LVEF (r = -0.28, P = 0.04). Washout was faster in a subgroup of 8 patients with reduced heart-rate variability (16.5% +/- 9.9% versus 10.3% +/- 8.3%; P = 0.04). Regional analysis revealed similar degrees of enhanced MIBG washout for infarcted (low perfusion, low MIBG uptake) and remote myocardium (normal perfusion, high MIBG uptake), whereas the border zone (normal perfusion, low MIBG uptake) showed a nonsignificant trend toward higher washout. CONCLUSION: After myocardial infarction, changes in MIBG kinetics occur specifically in the myocardium, whereas kinetics in lung and liver remain unchanged. Even in patients with left-ventricular function preserved by reperfusion therapy, MIBG washout is abnormal and globally increased. Enhanced washout may reflect increased sympathetic nerve tone and represent increased catecholamine turnover or impaired reuptake in the subacute phase of myocardial infarction.

3-Iodobenzylguanidine↗
PubMed1996

Variability of ventricular premature complexes and mortality risk.

A method using a parameter from the field of nonlinear dynamics to quantify the variability of ventricular premature complexes (VPCs) is presented. One hundred patients with coronary artery disease and > or = 10 VPCs/hour were included in the study. The RR intervals were plotted in a three-dimensional artificial phase space, and the structures in phase space were quantified by the local scaling indices, alpha. In the frequency distribution histogram, n(alpha), for each patient, the maximum of the ventricular ectopies alpha VPC, adjusted to the VPC frequency, was assessed; alpha VPC was used as the risk indicator. Endpoints were total mortality and sudden cardiac death. During follow-up (mean 3.1 years), 28 out of 100 patients died, 16 suddenly; alpha VPC had a significant prognostic impact and was independent from other risk indicators, such as left ventricular ejection fraction (LVEF). Patients who died during follow-up were characterized by a high alpha VPC. The optimal discrimination of high risk patients and low risk patients occurred at alpha VPC = 3.0. After 4 years, the survival rate of patients with a alpha VPC > 3.0 was 59%, in contrast to 97% in patients with alpha VPC < or = 0.3. As to the sudden death mortality, the survival rates were 74% and 97%, respectively. The difference between the groups were significant for both endpoints. Patients with an increased VPC variability (i.e., alpha VPC > 3.0) were at enhanced risk of sudden death and total mortality risk; alpha VPC was independent from other risk indicators such as the LVEF or heart rate variability parameters.

Adolescent↗
PubMed1994

Effects of 12 months quinapril therapy in asymptomatic patients with chronic aortic regurgitation.

This study was performed to assess the effects of one year of ACE inhibition with quinapril on left ventricular performance and morphology in asymptomatic patients with chronic aortic regurgitation. Pre- and afterload reduction is known to have beneficial effects in patients with chronic aortic regurgitation. To date, no controlled study has been reported analyzing long term influence of ACE inhibitor treatment on asymptomatic patients with chronic aortic regurgitation. Twelve asymptomatic patients with isolated moderate to severe chronic aortic regurgitation, no coronary disease on coronary angiography and no previous vasodilator treatment were studied under control conditions and after three and 12 months of quinapril therapy (10-20 mg/day) using echocardiography and simultaneous right heart catheterization and radionuclide ventriculography at rest and during supine bicycle exercise. After one year quinapril therapy regurgitant fraction fell by 17% compared to control before therapy (p = 0.001), left ventricular enddiastolic volume at rest was reduced from 150 +/- 33 to 128 +/- 30 ml/m2 (p = 0.0003) and endsystolic volume decreased from 55 +/- 27 to 44 +/- 28 ml/m2 (p = 0.0005). Left ventricular ejection fraction at rest averaged 0.64 +/- 0.11 at control and increased after one year therapy to 0.67 +/- 0.11 (p = 0.05). With maximum exercise (100 W), ejection fraction failed to rise at control; after one year therapy with quinapril it increased to 0.70 +/- 0.15 (p = 0.019). Moreover, after one year quinapril therapy there was a significant reduction of 35% in left ventricular mass compared to control.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Quinapril therapy in patients with chronic mitral regurgitation.

Pre- and afterload reduction is known to have beneficial effects in patients with chronic mitral regurgitation. To date, no controlled study has been reported analyzing the long term influence of angiotensin-converting enzyme inhibitor treatment on patients with chronic mitral regurgitation. Therefore the aim of this study was to assess the effects of one year angiotensin-converting enzyme inhibition with quinapril on myocardial performance in patients with chronic mitral regurgitation. Twelve patients with moderate to severe isolated chronic mitral regurgitation and no coronary disease on coronary angiography were studied under control conditions and followed up until one year of quinapril therapy (10-20mg/day) using echocardiography and simultaneous right heart catheterization, and radionuclide ventriculography at rest and exercise. As the result of a significant pre- and afterload reduction after one year quinapril treatment regurgitant fraction fell from 0.43 +/- 0.10 at control before therapy to 0.25 +/- 0.08 (p = 0.0001), left ventricular end-diastolic volume was reduced from 146 +/- 26 to 109 +/- 24 ml/m2 (p = 0.0001) and end-systolic volume decreased from 63 +/- 43 to 47 +/- 29 ml/m2 (p = 0.02). Left ventricular ejection fraction at control averaged 0.59 +/- 0.20 at rest, increased to 0.65 +/- 0.21 with maximum exercise and was unchanged after one year quinapril therapy. After one year treatment left ventricular mass was reduced by 15% (p = 0.0004) and septal wall thickness decreased from 11.8 +/- 0.7 to 10.8 +/- 0.8 mm (p = 0.0006). Moreover, there was significant functional improvement of nearly one NYHA class after one year quinapril therapy. In conclusion, in patients with chronic mitral regurgitation long term angiotensin-converting enzyme inhibition with quinapril reduces regurgitation and decreases left ventricular size and mass thereby demonstrating functional improvement. In addition, these data suggest that angiotensin-converting enzyme inhibition might have the potential of delaying mitral valve surgery.

Adult↗
PubMed1993

[Ventricular fibrillation and silent myocardial ischemia in a patient without anatomic heart disease].

A 44-year-old man, apparently without heart disease, suddenly collapsed with loss of consciousness. Ventricular fibrillation was documented when an external defibrillator was connected. After cardiopulmonary resuscitation and intubation he quickly regained consciousness. Clinical examination together with echocardiography, coronary angiography and electrophysiological tests discovered no abnormalities. Biochemical tests were normal except for slightly abnormal liver functions. Several long-term ECG recordings documented asymptomatic S-T elevations. During one such episode there occurred a polymorphous ventricular tachycardia of brief duration. Because the S-T elevations persisted, despite the administration of gallopamil (50 mg twice daily for one week), a defibrillator was implanted. Gallopamil was then discontinued. Long-term ECG monitoring subsequently revealed four episodes of marked S-T elevations, three of which accompanied by ventricular arrhythmias. After resuming gallopamil, now at a dose of 50 mg three times daily, further ECG monitoring showed no abnormalities.

Adult↗
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↗
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↗
PubMed1989

Assessing antiarrhythmic drug efficacy: multivariate considerations.

The spontaneous variability of ventricular arrhythmias is the major problem in assessing antiarrhythmic drug efficacy. Efficacy is usually assessed on one form of ventricular premature beats, namely either single beats (VPC) or more complex forms like couplets or salvos. The reduction rates required to assume efficacy with a confidence of 95 per cent are 63 per cent for VPCs, 92 per cent for couples or 96 per cent for salvos. These rates are valid for two Holter electrocardiogram recordings within one week; otherwise the rates are higher and close to 100 per cent. In this paper we extend our ratio method for calculating these criteria to consider two or all three forms of ventricular premature beats simultaneously. The method is based on the first principal component. For use in practice we decided to calculate fixed criteria for each form of ventricular premature beats. For the combination of VPCs and couplets and a confidence level of 95 per cent, reduction rates of 42 per cent for VPC and 87 per cent for couplets are required. Both criteria must be fulfilled to assume the efficacy of a drug. These criteria are lower than those for each form alone. For all three forms together, reduction rates of 28, 72 and 88 per cent for VPC, couplets and salvos respectively are required.

Anti-Arrhythmia Agents↗
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↗