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Biomedical subjects

M Malik

Publications and source records attributed to M Malik.

At least 145 records · Page 8Linked to original sources
PubMed1996

Use of ventricular premature complexes for risk stratification after acute myocardial infarction in the thrombolytic era.

The independent predictive role of ventricular premature complex (VPC) frequency in the stratification of mortality risk after acute myocardial infarction (AMI) was established in the prethrombolytic era by extensive multicenter trials. Thrombolysis has lead to important changes in the natural history of patients after AMI, so that reassessment of established risk factors is now required. The prognostic significance of VPCs was assessed in 680 patients, of whom 379 received early thrombolytic therapy. All patients underwent 24-hour Holter monitoring in a drug-free state between 6 and 10 days after AMI. Patients were followed up for 1 to 8 years. During the first year of follow-up, cardiac death occurred in 33 patients, sudden death in 24, and sustained ventricular tachycardia in 20. Mean VPC frequency was significantly higher in patients who died of cardiac causes, in those who died suddenly, and in those with arrhythmic events during the first year of follow-up. This was also true when patients who did and did not undergo thrombolysis were considered separately. The positive predictive accuracy of VPC frequency in predicting adverse cardiac events was greater in patients who did than did not undergo thrombolysis. At a sensitivity level of 40%, the positive predictive accuracy for cardiac mortality and arrhythmic events for the group with thrombolysis was 19.4% and 25.8%, respectively, compared with 16% and 16% for those without thrombolysis. Moreover, the highest VPC frequency for the dichotomy of patients into high-and low-risk groups was 25 VPCs/hour for patients without thrombolysis. VPC frequency appears to be more highly predictive of prognosis after AMI in patients who have undergone thrombolysis than in those who have not, but the optimal frequency for dichotomy is higher in the former.

Adult↗
PubMed1996

Comparison of time domain and spectral turbulence analysis of the signal-averaged electrocardiogram for the prediction of prognosis in idiopathic dilated cardiomyopathy.

BACKGROUND: Despite significant advances in the treatment of heart failure, the prognosis of patients with idiopathic dilated cardiomyopathy remains poor. Although several of prognostic variables have been shown to be useful in risk stratification of patients with idiopathic dilated cardiomyopathy, their predictive accuracy is low and clinical usefulness uncertain. HYPOTHESIS: This study was undertaken to assess the signal-averaged electrocardiogram (SAECG) in patients with idiopathic dilated cardiomyopathy and to compare the ability of time domain and spectral turbulence analytic techniques to predict clinical outcome. METHODS: SAECG analysis was performed in 80 patients with idiopathic dilated cardiomyopathy. Nineteen patients had left bundle-branch block and eight were taking low-dose amiodarone for life-threatening arrhythmias. Conventional time domain and spectral turbulence analyses of the SAECG were performed using Del Mar 183 software. RESULTS: During a follow-up of 27 +/- 19 months, 24 patients developed progressive heart failure, while the others remained clinically stable. Late potentials were detected in 28% of patients and were equally frequent in patients with and without progressive heart failure (38 vs. 23%, p = 0.20). Spectral turbulence analysis was abnormal in 34% of patients, and patients with abnormal results developed progressive heart failure more frequently than those with normal results (50 vs. 17%, p = 0.01). All spectral turbulence analysis parameters were significantly different in patients with progressive heart failure compared with those who remained clinically stable (p < or = 0.01). Furthermore, progressive heart failure-free survival at 2 years was significantly lower in patients with abnormal compared with normal results (63 vs. 87%; p < 0.05), but was similar in patients with and without late potentials (72 vs. 83%; p = 0.30). The relative risk for developing progressive heart failure using spectral turbulence analysis was 3.4 (95% confidence interval 1.2-9.7) and 2.8 (95% confidence interval 1.1-8.7) using time domain analysis. The sensitivity, specificity, and the positive and negative predictive accuracy for identifying patients who developed progressive heart failure were 50, 83, 50, and 83%, respectively, (p = 0.01) for spectral turbulence analysis, and 36, 85, 45 and 80%, respectively, (p = 0.09) for time domain analysis. CONCLUSION: Abnormalities in the SAECG of patients with idiopathic dilated cardiomyopathy are common and appear to provide a noninvasive marker for development of progressive heart failure.

Adult↗
PubMed1996

QT interval change with age in an overtly healthy older population.

BACKGROUND: Prolonged QT interval on the surface electrocardiogram (ECG) is known to be associated with arrhythmias, coronary heart disease, and sudden cardiac death. Increased QT dispersion has also been related to arrhythymias which are more frequent in the elderly. HYPOTHESIS: This study investigated the relationship between aging, QT interval, and QT dispersion. METHODS: Normal resting ECGs were recorded from 96 healthy subjects (73 women, age range 40-102 years). No subject had symptoms or signs of heart disease and none was on medication affecting cardiac function. All had normal heart size on chest x-ray and normal electrolytes. Using a digitizing board, the RR and QT intervals were measured on each lead of each ECG, excluding only the leads in which the T wave was not visible. Mean RR, mean QT interval, and heart rate-adjusted QTc interval (standard Bazet's formula) were obtained from these measurements. Further, QT dispersion was calculated for each ECG as (1) the difference between the maximum and minimum QT interval, and (2) as the coefficient of variance of QT interval of all measurable leads. RESULTS: A significant correlation between aging and prolonged QTc was noted in the total population (r = 0.43, p < 0.05), as well as in men (r = 0.4, p < 0.05) and women (r = 0.23, p < 0.05) separately. There was no association between QT dispersion and increasing age regardless of the method of calculation (r = -0.04, r = -0.08 respectively, both NS). CONCLUSION: The rate-adjusted QT interval is prolonged with increasing age and may contribute to the increased risk of ventricular arrhythmias and cardiac mortality in elderly patients.

Adult↗
PubMed1996

Predictive power of increased heart rate versus depressed left ventricular ejection fraction and heart rate variability for risk stratification after myocardial infarction. Results of a two-year follow-up study.

OBJECTIVES: The aim of this study was to compare the predictive value of mean RR interval assessed from predischarge Holter recordings with that of heart rate variability and left ventricular ejection fraction for risk stratification after myocardial infarction. BACKGROUND: Heart rate variability is a powerful tool for risk stratification after myocardial infarction. Although heart rate variability is related to heart rate, little is known of the prognostic value of 24-h mean heart rate. METHODS: A total of 579 patients surviving the acute phase of myocardial infarction were followed up for at least 2 years. Predischarge heart rate variability, 24-h mean RR interval and left ventricular ejection fraction were analyzed. RESULTS: During the first 2 years of follow-up, there were 54 deaths, 42 of which were cardiac (26 sudden). Shorter mean RR interval was a better predictor of all-cause mortality as well as cardiac and sudden death than depressed left ventricular ejection fraction. Depressed heart rate variability predicted the risk of death better than mean RR interval for sensitivities < 40%. For sensitivities > or = 40%, mean RR interval was as powerful as heart rate variability. All three variables performed equally well in predicting nonsudden cardiac death. For cardiac death prediction, a left ventricular ejection fraction < 35% had a 40% sensitivity, 78% specificity and 14% positive predictive accuracy; a mean RR interval < 700 ms had a 45% sensitivity, 85% specificity and 20% positive predictive accuracy; and a heart rate variability < 17 U had a 40% sensitivity, 86% specificity and 20% positive predictive accuracy. CONCLUSIONS: Predischarge 24-h mean heart rate is a strong predictor of mortality after myocardial infarction that can compete with left ventricular ejection fraction and heart rate variability.

Cohort Studies↗
PubMed1996

Distinction between arrhythmic and nonarrhythmic death after acute myocardial infarction based on heart rate variability, signal-averaged electrocardiogram, ventricular arrhythmias and left ventricular ejection fraction.

OBJECTIVES: We investigated whether heart rate variability, the signal-averaged electrocardiogram (ECG), ventricular arrhythmias and left ventricular ejection fraction predict the mechanism of cardiac death after myocardial infarction. BACKGROUND: Postinfarction risk stratification studies have almost exclusively focused on predicting the risk of arrhythmic death. The factors that identify and distinguish persons at risk for arrhythmic and nonarrhythmic death are poorly known. METHODS: Heart rate variability, the signal-averaged ECG, ventricular arrhythmias and left ventricular ejection fraction were assessed in 575 survivors of acute myocardial infarction. The patients were followed up for 2 years; arrhythmic and nonarrhythmic cardiac deaths were used as clinical end points. During the follow-up period, 47 cardiac deaths occurred, 29 (62%) arrhythmic and 18 (38%) nonarrhythmic. RESULTS: All risk factors were associated with cardiac mortality in univariate analysis. With the exception of left ventricular ejection fraction, they were also predictors of arrhythmic death. Depressed heart rate variability (p < 0.001), ventricular ectopic beats (p < 0.001) and low ejection fraction (p < 0.001) were related to nonarrhythmic death. In multivariate analysis, depressed heart rate variability (p < 0.001) and runs of ventricular tachycardia (p < 0.05) predicted arrhythmic death. Nonarrhythmic death was associated with depressed heart rate variability (p < 0.001), ventricular ectopic beats (p < 0.001) and low ejection fraction (p < 0.01). By selecting patients with depressed heart rate variability, long filtered QRS duration or ventricular arrhythmias and excluding patients with the lowest ejection fraction, we identified a group in which 75% of deaths were arrhythmic. Similarly, by selecting patients with a low ejection fraction and excluding patients with the lowest heart rate variability, we identified a group in which 75% of deaths were nonarrhythmic. CONCLUSIONS: Arrhythmic death was associated predominantly with depressed heart rate variability and ventricular tachycardia runs, and nonarrhythmic death with low ejection fraction, ventricular ectopic beats and depressed heart rate variability. A combination of risk factors identified patient groups in which a majority of deaths were either arrhythmic or nonarrhythmic.

Electrocardiography↗
PubMed1996

Patients treated with unfractionated heparin during open heart surgery are at high risk to form antibodies reactive with heparin:platelet factor 4 complexes.

Recent studies have demonstrated a strong association between type II (immunologically mediated) heparin-induced thrombocytopenia/thrombosis (HITP) and antibodies reactive with complexes consisting of heparin and platelet factor 4 (PF4), a heparin-binding protein normally found in platelet-alpha granules. However, the frequency with which such antibodies develop in patients given treatment with heparin has not yet been defined. We studied the development of heparin:PF4-specific antibodies in 51 patients who received a single dose of unfractionated heparin (UFH) during cardiac catheterization and were then given UFH or low-molecular-weight heparin (LMWH) again during and after open heart surgery. Eleven of the 51 patients (22%) had antibodies reactive with heparin:PF4 when they were admitted for cardiac surgery; these antibodies were mainly of the immunoglobulin M (IgM) class and were apparently stimulated by exposure to UFH at cardiac catheterization. Seventeen of 34 patients (50%) without preexisting antibody who were given UFH during and for 1 to 3 days after surgery formed immunoglobulin G antibodies or IgM antibodies (or both) by the sixth postoperative day. Overall, 27 of 44 patients (61%) who were given UFH at surgery had antibodies by the time of hospital discharge. None of 6 patients without preexisting antibody who were given LMWH at surgery formed antibodies (p < 0.03). However, LMWH was given as a single injection only on the day of surgery. The titer of the antibodies formed by patients receiving UFH ranged from 1:10 to 1:200, significantly lower than those in patients with a clinical diagnosis of HITP. Moderate thrombocytopenia was common after open heart surgery, but platelet levels in patients who had preexisting antibodies or formed new antibodies did not differ significantly from those in patients without antibody. Clinically significant thrombosis did not develop in any patient and HITP was not diagnosed in any patient. Antibodies reactive with heparin:PF4 formed in only 3 of 66 patients (4.5%) undergoing other types of surgery. One of these patients had been given UFH 3 months previously; the other 2 may have been exposed to heparin used to flush intravenous lines postoperatively. No antibodies reactive with heparin:PF4 were found in any of 108 normal subjects. We conclude that UFH is more immunogenic than has been thought and that patients exposed to this anticoagulant during open heart surgery are at high risk to form low titer (</= 1:200) antibodies reactive with heparin:PF4. Further studies are needed to determine whether such antibodies are clinically significant--that is, whether sensitized patients are at risk to develop HITP if heparin treatment is continued for more than 1 to 3 days or is reinstituted at a later date.

Adult↗
PubMed1996

If Dr. Bazett had had a computer....

The original data of 109 pairs of RR and QT intervals published by Dr. Bazett in 1920 were subjected to a computerized optimization of the QT/RR relationship. Four generic formulae expressing QT interval as alpha + beta RR mu, alpha + beta e mu RR, alpha + beta e(1/mu RR), and alpha + beta ln mu(10 x RR) were used, and for each formula, optimum combinations parameters alpha, beta, and mu were established that lead to minimum differences between the actual QT interval intervals and values predicted by the model. The results show that independent of the generic formula used, parameters of the model can be selected that provide a close fit of the measured values. Compared to the optimum models obtained in this way, the optimum fit of the Bazett model, QT = beta RR1/2, overestimates the QT intervals for slow heart rates. In addition to demonstrating the procedure of obtaining an optimum QT/RR model for a given data set, the study suggests that critical understanding of the principal limitations of every QT/RR model is more important than its mathematical form.

Computer Simulation↗
PubMed1996

Stepwise strategy of using short- and long-term heart rate variability for risk stratification after myocardial infarction.

Independent of other established risk factors, depressed heart rate variability (HRV) has been shown to be a powerful predictor of cardiac events after MI. Unfortunately, the need of 24-hour ECG recording and subsequent laborious editing of Holter data limits the clinical use of long-term HRV. In order to perform post-MI risk stratification more efficiently, we evaluated the value of short-term HRV estimates for preselection of patients who might benefit from long-term HRV assessment. Two measures were assessed from 24-hour ambulatory ECGs recorded in 729 survivors of acute MI prior to hospital discharge. In addition to a complete 24-hour HRV index, a standard deviation of normal-to-normal RR intervals (SDNN) was obtained from the first stationary and ectopic free 5-minute segment of the Holter recording. Predictive power (relation between positive predictive accuracy and sensitivity) of a complete 24-hour HRV index in identifying patients who suffered from cardiac mortality or arrhythmic events during a 2-year follow-up was compared to the predictive power of assessing the 24-hour HRV index limited to 50%, 40%, or 20% of patients with the lowest values of 5-minute SDNN. The HRV index was significantly lower in patients who died (19 +/- 11 units) or had an arrhythmic event (AE) (18 +/- 11 units) compared to those who survived without an event (28 +/- 10 resp. 27 +/- 11 units; P < 0.001). Similarly, 5-minute SDNN was significantly lower in patients who died (25 +/- 12 ms) or suffered an AE (26 +/- 13 ms) compared to survivors (40 +/- 19 ms resp. 39 +/- 19 ms; P < 0.001). When limited to patients with depressed 5-minute SDNN, assessment of the HRV index performed better than 5-minute SDNN alone in positive prediction of cardiac events. Preselected assessment of the lowest HRV index in 50% to 20% of the total population yielded a 2-year cardiac event prediction rate as high as analysis of the HRV index in all patients. Long-term HRV assessment for risk stratification after MI in patients preselected by depressed short-term SDNN is safe and efficient, and allows a practical identification of patients with the highest likelihood of cardiac events during long-term follow-up.

Aged↗
PubMed1996

Changes in heart rate variability with age.

Depressed heart rate variability (HRV) after a myocardial infarction is associated with increased mortality. This is thought to be due to reduced parasympathetic activity and heightened sympathetic activity. Aging is associated with depressed HRV, but little is known of the affect of aging on parasympathetic activity. This study examined 56 healthy subjects (age range 40-102 years; 39 women). None had a history of heart disease or were on medication that would affect cardiac function. All had normal resting ECGs, normal heart size on chest X ray, and normal electrolytes. In all subjects, 24-hour Holter recordings were performed and used to measure HRV. In particular, the study examined the affect of age on HRV triangular index, which gives an estimate of overall HRV, and on RMSSD (square root of the mean squared differences of successive normal-to-normal RR intervals), which gives an estimate of short-term components of HRV and is thought to reflect the overall extent of vagal modulations of heart rates. Both these parameters were compared in patients younger and older than 70 years. Each recording lasted at least 17 hours; the majority of recordings were longer than 20 hours. There was a significant decrease in HRV triangular index with age (r = -0.4, P < 0.05) and no significant change in RMSSD with age(r = -0.08, P = NS). There was a significant difference in HRV index in those > 70 years compared with those < 70 years (38.0 +/- 9.3 vs 31.0 +/- 11, respectively, P < 0.02). There was no significant difference in RMSSD between the two age groups (26.7 +/- 8.2 ms vs 28.4 +/- 11.3 ms, respectively, P = NS). Thus, the study concludes that aging reduces the global measure of HRV and may reflect reduced responsiveness of autonomic activity to external environmental stimuli with age. However, the time-domain short-term components of HRV are not affected by age and, therefore, the fast and presumably vagal modulations of heart rate appear to be maintained.

Adult↗
PubMed1996

Effect of digoxin on the ventricular rate variability during paroxysmal atrial fibrillation.

This study investigated whether the irregularity of ventricular cycle length during atrial fibrillation (AF) is affected by digoxin. Patients (n = 41) with paroxysmal AF enrolled in a randomized crossover comparison of digoxin and placebo underwent 24-hour ambulatory monitoring during each treatment. Tapes containing AF episodes lasting at least 2 minutes were selected (24 recordings on placebo and 17 on digoxin). The mean (mRR) and standard deviation (SDRR) of RR intervals was calculated for each 30-second segment of AF. The resulting SDRR values were clustered according to bins of mRR values ranging from 350-650 ms in 25-ms steps. In each bin, the SDRR values of all placebo and all digoxin recordings were statistically compared for the top 5, 10, and 15 percentiles of each bin which represented the extremes of ventricular cycle length irregularity during AF. There were no significant differences between the total data of SDRR values in individual bins of mRR. However, the top 5, 10, and 15 percentiles of SDRR values corresponding to mRR values from 350-550 ms were significantly reduced by digoxin (P < 0.0001). The study concludes that although digoxin does not influence the mean variability of RR cycles during AF paroxysms, it suppresses episodes in which a fast ventricular response is associated with extreme variability of RR periods.

Anti-Arrhythmia Agents↗
PubMed1996

Is vagal innervation to the atrioventricular node impaired after radiofrequency ablation of the slow atrioventricular nodal pathway?

To assess the potentially adverse effects of RF catheter ablation (RFCA) of the slow AV nodal pathway on the parasympathetic innervation to the AV node in patients with AV nodal reentrant tachycardia (AVNRT), AV nodal conduction was evaluated following vagal stimulation by means of a phenylephrine bolus injection (200 micrograms) before and after RFCA in ten patients (mean age, 37 +/- 14 years). Nine patients with AV reentrant tachycardia (AVRT) due to a left free wall accessory pathway served as a control group (mean age of 37 +/- 12 years). Whereas no prolongation of the AH interval was observed in the AVNRT group following the phenylephrine bolus during sinus rhythm, despite a significant slowing in sinus rate, phenylephrine administration in AVRT patients was associated with both slowing of the sinus rate and prolongation of the AH interval. Following successful RFCA, the same responses were observed. To delineate the indirect effect of heart rate on AV conduction in response to the phenylephrine bolus, the AH interval was also measured during fixed atrial pacing. A marked prolongation of the AH interval occurred in both groups following phenylephrine administration. This prolongation was biphasic in 50% of AVNRT patients before ablation, suggesting a predominant effect of vagal stimulation on the fast AV nodal pathway. RFCA was associated with disappearance of discontinuous AV conduction in all but one patient with AVNRT. Vagal stimulation caused the same amount of AH interval prolongation as before RFCA in both study groups. In conclusion, patients with AVNRT have a preserved modulation of AV nodal conduction in response to vagal stimulation during sinus rhythm. In addition, vagal stimulation seems to exert a predominant effect on the fast AV nodal pathway. RFCA of the slow AV nodal pathway in patients with AVNRT does not cause detectable damage to the vagal innervation to the AV node.

Adult↗
PubMed1996

Decreased heart rate variability in patients with congestive heart failure and chronotropic incompetence.

UNLABELLED: Heart rate variability was studied in 41 patients (aged 48 +/- 12 years) with congestive heart failure secondary to idiopathic dilated cardiomyopathy. All patients underwent a treadmill exercise test and 24-hour Holter ECG monitoring. Chronotropic incompetence was defined as the failure to achieve > or = 80% of the predicted maximal heart rate response given by 220--age (years) at peak exercise. Spectral heart rate variability was analyzed from 24-hour Holter ECGs 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. The standard deviation of all normal RR intervals (SDNN) was also computed. Chronotropic incompetence was observed in ten patients. Peak oxygen consumption was significantly lower in patients with chronotropic incompetence compared with those without chronotropic incompetence. The total (5.11 +/- 1.26 ln [ms2] vs 6.41 +/- 0.92 ln [ms2]; P = 0.009) and low (3.38 +/- 1.65 ln [ms2] vs 5.45 +/- 1.34 ln [ms2]; P = 0.003), but not the high (3.42 +/- 1.04 ln [ms2] vs 4.00 +/- 1.12 ln [ms2]; P = 0.249) frequency components of heart rate variability were significantly lower in patients with chronotropic incompetence, although there was no significant difference in mean heart rate (88 +/- 20 beats/min vs 86 +/- 15 beats/min; P = 0.831) or left ventricular ejection fraction (22% +/- 10% vs 24% +/- 10%; P = 0.619). SDNN was also significantly lower in patients with chronotropic incompetence compared with those without chronotropic incompetence (64 +/- 34 ms vs 102 +/- 37 ms; P = 0.030). CONCLUSIONS: The observation that heart rate variability is significantly decreased in patients with congestive heart failure who have chronotropic incompetence suggests that chronotropic incompetence may relate to an abnormal autonomic influence on the heart in these patients.

Autonomic Nervous System↗
PubMed1996

Changes of QT intervals associated with postural change in patients with chronic atrial fibrillation.

Although different computerized systems have been developed to localize specific patterns in electrocardiographic (ECG) signals, it is still difficult to detect T waves and measure QT intervals during atrial fibrillation. This article demonstrates the use of an auto-correlation (ECG) based system that was used to investigate the dynamicity of QT intervals related to active postural change in patients with chronic atrial fibrillation. Twenty patients (9 male, mean age 63 years) with chronic atrial fibrillation (8 idiopathic, 12 organic heart disease) were examined. Seventeen of these patients were on digoxin, but patients with other conditions potentially affecting the autonomic nervous system were not included. A 3-channel ECG was recorded digitally during active postural change from supine to standing. Data were first analyzed by the Burdick Altair system and subsequently processed using an in-house software package evaluating auto-correlations of ECG signals. An ECG channel with suitable repolarization patterns was found in 15 patients. The mean QT interval of 409.8 +/- 11.1 ms (mean +/- SE) recorded during supine position shortened to 401.9 +/- 9.89 ms during the first minute of active standing (P < 0.05) and to 394.8 +/- 10.0 ms during the second minute of active standing (P < 0.005). It did not further change during the subsequent minutes of active standing. The study shows that automatic detection of QT intervals during atrial fibrillation is possible. Although the effect of position change of the heart cannot be completely excluded, the study suggests that QT interval is changed directly by autonomic nervous mechanisms rather than indirectly via the mean heart rate.

Atrial Fibrillation↗
PubMed1996

Spectral turbulence versus time-domain analysis of signal-averaged ECG used for the prediction of different arrhythmic events in survivors of acute myocardial infarction.

INTRODUCTION: Spectral turbulence analysis of the signal-averaged ECG (SAECG) combines spectral analysis with statistical evaluation of spectrograms of individual parts of the QRS complex. It has been suggested that it may be superior to conventional time-domain analysis of the SAECG. METHODS AND RESULTS: This study compared the power of conventional time-domain (40 to 250 Hz) and spectral turbulence analyses of SAECG for the prediction of cardiac death, ventricular tachycardia, sudden arrhythmic death, and arrhythmic events (ventricular tachycardia or fibrillation, and/or sudden arrhythmic death) after acute myocardial infarction in 603 patients. The population excluded patients with bundle branch block and other conduction abnormalities. During the first 2 years of follow-up, there were 40 cardiac deaths, 21 cases of ventricular tachycardia, 1 sudden arrhythmic deaths, and 29 arrhythmic events. The positive predictive accuracy of spectral turbulence analysis was significantly higher than time-domain analysis for cardiac death at most levels of sensitivity (e.g., 26% vs 20% at 40% sensitivity, P < 0.05). The positive predictive accuracies of the two techniques were not statistically different for the prediction of ventricular tachycardia. For the prediction of sudden arrhythmic death and arrhythmic events, the positive predictive accuracy of spectral turbulence was better than that of time-domain analysis only at the higher levels of sensitivity (9% vs 2%, P < 0.001 for sudden arrhythmic death at 60% sensitivity, and 14% vs 11%, P < 0.05 for arrhythmic events at 60% sensitivity). CONCLUSIONS: Spectral turbulence analysis is essentially equivalent to time-domain analysis for the prediction of arrhythmic events after myocardial infarction. However, it performed significantly better than time-domain analysis for the prediction of cardiac death.

Acute Disease↗