Effects of anisotropic myocardial conductivity in model of defibrillation current density distribution.
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Anisotropy↗
Biomedical subjects
M Malik
Publications and source records attributed to M Malik.
Computation of multifactorial receiver operator and predictive accuracy characteristics.
The computation of the so-called receiver operator characteristics (i.e. functions that assign the maximum specificity to each value of sensitivity) is simple when the characteristics are based on univariate data. On the contrary, multivariate characteristics are difficult to compute, as the complexity of their calculation increases exponentially with the dimension of the data. This paper describes an algorithm for computation of multivariate receiver operator characteristics and derived functions (namely positive and negative predictive characteristics). The algorithm is based on several concepts that increase its computational efficiency. The most important of them is a pre-sorting of the data in each dimension and the division of each dimension into groups in which the positive and negative cases are 100% stratified. The paper also presents a risk stratification study that utilised this algorithm. The study was aimed at identifying those survivors of acute myocardial infarction who are at risk of early death. A cohort of 539 patients was stratified based on time-domain (three variables) and spectral turbulence (six variables) indices of signal-averaged electrocardiogram. The computing times of the algorithm in this study are presented in the text, and the efficiency of the computation is discussed in detail.
Algorithms↗
Spectral turbulence analysis versus time-domain analysis of the signal-averaged ECG in survivors of acute myocardial infarction.
This study compared the time-domain and spectral turbulence analyses of signal-averaged electrocardiogram (ECG) for the prediction of risk after acute myocardial infarction. Signal-averaged ECGs were recorded in 553 survivors of acute myocardial infarction before hospital discharge. The study excluded cases with bundle branch block and other conduction abnormalities, and patients were followed for at least 1 year. During the first year of the follow-up period, 30 patients died and 20 presented with ventricular tachycardia/fibrillation. The signal-averaged ECG recordings were analyzed using conventional time domain at 40-250 Hz and spectral turbulence analyses. The indices provided by both types of analysis were compared in patients with and without endpoints. The optimum positive predictive characteristics were calculated for the prediction of all cause mortality and of ventricular tachycardia based on the time domain and on the spectral turbulence indices. Spectral turbulence analysis provided significantly lower positive predictive accuracy (14.5% at 40% sensitivity) than the time-domain analysis (26.7% at 40% sensitivity) for prediction of ventricular tachycardia/fibrillation during 1 year after infarction (P < .01). However, spectral turbulence analysis provided significantly higher positive predictive accuracy (27.2% at 30% sensitivity) than the time-domain analysis (16.9% at 30% sensitivity) for the prediction of 1-year all-cause mortality (P < .01). Thus, spectral turbulence analysis was inferior to the time-domain analysis in predicting ventricular tachycardia/fibrillation during the first year after myocardial infarction, but it was more powerful in predicting 1-year mortality.
Aged↗
Data protection and security.
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Algorithms↗
Short- and long-term reproducibility of QT, QTc, and QT dispersion measurement in healthy subjects.
The study investigated interobserver and intrasubject reproducibility of QT interval duration and dispersion measured in standard 12-lead ECGs recorded at 25 mm/sec. Twenty-eight healthy volunteers were studied. Each underwent four ECG recordings, which were performed 1, 7, and 30 days apart. Two independent observers analyzed each ECG record. In each lead with a distinguishable T wave pattern, the RR interval, Q-peak of T interval, and Q-end of T interval were measured using a digitizing board with a 0.1-mm resolution. From each recording the following measures were derived: the maximum, minimum, and mean QT interval; maximum, minimum, and mean heart rate corrected QT interval (QTc); QT and QTc dispersion (the difference between the maximum and minimum QT interval among the 12 leads); and adjusted QT and QTc dispersion (dispersion divided by the square root of the number of leads measured). The interobserver and short-term (1 day) and long-term (1 week and 1 month) reproducibility of individual indices was assessed by computing the relative errors and comparing them by a standard sign test. In addition, the distributions of maximum and minimum QTc values among electrocardiographic leads, and the differences between QT-end and QT-peak based measurements were investigated. The results showed that: (1) the measurement of the QT interval from standard ECG recordings is feasible and not operator dependent (interobserver relative error < 4%); (2) the duration of the QT interval in healthy volunteers is stable and its short- and long-term reproducibility is high (intrasubject relative error < 6%); (3) parameters that characterize dispersion of the QT interval in the 12-lead ECG are highly nonreproducible, both between subsequent recording (relative error of 25%-35%) and between observers (relative error 28%-33%), the reproducibility of QT dispersion is significantly lower than that of QT duration (P < 0.01); and (4) the duration of the entire QT interval correlates only weakly with the duration of the Q-peak of T interval.
Adult↗
Influence of filtering techniques on the time-domain analysis, diagnosis, and clinical use of signal-averaged electrocardiogram.
In order to investigate the effect of different filtering techniques on the time-domain analysis of signal-averaged electrocardiogram (SAECG), recordings of 1,192 subjects were analyzed using Butterworth and Del Mar filters, both set at 40-250 Hz high and low pass frequencies. The recordings were taken from six clinically defined groups: (a) survivors of acute myocardial infarction (n = 553); (b) patients with sustained symptomatic postinfarction ventricular tachycardia (n = 89); (c) patients with hyperthropic cardiomyopathy (n = 219); (d) patients with dilated cardiomyopathy (n = 76); (e) direct relatives of patients with dilated cardiomyopathy (n = 170); and (f) normal healthy volunteers (n = 85). The study investigated differences between the SAECG results reported with both filters in three individual aspects: (1) numerical values of individual time-domain SAECG variables; (2) differences in SAECG findings of patients with postinfarction ventricular tachycardia and pair matched patients with uncomplicated follow-up after acute infarction; and (3) the power of SAECG findings to predict high risk of arrhythmic complication (sudden death and/or sustained ventricular tachycardia) among survivors of acute myocardial infarction. Compared with the Butterworth filter, the Del Mar filter led to a systematic difference of +8% in total QRS duration, was equally powerful in distinguishing between the pair matched patients with and without postinfarction ventricular tachycardia, and was statistically significantly more powerful in identifying those survivors of acute infarction who were at high risk of arrhythmic complications. The study concludes that the use of different filters may produce discordant results of SAECG analysis. Normal and abnormal values for various types of SAECG recording and analysis have to be established individually for different equipment and different software settings. These optimal cut-offs of SAECG variables should also take into account the clinical characteristics of patient groups.
Cardiomyopathy, Dilated↗
Is the computer precise all the time?
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Computers↗
Relationship between short- and long-term measurements of heart rate variability in patients at risk of sudden cardiac death.
Because of technical difficulties in analyzing heart rate variability (HRV) from ambulatory Holter recordings over 24-hour periods, short-term recordings are more practical for the clinical application of HRV. However, the relationship between short- and long-term recordings is unclear. In this study, short-term (10 min) electrocardiograms were assessed in the supine position, during passive head-up tilt and on standing in 15 patients (aged 39 +/- 14 years) with ventricular tachycardia/fibrillation not associated with coronary artery disease. Spectral HRV was computed as total frequency (TF: 0.01-1.00 Hz), low frequency (LF: 0.04-0.15 Hz), and high frequency (HF: 0.15-0.40 Hz) components. The short-term HRV parameters were compared with those obtained from long-term (24 hour) recordings from the same patients. There was a significant decrease in the HF component of HRV and a significant increase in LF/HF ratio during passive tilt or active standing compared with supine recordings, but no significant changes were observed in the TF or LF components. All frequency components of HRV for the 24-hour periods showed significant correlation with the values from short-term recordings (tau ranged from 0.67-0.87). Stepwise multivariate regression analysis showed that both the TF and HF components of HRV over 24 hours were predominantly related to the corresponding frequency components of HRV in the supine position, while the LF component of HRV over 24 hours was predominantly related to that on standing. Our observations suggest that the short-term HRV is related to the long-term value, but global HRV over 24 hours cannot completely be replaced by the short-term recordings.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Ambulatory assessment of the QT interval in patients with hypertrophic cardiomyopathy: risk stratification and effect of low dose amiodarone.
This study aims to assess the dynamics of the QT interval in patients with hypertrophic cardiomyopathy (HCM). Three consecutive QT intervals and the preceding RR intervals were measured on 24 hour ambulatory electrocardiograms at 30-minute intervals in ten high risk patients with HCM (sudden cardiac death [SCD] and/or documented ventricular fibrillation), aged 29 +/- 17 years, compared with ten age and sex matched low risk patients with HCM (no syncope, no adverse family history, and no ventricular tachycardia on Holter monitoring), and ten normal subjects. Another ten patients who were on amiodarone therapy (200-mg daily) were also studied. Patients with intraventricular conduction defects were excluded. There were 4,424 pairs of QT intervals and their preceding RR intervals were measured in this study. A nonsignificant prolongation in the QT interval and a significant prolongation in QTc values (Bazett's and Fridericia's formulas) were demonstrated in patients with HCM compared with normals. There were no significant differences in the QT and QTc between high and low risk patients. The slope of regression line for the QT against RR interval was significantly different between normals and HCM (0.1583 +/- 0.040 vs. 0.2017 +/- 0.043, P < 0.05), but not between high and low risk patients. Amiodarone significantly prolonged the QT and QTc without significantly altering the slope of the regression line (0.2017 +/- 0.043 vs 0.2099 +/- 0.037, NS). Our findings support the observations that there is a prolonged QT interval in patients with HCM and that there is no significant use dependent effect of amiodarone on ventricular repolarization.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
QT dispersion: problems of methodology and clinical significance.
QT dispersion is defined as the difference in QT interval between the different leads of the surface 12-lead ECG. This may provide an indirect measure of the underlying inhomogeneity of myocardial repolarization, which is believed to be important in arrhythmogenesis. Methodology for determining QT dispersion varies significantly between studies, and the results of these studies need to be interpreted in light of the methodology used. Although QT dispersion is developing into an important research tool, as yet it has no established role in clinical practice. Once standardization of methodology is achieved a clinical role may emerge, particularly in the assessment of patients before and after intervention aimed at reduction of arrhythmia risk.
Anti-Arrhythmia Agents↗
Decreased heart rate variability in survivors of sudden cardiac death not associated with coronary artery disease.
BACKGROUND: Although heart rate variability has already been studied in survivors of sudden cardiac death secondary to coronary artery disease, an assessment of heart rate variability in survivors of sudden cardiac death not associated with coronary artery disease has not been made. METHODS: 10 patients with aborted sudden cardiac death not associated with coronary artery disease (seven patients with primary ventricular fibrillation and three with unclassified mild cardiomyopathy) underwent two channel 24 hour Holter monitoring in a drug free state. All subjects were in sinus rhythm and had normal atrioventricular conduction and normal cardiac function. Spectral heart rate variability was analysed on a Holter analysis system and was expressed as total (0.01-1.00 Hz), low (0.04-0.15 Hz) and high (0.15-0.40 Hz) frequency components for each hour. Heart rate variability index was calculated for the 24 hour periods. 10 age and sex matched healthy subjects were taken as a control group. RESULTS: The spectral heart rate variability over 24 hours was significantly lower in survivors of sudden cardiac death than in controls (total 38(15) v 48(14) ms; low, 25(11) v 32(13) ms; and high, 13(8) v 18(8) ms; p < 0.05 for all comparisons). The differences in the ratio of low/high (2.19(0.76) v 1.98(0.50), p = 0.132), mean heart rate (77(12) v 69(12) beats/min, p = 0.070), and heart rate variability index (38(12) v 44(16), p = 0.287) over 24 hours between survivors of sudden cardiac death and controls did not reach significance. Comparisons of the hourly heart rate variability over the 24 hour period between the two groups showed that the differences in all components of heart rate variability, low/high ratio and mean heart rate were highly significant. Furthermore, there was no significant difference in the maximum hourly heart rate variability over the 24 hour period. The minimum hourly heart rate variability was, however, significantly lower in survivors of sudden cardiac death than in controls (total, 20(8) v 28(4) ms; low, 12(6) v 17(3) ms; high, 6(2) v 8(2) ms; p < 0.05 for all comparisons). CONCLUSIONS: These findings suggest that there is abnormal autonomic influence on the heart in patients without coronary artery disease at risk of sudden cardiac death. Hourly analysis of heart rate variability throughout the 24 hour period may provide additional information important in the identification of high risk patients.
Adolescent↗
Heart rate variability and clinical cardiology.
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Heart Diseases↗
Temporal influences on the prediction of postinfarction mortality by heart rate variability: a comparison with the left ventricular ejection fraction.
OBJECTIVE: To examine the influence of the duration of follow up on the values of heart rate variability (HRV) and the left ventricular ejection fraction (LVEF) for predicting mortality after infarction. BACKGROUND: HRV is an index of autonomic balance that identifies patients at a high risk of arrhythmic events. The index is most depressed during the first few weeks after myocardial infarction whereas left ventricular function tends to deteriorate with time. HYPOTHESIS: The value of depressed HRV measured before discharge from hospital for predicting mortality after infarction should decline with time. METHODS: The HRV and the LVEF were assessed in 433 survivors of a first acute myocardial infarction: HRV < 20 units and LVEF < 40% were taken as cut off points. Kaplan-Meier survival functions for total cardiac mortality and sudden cardiac death were calculated for the whole five year follow up period and for different intervening periods. RESULTS: During follow up of four weeks to five years there were 46 (10.6%) deaths and 15 (3.5%) patients died suddenly. Within the whole follow up period, HRV < 20 units and LVEF < 40% were both strongly associated with total cardiac mortality (p < 0.0001), but HRV was an independent predictor of total cardiac mortality only during the first six months of follow up. There were no deaths predicted by HRV < 20 units after the first year of follow up whereas LVEF < 40% had a sensitivity of 43% and a positive predictive accuracy of 9% for predicting death during this period. HRV < 20 units was better than LVEF < 40% in predicting sudden deaths during the first year of follow up but was an independent predictor only of those sudden deaths occurring within six months of infarction. CONCLUSIONS: The duration of follow up affects the prediction of sudden death and total cardiac mortality from HRV. Reduced HRV as measured before discharge from hospital does not seem to retain independent prognostic value after six months of follow up. These findings have potential implications for the serial evaluation of HRV and for the prevention of sudden death after myocardial infarction.
Death, Sudden, Cardiac↗
Adjustment of QT dispersion assessed from 12 lead electrocardiograms for different numbers of analysed electrocardiographic leads: comparison of stability of different methods.
OBJECTIVE: Normal electrocardiographic recordings were analysed to establish the influence of measurement of different numbers of electrocardiographic leads on the results of different formulas expressing QT dispersion and the effects of adjustment of QT dispersion obtained from a subset of an electrocardiogram to approximate to the true QT dispersion obtained from a complete electrocardiogram. SUBJECTS AND METHODS: Resting 12 lead electrocardiograms of 27 healthy people were investigated. In each lead, the QT interval was measured with a digitising board and QT dispersion was evaluated by three formulas: (A) the difference between the longest and the shortest QT interval among all leads; (B) the difference between the second longest and the second shortest QT interval; (C) SD of QT intervals in different leads. For each formula, the "true" dispersion was assessed from all measurable leads and then different combinations of leads were omitted. The mean relative differences between the QT dispersion with a given number of omitted leads and the "true" QT dispersion (mean relative errors) and the coefficients of variance of the results of QT dispersion obtained when omitting combinations of leads were compared for the different formulas. The procedure was repeated with an adjustment of each formula dividing its results by the square root of the number of measured leads. The same approach was used for the measurement of QT dispersion from the chest leads including a fourth formula (D) the SD of interlead differences weighted according to the distances between leads. For different formulas, the mean relative errors caused by omitting individual electrocardiographic leads were also assessed and the importance of individual leads for correct measurement of QT dispersion was investigated. RESULTS: The study found important differences between different formulas for assessment of QT dispersion with respect to compensation for missing measurements of QT interval. The standard max-min formula (A) performed poorly (mean relative errors of 6.1% to 18.5% for missing one to four leads) but was appropriately adjusted with the factor of 1/square root of n (n = number of measured leads). In a population of healthy people such an adjustment removed the systematic bias introduced by missing leads of the 12 lead electrocardiogram and significantly reduced the mean relative errors caused by the omission of several leads. The unadjusted SD was the optimum formula (C) for the analysis of 12 lead electrocardiograms, and the weighted standard deviation (D) was the optimum for the analysis of six lead chest electrocardiograms. The coefficients of variance of measurements of QT dispersion with different missing leads were very large (about 3 to 7 for one to four missing leads). Independently of the formula for measurement of QT dispersion, omission of different leads produced substantially different relative errors. In 12 lead electrocardiograms the largest relative errors (> 10%) were caused by omitting lead aVL or lead V1. CONCLUSIONS: Because of the large coefficients of variance, the concept of adjusting the QT dispersion for different numbers of electrocardiographic leads used in its assessment is difficult if not impossible to fulfil. Thus it is likely to be more appropriate to assess QT dispersion from standardised constant sets of electrocardiographic leads.
Adult↗
Changes in triiodothyronine (T3) mononuclear leukocyte receptor kinetics after T3 administration and multiple cold-air exposures.
Repeated cold-air exposures increase human triiodothyronine (T3) plasma clearance rates. To study the response of the nuclear T3 receptor (NT3R) in this condition, binding characteristics were analyzed in human mononuclear leukocytes (MNL). In addition, we supplemented one group of individuals with a daily oral replacement dose of T3 to isolate the influence of serum thyroxine (T4) and thyrotropin (TSH) levels on receptor kinetics. The subjects were exposed to cold air (4 degrees C) twice/d, 30 min/exposure, for a total of 80 exposures. The T3-subjects received placebo [n = 8] and the T3 + subjects received T3 (30 micrograms/d) [n = 8] in a double-blind fashion. Mononuclear leukocytes were isolated from peripheral blood before the cold exposure and drug regimen began, and then after every 20 exposures. The dissociation constant (Kd) and maximum binding capacity (MBC) of the NT3R values were log transformed to minimize between-subject variability. In the T3+ group, serum total thyroxine (TT4), free T4 (FT4), and TSH were approx 50% lower than both basal and T3-values. The log10Kd increased 0.304 +/- 0.139 (p < 0.04) and the log10MBC increased 0.49 +/- 0.10 (p < 0.001) in the T3+ subjects compared to baseline. This change in MBC represents a 311% increase in the MBC over baseline and a fivefold increase over placebo-treated subjects. The T3- group showed no change in MBC over the study. These results describe for the first time the rapid modulation of the NT3R in response to the combined influence of cold exposure and reduced circulating T4 and TSH.
Adaptation, Physiological↗
Do patients with neurally mediated syncope have augmented vagal tone?
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Adolescent↗
Components of heart rate variability--what they really mean and what we really measure.
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Heart Rate↗
Long-term echocardiographic follow-up of acromegalic heart disease.
Heart muscle disease in acromegaly manifests usually as cardiac hypertrophy. Based on a retrospective analysis, it was suggested that cardiac hypertrophy is slowly reversible after normalization of plasma growth hormone levels. The reversibility of acromegalic heart muscle disease during and after treatment of acromegaly was studied prospectively. A cohort of 78 patients was examined echocardiographically in 1981, and 38 survivors of this group were reexamined 10 years later. Patients were classified according to original hormonal activity in 1981, and change in hormonal activity during follow-up into the following 4 groups: group I--hormonally inactive for entire follow-up (n = 10); group II--hormonally active for entire follow-up (n = 11); group III--initially hormonally inactive with later resurgence (n = 6); and group IV--initially hormonally active with later normalization of growth hormone levels (n = 11). No significant echocardiographic changes occurred during follow-up in group I. Left ventricular posterior wall and septal diastolic thickness, and left ventricular mass increased significantly (all p < 0.05) in group II. Left ventricular posterior wall thickness, mass and diastolic volume increased significantly (p < 0.05, < 0.01 and < 0.001, respectively) in group III. On the contrary, there were significant decreases in left ventricular mass, and both diastolic and systolic left ventricular volumes (p < 0.01, < 0.05 and < 0.05, respectively) in group IV. It is concluded that both hypertrophy and dilatation of the left ventricle in acromegaly are slowly reversible after successful treatment. On the contrary, continuing or relapsed hyperproduction of growth hormone causes further deterioration of acromegalic heart disease.
Acromegaly↗