The impact of QT lag compensation on dynamic assessment of ventricular repolarization: reproducibility and the impact of lead selection.

In cardiac disease, abnormalities exist in the rate-corrected QT interval and the relationship between QT and heart rate. The QT/RR relationship is known to be dynamic and show circadian variation. The availability of automated methods for measurement of QT and RR intervals allows monitoring of the QT/RR relationship and may provide insights into arrhythmia onset. Using a method for analyzing 24-hour recordings that incorporates beat-by-beat QT and RR measurement and an automated mechanism for compensating for lag in adaptation of QT to changes in RR, the authors evaluated the impact of lag compensation on assessment of the QT/RR relationship, reproducibility, and the effect of lead selection in 15 normal subjects. The QT/RR relationship is continuously estimated from the lag compensated data over a 5-minute scrolling time frame. The relationship is expressed as an exponential formula, QT = QTo.RRJ where QTo is the QT interval at a standardized RR interval of 1 second and J is a variable exponent. We found that the use of lag compensation significantly improves the mean 24-hour correlation between QT and RR data (r = 0.87 vs 0.65). The 24-hour mean of QTo and J were highly reproducible (coefficients of variation 2% and 8%, respectively). The mean 24-hour QT/RR relationship for the population was QT = 0.415.(RR)0.32. There was a small difference between leads in QTo and J. Compensating for QT adaptation lag provides a means of assessing the QT/RR relationship over long and short periods. This method allows investigation of the effect of acute interventions on the dynamic QT/RR relationship, which has previously been restricted by the presence of QT hysteresis.

The relationship between QT intervals and mortality in ambulant patients with chronic heart failure. The united kingdom heart failure evaluation and assessment of risk trial (UK-HEART)

AIMS: Mortality in patients with heart failure remains high and is difficult to predict. QT interval parameters on a 12-lead ECG have been shown to predict arrhythmic events in patients with a variety of myocardial diseases. There is some, but not consistent, evidence that QT interval parameters may act as predictors of mortality, in particular sudden death, in patients with heart failure. In an adequately powered prospective study we have studied QT interval parameters in patients with stable chronic heart failure in order to determine whether they are predictive of all-cause mortality or mode of death. METHODS AND RESULTS: Five hundred and fifty-four ambulant outpatients with chronic heart failure were recruited. A 12-lead ECG, chest radiograph, echocardiogram, 24 h ambulatory electrocardiogram and serum for biochemical analysis were obtained at baseline. Patients were followed for 471+/-168 days. QT intervals were measured in all leads blinded to patient's characteristics and outcome, were corrected for heart rate, and the maximum QT intervals, and QT dispersion (range of QT intervals) were determined. The same parameters were determined for JT intervals. The primary end-point was all-cause mortality, secondary end-points were sudden cardiac death and death due to progressive heart failure. Multivariate analysis with the Cox's proportional hazards model was used to determine which variables were independently related to outcome. Four hundred and ninety-five patients had analysable ECGs at study entry and of these 71 died during follow-up. The heart rate corrected QT dispersion and maximum QT interval were significant univariate predictors of all-cause mortality (P=0.026 and <0.0001 respectively), and also of sudden death and progressive heart failure death, but were not related to outcome in the multivariate analysis. The independent predictors of all-cause mortality were cardiothoracic ratio (P=0.0003), creatinine (P=0.0009), heart rate (P=0.007), echocardiographically derived left ventricular end-diastolic dimension (P=0.007) and ventricular couplets on 24 h electrocardiographic monitoring (P=0.015). CONCLUSION: In an adequately powered prospective study none of the QT or JT parameters were shown to be independent predictors of outcome in patients with mild to moderate congestive heart failure. These variables do not therefore add to the prognostic information which can be gained from simple radiographic, biochemical, echocardiographic and Holter data in this group of patients.

Prospective study of heart rate variability and mortality in chronic heart failure: results of the United Kingdom heart failure evaluation and assessment of risk trial (UK-heart).

BACKGROUND: Patients with chronic heart failure (CHF) have a continuing high mortality. Autonomic dysfunction may play an important role in the pathophysiology of cardiac death in CHF. UK-HEART examined the value of heart rate variability (HRV) measures as independent predictors of death in CHF. METHODS AND RESULTS: In a prospective study powered for mortality, we recruited 433 outpatients 62+/-9.6 years old with CHF (NYHA functional class I to III; mean ejection fraction, 0.41+/-0.17). Time-domain HRV indices and conventional prognostic indicators were related to death by multivariate analysis. During 482+/-161 days of follow-up, cardiothoracic ratio, SDNN, left ventricular end-systolic diameter, and serum sodium were significant predictors of all-cause mortality. The risk ratio for a 41.2-ms decrease in SDNN was 1.62 (95% CI, 1.16 to 2.44). The annual mortality rate for the study population in SDNN subgroups was 5.5% for >100 ms, 12.7% for 50 to 100 ms, and 51.4% for <50 ms. SDNN, creatinine, and serum sodium were related to progressive heart failure death. Cardiothoracic ratio, left ventricular end-diastolic diameter, the presence of nonsustained ventricular tachycardia, and serum potassium were related to sudden cardiac death. A reduction in SDNN was the most powerful predictor of the risk of death due to progressive heart failure. CONCLUSIONS: CHF is associated with autonomic dysfunction, which can be quantified by measuring HRV. A reduction in SDNN identifies patients at high risk of death and is a better predictor of death due to progressive heart failure than other conventional clinical measurements. High-risk subgroups identified by this measurement are candidates for additional therapy after prescription of an ACE inhibitor.

Effects of digoxin on time domain measures of heart rate variability in patients with stable chronic cardiac failure: withdrawal and comparison group studies.

The effect on heart rate variability of adding digoxin to a diuretic and ACE inhibitor was studied in patients with chronic stable cardiac failure. Digoxin was found to increase heart rate variability, especially those measures of heart rate variability thought to represent parasympathetic activity. The withdrawal of digoxin led to a decrease in heart rate variability to pre-treatment levels. Whilst digoxin in standard doses does not alter prognosis in chronic cardiac failure, it does have potentially beneficial neurohumoral effects. If the increase in heart rate variability, which represents beneficial neurohumoral modulation, can be divorced from the potentially detrimental effects, perhaps by using smaller doses, then there may be a role for digoxin in the treatment of chronic cardiac failure.

The correction of autonomic dysfunction in cirrhosis by captopril.

BACKGROUND/AIMS: Vagal dysfunction is reported in about 70% of patients with cirrhosis, irrespective of aetiology, as detected by cardiovascular reflex tests. We have previously shown that RR-variability on 24-h ECG is a more sensitive marker of vagal dysfunction in cirrhosis. Angiotensin II inhibits vagal function in animals, and it is elevated in cirrhosis and may be the cause of the vagal dysfunction. Our aim was to observe the effect of captopril on vagal dysfunction in cirrhosis. METHODS: Eight patients with cirrhosis (biopsy proven, male two, female six, mean age 54.25) had 24-h ECG RR-variability performed. They then received captopril 25 mg t.d.s. for 48 h. The 24-h ECG was repeated on therapy. RESULTS: Mean blood pressure remained unchanged: baseline 89.8 +/- 4.8 mmHg (mean +/- sem) versus 91.8 +/- 5.9 mmHg, p = not significant. Median baseline RR-variability was 791 (range 18-5344) counts/24 h and increased in all but one patient, with captopril, to 1548 (56-4824) p = 0.008. Three increased into the normal range. CONCLUSION: The vagal dysfunction of cirrhosis is caused by neuromodulation by angiotensin II and is not due to a neuropathy.

Dynamic QT interval analysis : methodological aspects.

Advances in electronic computing have enabled continuous tracking of the QT Interval from 24 hour ambulatory ECG recordings. With proper attention to appropriate lead selection and good hook-up technique the variations in QT can be followed for hours with an uncertainty of only a few milliseconds rms.

Caffeine restriction has no role in the management of patients with symptomatic idiopathic ventricular premature beats.

OBJECTIVE: To assess the role of caffeine restriction in the management of patients with symptomatic idiopathic ventricular premature beats. DESIGN: A randomised, double blind, 6 week intervention trial incorporating dietary caffeine restriction, caffeinated coffee, and decaffeinated coffee. SETTING: Cardiac outpatient clinic. PATIENTS: 13 patients with symptomatic frequent idiopathic ventricular premature beats. MAIN OUTCOME MEASURES: Weekly measures of serum caffeine concentration, coffee consumption, visual analogue score of palpitations, and 24 hour ventricular premature beat frequency. RESULTS: The interventions achieved significant alterations in serum caffeine concentrations (P < 0.001) which correlated with coffee consumption (r = 0.70; P < 0.001). Visual analogue palpitation scores showed a small, but significant correlation with ventricular premature beat frequencies (r = 0.34; P = 0.003). However, there were no significant changes in palpitation scores or ventricular premature beat frequencies during the intervention weeks and no significant correlations were found between these variables and serum caffeine concentrations. CONCLUSIONS: Caffeine restriction has no role in the management of patients referred with symptomatic idiopathic ventricular premature beats.

Prognostic significance of heart rate variability in post-myocardial infarction patients in the fibrinolytic era. The GISSI-2 results. Gruppo Italiano per lo Studio della Sopravvivenza nell' Infarto Miocardico.

BACKGROUND: Studies performed before the introduction of fibrinolysis showed that a low heart rate variability (HRV) is associated with higher mortality in post-myocardial infarction (MI) patients. We evaluated whether HRV adds information relevant to risk stratification in patients treated with fibrinolysis as well. METHODS AND RESULTS: From 24-hour ECG recordings obtained at discharge in patients treated with recombinant tissue-type plasminogen activator or streptokinase, we measured several time-domain indexes of HRV: standard deviation (SDNN), root-mean-square of successive differences (RMSSD), and number of RR interval increases > 50 ms ("NN50+"). The prognostic value of HRV for total and cardiovascular mortality was assessed. Of 567 patients with valid recordings, 52 (9.1%) died during the 1000 days of follow-up, 44 (7.8%) of cardiovascular causes. All indexes of low HRV were able to identify patients (16% to 18% of total population) with a higher total mortality (20.8% to 24.2% versus 6.0% to 6.8%, depending on index used). The independent predictive value of low HRV was confirmed by the adjusted analysis with the following relative risks: NN50+, 3.5 (95% CI, 1.9 to 6.7); SDNN, 3.0 (95% CI, 1.55 to 5.9); and RMSSD, 2.8 (95% CI, 1.5 to 5.3). Advanced age, previous MI, Killip class at entry, and use of digitalis were also independent predictors. Similar data were obtained for cardiovascular mortality. CONCLUSIONS: Time-domain indexes of HRV retain their independent prognostic significance even in post-MI patients of all ages treated with fibrinolysis.

Measurement of parasympathetic activity from 24-hour ambulatory electrocardiograms and its reproducibility and sensitivity in normal subjects, patients with symptomatic myocardial ischemia, and patients with diabetes mellitus.

The parasympathetic nervous system plays a major role in the pathophysiology of many cardiovascular disease, particularly in modulating myocardial electrical stability. Measurements of heart rate variability have been widely used to assess parasympathetic activity. The reproducibility of measurements obtained from 24-hour ambulatory electrocardiograms has not been well documented. We have developed a technique for measuring parasympathetic activity from clinical quality 24-hour ambulatory electrocardiograms by counting beat-to-beat increases in RR interval that are > 50 ms. To determine the reproducibility and sensitivity of our technique, we analyzed repeated 24-hour electrocardiograms of 173 subjects (19 normal subjects, 67 patients with ischemic heart disease, and 87 diabetics) followed up over periods of 2 to 16 weeks. In all subject groups, mean values for repeated measurements were virtually identical. Measurements were stable in all 3 groups throughout the course of the study, as assessed by intraclass correlation coefficients. This technique is sensitive enough to detect relatively small changes in parasympathetic activity in subjects, as demonstrated by the calculated Bland and Altman coefficients of repeatability. Reproducibility and sensitivity of our technique are particularly good in normal subjects and in patients with ischemic heart disease. The results obtained with this technique imply that other related measurements of parasympathetic activity will show similar excellent short- and long-term reproducibility and sensitivity.

Autonomic function in cirrhosis assessed by cardiovascular reflex tests and 24-hour heart rate variability.

OBJECTIVES: To assess the prevalence of autonomic dysfunction in cirrhosis and to observe the effect of disease severity on autonomic dysfunction. METHODS: Seventy patients with cirrhosis (Child's class A, 42; Child's class B, 10; and Child's class C, 15) (45 alcoholic, 15 primary biliary cirrhosis, five chronic active hepatitis, and eight idiopathic) underwent standard cardiovascular reflex tests. In addition, in 40 patients, 24-h ECG RR variability tests were performed to detect autonomic dysfunction. RESULTS: Forty-two of 70 (60%) patients had abnormalities of cardiovascular reflex function of varying severity, whereas 24 of 34 (70%) had 24-h RR counts with the 95% age-related tolerance. The prevalence of abnormality increased with increasing severity of liver disease but not with different etiologies. CONCLUSION: Irrespective of etiology, there is a high prevalence of autonomic dysfunction in cirrhosis, and it is related to disease severity: the mechanism is unknown.

Cardiac effects of sodium stibogluconate: myocardial, electrophysiological and biochemical studies.

The pentavalent antimonial sodium stibogluconate is the mainstay of anti-leishmanial therapy. Sodium stibogluconate is less cardiotoxic than antimony and the trivalent derivatives, but has been associated with dose-related electrocardiographic changes. The effect of the currently-used regimen of sodium stibogluconate (20 mg/kg/day for 20 days) on cardiac function is uncertain. We studied 12 soldiers, mean age 24 years, with proven cutaneous leishmaniasis treated with this regimen. There were no significant changes in echocardiographic indices of left ventricular systolic or diastolic function during treatment. Indices of myocardial electrical stability (heart-rate variability and episodes of overt supraventricular and ventricular arrhythmias) were unchanged, but there was a reversible decrease in T-wave amplitude during treatment. Systolic and diastolic blood pressure fell and the heart rate increased during treatment. This regimen of sodium stibogluconate does not measurably impair left ventricular systolic or diastolic function. Minor T-wave changes occur during treatment, but there is no increase in arrhythmia frequency or change in heart-rate variability. In most young fit patients, this regimen has no cardiac side-effects. However, idiosyncratic reactions cannot be excluded, and patients with malnutrition, impaired renal function or pre-existing heart disease may be more sensitive to any cardiotoxic properties of sodium stibogluconate.

Cardiac parasympathetic activity in severe uncomplicated coronary artery disease.

BACKGROUND: Previous studies have suggested that coronary artery disease is independently associated with reduced cardiac parasympathetic activity, and that this is important in its pathophysiology. These studies included many patients with complications that might be responsible for the reported autonomic abnormalities. OBJECTIVE: To measure cardiac parasympathetic activity in patients with uncomplicated coronary artery disease. PATIENTS AND METHODS: 44 patients of mean (SD) age 56 (8) with severe uncomplicated coronary artery disease (symptoms uncontrolled on maximal medical treatment; > 70% coronary stenosis at angiography; normal ejection fraction; no evidence of previous infarction, diabetes, or hypertension). Heart rate variability was measured from 24 hour ambulatory electrocardiograms by counting the number of times successive RR intervals exceeded the preceding RR interval by > 50 ms, a previously validated sensitive and specific index of cardiac parasympathetic activity. RESULTS: Mean (range) of counts were: waking 112 (range 6-501)/h, sleeping 198 (0-812)/h, and total 3912 (151-14 454)/24 h. These mean results were unremarkable, and < 10% of patients fell below the lower 95% confidence interval for waking, sleeping, or total 24 hour counts in normal people. There was no relation between the severity of coronary artery disease or the use of concurrent antianginal drug treatment and cardiac parasympathetic activity. CONCLUSION: In contrast with previous reports no evidence of a specific independent association between coronary artery disease and reduced cardiac parasympathetic activity was found. The results of previous studies may reflect the inclusion of patients with complications and not the direct effect of coronary artery disease itself.

Differing patterns of cardiac parasympathetic activity and their evolution in selected patients with a first myocardial infarction.

OBJECTIVES: The purpose of the study was to compare cardiac parasympathetic activity during the early and convalescent phases of acute anterior and inferior myocardial infarction. BACKGROUND: Previous studies have shown that cardiac parasympathetic activity may vary with the site of infarction and that recovery may occur after infarction. METHODS: Cardiac parasympathetic activity was measured from 24-h electrocardiograms by counting the number of times that successive RR intervals (counts) differed by > 50 ms. Recordings began within 12 h of admission and at 7, 42 and 140 days after acute myocardial infarction in 20 patients (mean age 57 +/- 7.9 years). All patients were treated with streptokinase, aspirin and oral beta-adrenergic blocking agents. RESULTS: For the entire group, mean total 24-h RR counts increased from 592 (range 78 to 3,812) at 48 h to 648 (range 109 to 5,473) at 7 days, 1,145 (range 162 to 6,268) at 42 days and 1,958 (range 344 to 9,632) at 140 days. Patients with anterior infarction had significantly lower counts (mean 277, range 78 to 2,708; n = 11) compared with those with inferior infarction (mean 2,172, range 897 to 3,812; n = 9) at 48 h (p < 0.05). There was no significant difference in counts between patients with anterior (mean 1,051, range 212 to 6,268) and inferior (mean 1,321, range 162 to 3,265) infarction after 42 or after 140 days (anterior: mean 1,655, range 344 to 9,632; inferior: mean 2,588, range 1,700 to 5,767). CONCLUSIONS: These data suggest that after anterior myocardial infarction there is impaired cardiac parasympathetic function that improves within 6 weeks, whereas in inferior infarction there is relative preservation of cardiac parasympathetic function.

Decreased cardiac parasympathetic activity in chronic heart failure and its relation to left ventricular function.

BACKGROUND: Activation of the sympathetic nervous system has been extensively studied in patients with chronic heart failure, but the parasympathetic nervous system has received relatively little attention. The objective in this study was to investigate cardiac parasympathetic activity in chronic heart failure and to explore its relation to left ventricular function. METHODS: Heart rate variability was measured from 24 hour ambulatory electrocardiograms by counting the number of times each RR interval exceeded the preceding RR interval by more than 50 ms (counts). This method provided a sensitive index of cardiac parasympathetic activity. RESULTS: Mean (range) of counts were: waking 48 (1-275)/h, sleeping 62 (0-360)/h, and total 1310 (31-7278)/24 h. These were lower than expected, and in 26 (60%) of the 43 patients counts fell below the lower 95% confidence intervals (95% CI) for RR counts in normal subjects. A significant correlation between total 24 hour RR counts and left ventricular ejection fraction was present (r = 0.49, p less than 0.05). CONCLUSIONS: These results indicate that most patients with chronic heart failure have reduced heart rate variability and therefore reduced cardiac parasympathetic activity. The degree of parasympathetic dysfunction is related to the severity of left ventricular dysfunction. This may be relevant to the high incidence of ventricular arrhythmias and poor prognosis of patients with chronic heart failure.

Effect of captopril on cardiac parasympathetic activity in chronic cardiac failure secondary to coronary artery disease.

Thirty-two patients with chronic cardiac failure underwent 24-hour ambulatory electrocardiographic monitoring on 2 separate occasions: 20 patients before and during treatment with captopril, and 12 acting as controls. Heart rate variability was calculated by counting the number of times successive RR interval differences were greater than 50 ms (this measurement being a reliable index of cardiac parasympathetic activity). During treatment with captopril, group mean total counts increased to 1,032 (range 48 to 7,437) from 482 (range 23 to 6,120) (p = 0.002). There was no change in mean hourly waking or sleeping heart rates. In the control group, no changes were seen: group mean total counts on the first occasion were 340 (range 120 to 3,255) and on the second occasion 400 (range 154 to 3,300) (p = not significant). These results show that treatment with angiotensin-converting enzyme inhibitors increases cardiac parasympathetic activity in patients with chronic cardiac failure. This may be relevant to the improved prognosis of this group of patients when treated with angiotensin-converting enzyme inhibitors.

Heart rate variability and cardiac arrhythmias in patients with chronic renal failure.

Heart rate variability was measured from 24-h electrocardiograms in 61 patients with end stage chronic renal failure. The method used counts the number of times successive RR intervals differ by more than 50 ms over the 24-h period, and is a reliable indicator of cardiac parasympathetic activity. Also analysed were the frequency and type of ectopic beats and other arrhythmias. Twenty-one subjects (34%) had varying numbers of ventricular ectopic beats, and twelve (20%) had frequent supraventricular ectopics. Total 24-h count values were abnormal in 30 (76%) of the 41 subjects whose tapes were technically suitable for this analysis. There were no sex differences, but those patients maintained on haemodialysis had significantly lower counts than those on continuous ambulatory peritoneal dialysis. We conclude that about three-quarters of patients with chronic renal failure have abnormal cardiac parasympathetic activity. This may increase susceptibility to cardiac arrhythmias and sudden death and contribute to the high mortality of patients with chronic renal failure.

Twenty four hour heart rate variability: effects of posture, sleep, and time of day in healthy controls and comparison with bedside tests of autonomic function in diabetic patients.

Heart rate variability was measured in 77 healthy controls and 343 diabetic patients by a count of the number of beat-to-beat differences greater than 50 ms in the RR interval during a 24 hour ambulatory electrocardiogram. In the healthy controls the lower 95% tolerance limits for total 24 hour RR interval counts were approximately 2000 at age 25, 1000 at 45, and 500 at 65 years. Six controls confined to bed after injury had normal 24 hour patterns of RR counts, while eight other controls showed loss of diurnal variation in both heart rate and RR counts during a period of sleep deprivation. RR counts in ten controls on and off night duty increased during sleep whenever it occurred. Nearly half (146) the 343 diabetic patients had abnormal 24 hour RR counts. The percentage of abnormal RR counts increased with increasing autonomic abnormality assessed by a standard battery of tests of cardiovascular autonomic function. A quarter of those with normal cardiovascular reflex tests had abnormal 24 hour RR counts. There were close correlations between 24 hour RR count results and the individual heart rate tests (r = 0.6). The assessment of cardiac parasympathetic activity by 24 hour RR counts was reliable. The diurnal variations in RR counts seen in the controls were probably related to sleep rather than either posture or time of day. The method was more sensitive than conventional tests of cardiovascular reflexes.

Heart rate variability in patients with ventricular arrhythmias: effect of antiarrhythmic drugs. Antiarrhythmic Drug Evaluation Group (ADEG).

The purpose of this study was to investigate whether heart rate variability could be reliably assessed in patients with ventricular arrhythmias and to evaluate whether it is affected by antiarrhythmic drugs. The study was based on an analysis of 239 ambulatory electrocardiographic (ECG) recordings obtained from 67 patients with frequent and complex ventricular arrhythmias enrolled in the Antiarrhythmic Drug Evaluation Group (ADEG) study. In each recording, after exclusion of premature ventricular complexes, the number of times during a 24 h period in which two consecutive sinus RR intervals differed by more than 50 ms was calculated. The total 24 h count from each recording was then used as an index of heart rate variability. This method is a reliable marker of cardiac parasympathetic activity. Recordings were analyzed at baseline (n = 56), during long-term treatment with amiodarone (n = 17), flecainide (n = 22) or propafenone (n = 17) and after washout in selected patients (n = 5). Despite the presence of a different number of arrhythmias, total 24 h counts in the same patient appeared reproducible over time (r = 0.83 between two different recordings, n = 49, p less than 0.0001). Baseline counts (median 1,698, range 26 to 13,648) were not correlated (r = 0.15) with the number of arrhythmias. The three antiarrhythmic drugs had a disparate effect on total 24 h counts: no change was observed in patients treated with amiodarone (median percent change [delta %]-8, p = NS), whereas a significant (p less than 0.025) decrease occurred in patients treated with flecainide (median delta % -56%) or propafenone (median delta % -64%).(ABSTRACT TRUNCATED AT 250 WORDS)

Autonomic neuropathy, QT interval lengthening, and unexpected deaths in male diabetic patients.

QT intervals were measured over RR intervals ranging from 500 ms to 1000 ms in 13 normal male subjects, 13 male diabetic subjects without and 13 with autonomic neuropathy. There was a close linear relationship between QT and RR in all subjects. The slope of the regression line was significantly greater in the autonomic neuropathy group than the normal group. Thirty-two male diabetic subjects with varying degrees of autonomic dysfunction had repeat QT measurements 3 (range 2-6) years later. QT and QTC lengthened significantly at the second visit, unrelated to age or time between recordings, but which corresponded with changes in autonomic function. Of 71 male diabetic subjects under 60 years followed for 3 years, 13 had died, 8 unexpectedly. Of those with autonomic neuropathy. QT and QTC were significantly longer in those who subsequently died, despite similar ages and duration of diabetes. We conclude that QT/RR interval relationships are altered in diabetic autonomic neuropathy, and that changes in QT length with time parallel changes in autonomic function. There may be an association between QT interval prolongation and the risk of dying unexpectedly in diabetic autonomic neuropathy.

QT interval length and diabetic autonomic neuropathy.

QT interval length was measured in ECG recordings from three groups of age-matched male subjects: 36 normal subjects, 41 diabetic patients without (DAN-ve), and 34 with (DAN+ve) autonomic neuropathy. ECG samples were selected from previously recorded 24-h ECGs on the basis of a clearly defined T wave and a steady RR interval over 2 min of around 750 ms (80 beats min-1). There were no significant differences in RR interval between the groups. The two diabetic groups had slightly longer QT measurements (normal 365 +/- 14 (+/- SD) ms, DAN-ve 373 +/- 18 ms, DAN+ve 375 +/- 23 ms, p = 0.05), and corrected QT (QTc) values (normal 423 +/- 15 ms, DAN-ve 430 +/- 20 ms, DAN+ve 435 +/- 24 ms, p = 0.05). Ten diabetic patients fell above our defined upper limit of normal for QTc (greater than mean + 2SD). There was a significant correlation in the DAN-ve group between the QT indices and 24-h RR counts (QT r = -0.38, p less than 0.01; QTc r = -0.40, p less than 0.01). We conclude that there are some small alterations in QT interval length in the steady state in diabetic autonomic neuropathy. The changes appear to be due to autonomic impairment, rather than diabetes per se.