Left ventricular hypertrophy increases transepicardial dispersion of repolarisation in hypertensive patients: a differential effect on QTpeak and QTend dispersion

BACKGROUND: Ventricular arrhythmias in left ventricular hypertrophy (LVH) are related to regional electrical heterogeneity. The significance of noninvasive electrocardiographic indices of electrical heterogeneity in LVH has not been established. The aim of the study was to investigate changes in the Tpeak-Tend interval (an index of transmural dispersion of repolarisation) in addition to other traditional electrocardiographic indices of electrical dispersion in patients with hypertensive LVH. METHODS: Consecutive patients were screened for the presence of hypertensive echocardiographic LVH and compared with a control group. LVH was identified as left ventricular mass > 134 g m-2 in men and > 110 g m-2 in women. Twelve-lead ECGs were analysed in respect of various indices of electrical dispersion. RESULTS: Left ventricular mass was greater in the LVH than in the control group (174 +/- 39 vs. 101 +/- 18 g m-2, P < 0.0001). The Tpeak-Tend interval was not affected by LVH. The main effect of LVH was an increase in QTpeak dispersion (40 +/- 13 vs. 53 +/- 21 ms, P < 0.05), which resulted from an increase in the maximum QTpeak interval (337 +/- 24 vs. 358 +/- 30 ms, P < 0.04), without any change in the minimum QTpeak interval. There was a significant correlation between the left ventricular mass index and QTpeak dispersion (r = 0.40; P < 0.01). In contrast, LVH did not exert any effect on QTend dispersion (65 +/- 21 vs. 65 +/- 16 ms, ns), because LVH increased both the maximum QTend interval (430 +/- 30 vs. 449 +/- 28 ms, P < 0.05) and the minimum QTend interval (365 +/- 29 vs. 384 +/- 27 ms, P < 0.04). CONCLUSIONS: Hypertensive LVH exerts a differential effect on QTpeak and QTend interval dispersion. The most likely explanation is that these changes reflect a nonuniform prolongation of action potential duration across the epicardium, leading to an increase in transepicardial dispersion of repolarisation.     

Effect of epirubicin-based chemotherapy and dexrazoxane supplementation on QT dispersion in non-Hodgkin lymphoma patients

BACKGROUND AND OBJECTIVE: Aim of the present study was to assess the effect of epirubicin-based chemotherapy on QT interval dispersion in patients with aggressive non-Hodgkin lymphoma (NHL), and the effect of dexrazoxane supplementation. Prolongation of QT dispersion may not only represent a sensitive tool in identifying the first sign of anthracycline-induced cardiotoxicity, but it may serve also in identifying patients who are at risk of arrhythmic events. METHODS: Twenty untreated patients, 相似文献   

Hypertensive stress increases dispersion of repolarization

Several electrocardiographic indices for repolarization heterogeneity have been proposed previously. The behavior of these indices under two different stressors at the same heart rate (i.e., normotensive gravitational stress, and hypertensive isometric stress) was studied. ECG and blood pressure were recorded in 56 healthy men during rest (sitting with horizontal legs), hypertensive stress (performing handgrip), and normotensive stress (sitting with lowered legs). During both stressors, heart rates differed <10% in 41 subjects, who constituted the final study group. Heart rate increased from 63 +/- 9 beats/min at rest to 71 +/- 11 beats/min during normotensive, and to 71 +/- 10 beats/min during hypertensive stress (P < 0.001). Systolic blood pressure was 122 +/- 15 mmHg at rest and 121 +/- 15 mmHg during normotensive stress, and increased to 151 +/- 17 mmHg during hypertensive stress (P < 0.001). The QT interval was larger during hypertensive (405 +/- 27) than during normotensive stress (389 +/- 26, P < 0.001). QT dispersion did not differ significantly between the two stressors. The mean interval between the apex and the end of the T wave (Tapex-Tend) of the mid-precordial leads was larger during hypertensive (121 +/- 17 ms) than during normotensive stress (116 +/- 15 ms, P < 0.001). The singular value decomposition T wave index was larger during hypertensive (0.144 +/- 0.071) than during normotensive stress (0.089 +/- 0.053, P < 0.001). Most indices of repolarization heterogeneity were larger during hypertensive stress than during normotensive stress. Hypertensive stressors are associated with arrhythmogeneity in vulnerable hearts. This may in part be explained by the induction of repolarization heterogeneity by hypertensive stress.     

Influence of electrolyte abnormalities on interlead variability of ventricular repolarization times in 12-lead electrocardiography

Increased QT dispersion (QT(d)) has been associated with increased risk for ventricular arrhythmias. Pathologic extracellular electrolyte concentrations may result in ventricular arrhythmias. The aim of this study was to evaluate the effect of electrolyte abnormalities on QT(d). Ten consecutive patients with isolated electrolyte abnormalities were selected for each of the following groups: hypokalemia, hyperkalemia, hypercalcemia, hypocalcemia, hypomagnesemia, and normal controls. Standard 12-lead electrocardiography was performed for each patient and average QT, JT, and RR intervals were calculated for each lead. Dispersion of QT, JT (JT(d)), and QTc (QTc(d)) intervals were calculated as the range between the longest and shortest measurements. Compared with controls, only patients with hypokalemia had a greater QT(d) (115 +/- 31 vs. 49 +/- 15 ms), JT(d) (116 +/- 34 vs. 52 +/- 12 ms), and QTc(d) (141 +/- 40 vs. 58 +/- 1 ms), (P < 0.05). In an experimental substudy, seven rats were maintained on K(+) and seven on Mg(2+)-free diet followed by normal diet. Experimental hypokalemia significantly increased QT(d) (10 +/- 4 to 37 +/- 7 ms), and QTc(d) (32 +/- 6 to 79 +/- 27 ms) (P < 0.05), whereas hypomagnesemia did not. Restoration of serum potassium resulted in normalization of dispersion (QT(d), 14 +/- 2; QTc(d), 34 +/- 6 ms). Hypokalemia increases the dispersion of ventricular repolarization that may be responsible for arrhythmias. Even though hyperkalemia, hypocalcemia, and hypercalcemia are known to affect ventricular repolarization, our study shows that they are not associated with increased dispersion.     

QTc dispersion and P-wave dispersion during migraine attacks

The aim of this study was to investigate increase of QTc dispersion and P-wave dispersion during migraine attacks. Fifty-five patients (16-65 years of age, 49 women, six men) with migraine were included in our study. Heart rate, QTc interval, maximum and minimum QTc interval, QTc dispersion, maximum and minimum P-wave duration and P-wave dispersion were measured from 12-lead ECG recording during migraine attacks and pain-free periods. ECGs were transferred to a personal computer via a scanner and then used for magnification of x400 by Adobe Photoshop software. Maximum QTc interval (454 +/- 24 ms vs. 429 +/- 23 ms, P < 0.001), QTc interval (443 +/- 26 ms vs. 408 +/- 22 ms, P < 0.001) and QTc dispersion (63 +/- 18 ms vs. 43 +/- 14 ms, P < 0.001) were found significantly higher during migraine attacks compared with pain-free periods. Maximum P-wave duration (107 +/- 11 ms vs. 100 +/- 11 ms, P < 0.001) and P-wave dispersion (45 +/- 13 ms vs. 35 +/- 13 ms, P < 0.001) were found higher during migraine attacks than pain-free periods. We concluded that migraine attacks are associated with increased QTc and P-wave dispersion compared with pain-free periods.     

QT dispersion in children with ventricular arrhythmia and a structurally normal heart

In adults, increased QT dispersion has been shown to predict arrhythmic risk as well as risk of sudden death in several clinical settings. It is not known whether or not QT dispersion is increased in children with idiopathic ventricular arrhythmia. We studied three groups of children: (1) 20 patients with idiopathic VT (aged 3-18 years; mean 11.2 years); (2) 30 patients with benign PVCs (aged 1-20 years; mean 10.5 years); and (3) 30 control subjects (aged 4-17 years; mean 12 years). Standard ECGs were reviewed and the dispersion of both QT and JT intervals was compared. No patient had structural heart disease or long QT syndrome. The QT and QTc dispersion (QT delta, QTc delta) among the three groups did not differ: QTc delta of the VT group was 70 ms +/- 30 ms, QTc delta of PVC patients was 60 ms +/- 30 ms, and the QTc delta of the control group was 65 ms +/- 30 ms. The JTc delta among the three groups did not differ as well: JTc delta of the VT group was 70 ms +/- 30 ms, the JTc delta of the PVC group was 60 msec +/- 25 msec, and the JTc delta of the control group was 70 ms +/- 30 ms. We conclude that QT and JT dispersion are not significantly altered in children with idiopathic VT or benign PVCs when compared to control subjects. QT dispersion is not a reliable marker for arrhythmic risk in children with idiopathic ventricular arrhythmias and structurally normal hearts.     

QT dispersion from body surface ECG does not reflect the spatial dispersion of ventricular repolarization in sheep

The correlation between the QT dispersion on body surface ECG and the dispersion in ventricular repolarization from the cardiac surface was studied in six sheep anesthetized with pentobarbital. The standard 12-lead body surface ECG and multiple ventricular epicardial ECGs were simultaneously recorded. The activation-recovery interval (ARI) was measured from the unipolar epicardial ECGs. The pooled QT dispersion from the six animals was significantly smaller than the pooled ARI dispersion (22.7 +/- 2.6 vs 33.0 +/- 6.9 ms, P < 0.01). There was no correlation between the QT and ARI dispersion. The unipolar epicardial ECGs were then converted into bipolar ECGs and epicardial QT intervals were subsequently acquired from these ECGs. The average value of epicardial QT dispersion from the six animals was similar to that of body surface ECG, but was less than the ARI dispersion (27.5 +/- 6.8 vs 33.0 +/- 6.9, P < 0.01). A good correlation between the epicardial QT dispersion and ARI dispersion was identified (r = 0.84, P < 0.05). In addition, a prolongation in ventricular repolarization, induced by an increase in coronary flow, elicited a pooled ARI dispersion of 62.3 +/- 6.2 ms (n = 6), which was larger than the simultaneously recorded body surface QT dispersion (28.3 +/- 9.8 ms, n = 6, P < 0.01). No correlation between the ARI and QT dispersion was found in the presence of the prolonged ventricular repolarization. In conclusion, QT dispersion from a 12-lead body surface ECG seems to underestimate the spatial dispersion of ventricular repolarization acquired from sheep epicardium.     

Temporary disturbances of the QT interval precede the onset of ventricular tachyarrhythmias in patients with structural heart diseases

An increase in sinus rate prior to ventricular tachyarrhythmias has been demonstrated in previous studies. There is no clear data available concerning changes in ventricular de- and repolarization prior to ventricular tachyarrhythmias, especially in patients with structural heart disease. Therefore, the aim of this study was to analyze the QT and QTc interval (Bazett's formula immediately before the onset of ventricular tachyarrhythmias in stored electrograms of patients with ICDs. The study analyzed 228 spontaneous ventricular tachyarrhythmia episodes in 52 patients (mean age 64 +/- 10 years, 49 men, 3 women) and compared them with 146 electrograms of baseline rhythm recorded during regular ICD follow-up. Mean ventricular cycle length (CL), QT interval, and QTc were measured before the onset of ventricular tachyarrhythmia and during baseline rhythm. Prior to ventricular tachyarrhythmias onset, CL was significantly shorter than during baseline rhythm (714 +/- 139 vs 828 +/- 149 ms, P < 0.0001). By contrast, the QT interval (430 +/- 67 ms) and QTc interval (518 +/- 67 ms) were significantly prolonged before the onset of ventricular tachyarrhythmias as compared to baseline rhythm (QT 406 +/- 67 ms, QTc 450 +/- 61 ms; P < 0.0001). CL, QT, and QTc changes were independent of concomitant treatment with antiarrhythmic drugs. Ventricular tachyarrhythmias are preceded by a significant prolongation of the QT and QTc intervals. This phenomenon may represent a greater than normal disparity of repolarization recovery times possibly facilitating the development of ventricular tachyarrhythmias.     

QT Duration and Dispersion in Patients with Anomalous Origins of Coronary Arteries

Background: Coronary artery anomalies have been reported to show various symptoms ranging from chest pain and dyspnea to cardio-respiratory arrest and sudden death. In this study, we attempted to assess the changes in QT interval duration and dispersion in anomalous origins of coronary arteries (AOCA).
Methods: Nineteen AOCA patients (mean age: 52 ± 11 years) and 30 healthy control subjects (mean age: 50 ± 12 years) were included in the study. Minimum and maximum corrected QT intervals, and corrected QT dispersion were calculated. The two groups were compared in terms of QT dispersion and QT duration.
Results: There was no difference between the two groups in terms of baseline demographic characteristics. Maximum corrected QT intervals (QTc max), minimum corrected QT intervals (QTc min), and corrected QT dispersion were higher in AOCA patients than controls (452 ± 38 vs 411 ± 25 ms [P = 0.0001], 402 ± 31 vs 383 ± 28 ms [P = 0.048], and 51 ± 30 vs 28 ± 12 ms [P = 0.001], respectively).
Conclusion: In the patients with anomalous origins of coronary arteries, QT dispersion that is an indicator of sudden cardiac death and arrhythmias frequency increased. QTc max, QTc min, and corrected QT dispersion are higher in patients with anomalous origin of the coronary artery than in control subjects.     

Effect of telmisartan on QT interval variability and autonomic control in hypertensive patients with left ventricular hypertrophy

Objectives

The aim of the study was to examine the effect of the antihypertensive AT1 receptors antagonist telmisartan on cardiovascular autonomic function and QT dispersion in hypertensive patients with LVH.

Methods

Twenty-five patients (18 males and seven women, mean age 49.8 ± 5.2 years) with mild essential arterial hypertension and LVH were compared with 25 age-matched healthy controls. All the participants underwent a complete clinical examination, including electrocardiogram for QT interval measurements and 24 h ambulatory ECG monitoring for measurement of heart rate variability. The ECG, 24 h ambulatory ECG, and echocardiogram were repeated after eight weeks of treatment.

Results

At baseline, hypertensive patients showed QT dispersion (p < 0.001) and QTc dispersion (p < 0.001) significantly higher than control subjects. An eight-week telmisartan treatment significantly reduced blood pressure (p < 0.0001), without significant change in left ventricular mass. Telmisartan-based treatment induced an increased vagal activity without significant change of sympathetic activity and a reduction of QT dispersion (p < 0.001) and QTc dispersion (p < 0.001).

Conclusions

These data suggest that therapy with telmisartan significantly improves the sympathovagal balance increasing parasympathetic activity, and cardiac electrical stability reducing the heterogeneity of ventricular repolarization in hypertensive subjects. These effects could contribute to reduce arrhythmias as well as sudden cardiac death in at-risk hypertensive patients.     

Left ventricular hypertrophy is associated with a stronger impairment of non-oxidative glucose metabolism in hypertensive patients

Abstract. Hypertensive patients with left ventricular hypertrophy (LVH) have a higher degree of hyper-insulinaemia than hypertensive patients without LVH. Obese patients with LVH have also been demonstrated to have a very low glucose disappearance rate after an intravenous glucose bolus. No studies have investigated the difference in insulin action and substrate oxidation in hypertensive patients with and without LVH. For this reason 36 subjects were enrolled for our study: (1) healthy control subjects ( n =10); (2) hypertensive patients without LVH ( n = 12); and (3) hypertensive patients with LVH ( n = 14). All subjects underwent an oral glucose tolerance test (OGTT, 75 g of glucose) and a euglycaemic hyperinsulinaemic glucose clamp (insulin infusion rate, 71 pmol(kgmin)^-1 for 120min). In this latter test indirect calorimetry allowed substrate oxidation determination. Echocardiographic methods allowed LVH assessment. Hypertensive patients with LVH had the lowest insulin-mediated nonoxidative glucose metabolism compared to hypertensive patients without LVH ( P <0.01) and to healthy subjects ( P < 0.001). In the whole group of hypertensive patients ( n = 26), partial correlations showed left ventricular mass index (LVMI) associated with fasting plasma insulin levels ( r = 0.44 P <0.005), insulin-mediated whole body glucose disposal ( r = -0.41 P <0.01) and nonoxidative glucose metabolism ( r = -0.33 P<0.04) independently of age, body weight, systolic blood pressure and plasma catechola-mines levels. In conclusion, our data provide evidence that LVH in hypertensive patients is associated with a worsening in nonoxidative glucose metabolism.     

Influence of posture and handgrip on the QT interval in left ventricular hypertrophy and in chronic heart failure

In certain disease states prolongation of the QT interval has been shown to be arrhythmogenic. Whether QTc interval changes with position and thus whether certain positions are more arrhythmogenic than others is not known for different diseases that predispose to arrhythmias, and was therefore studied. Patients with left ventricular hypertrophy and heart failure, and the appropriate matched controls, were recruited. Subjects were studied in the lying, sitting, standing and squatting positions and had QT intervals determined by computer algorithm 2 min after each position change. After resting, QT interval was determined while the subjects performed maximum handgrip exercise with their dominant hand. QT intervals were rate-corrected using Bazett's method. QTc interval is prolonged in heart failure patients compared with either left ventricular hypertrophy or control subjects in the lying and sitting position, but not in the standing or squatting position. The QTc intervals for heart failure and control subjects were, respectively, 443+/-7 ms versus 421+/-6 ms when lying (P<0.05), 451+/-10 ms versus 419+/-6 ms when sitting (P<0.05), 429+/-10 versus 414+/-7 ms when standing (P not significant) and 437+/-10 versus 419+/-8 ms when squatting (P not significant). The values for patients with hypertrophy did not differ from control values. Maximum handgrip does not affect the QTc interval in heart failure, but prolongs it in both the hypertrophy and control groups. Position and static exercise are important modifiers of QTc interval and their effect depends on the condition of the left ventricle.     

Prolonged QRS duration increases QT dispersion but does not relate to arrhythmias in survivors of acute myocardial infarction

QT dispersion has been suggested and disputed as a risk marker for ventricular arrhythmias after myocardial infarction. Delayed ventricular activation after myocardial infarction may affect arrhythmic risk and QT intervals. This study determined if delayed activation as assessed by (1) QRS duration in the 12-lead ECG and by (2) late potentials in the signal-averaged ECG affects QT dispersion and its ability to assess arrhythmic risk after myocardial infarction. QT duration, JT duration, QT dispersion, and JT dispersion were compared to QRS duration in the 12-lead ECG and to late potentials in the signal-averaged ECG recorded in 724 patients 2-3 weeks after myocardial infarction. Prolonged QRS duration (> 110 ms) and high QRS dispersion increased QT and JT dispersion by 12%-15% (P < 0.05). Presence of late potentials, in contrast, did not change QT dispersion. Only the presence of late potentials (n = 113) was related to arrhythmic events during 6-month follow-up. QT dispersion, JT dispersion, QRS duration, and QRS dispersion were equal in patients with (n = 29) and without arrhythmic events (QT disp 80 +/- 7 vs 78 +/- 1 ms, JT disp 80 +/- 6 vs 79 +/- 2 ms, mean +/- SEM, P > 0.2). In conclusion, prolonged QRS duration increases QT dispersion irrespective of arrhythmic events in survivors of myocardial infarction. Presence of late potentials, in contrast, relates to arrhythmic events but does not affect QT dispersion. Therefore, QT dispersion may not be an adequate parameter to assess arrhythmic risk in survivors of myocardial infarction.     

Serum quinidine concentrations and effect on QT dispersion and interval

OBJECTIVE: To establish a relationship between serum quinidine concentrations (SQCs) and QT interval dispersion, compared with corresponding QT intervals, in order to identify a reason why many reports describe torsade de pointes as occurring at subtherapeutic concentrations. DESIGN: Retrospective study. SETTING: University teaching hospital. PARTICIPANTS: Eleven patients with atrial arrhythmias managed with quinidine therapy. MAIN OUTCOME MEASURES: Patients with subtherapeutic (<2 microg/mL) and therapeutic (2-5 microg/mL) SQCs with corresponding 12-lead electrocardiograms (ECGs) (25 mm/sec) and baseline ECG were evaluated for QT interval dispersion, calculated as the maximum minus the minimum QT interval on the 12-lead ECG. RESULTS: Mean +/- SD subtherapeutic and therapeutic SQCs were 1.48 +/- 0.39 microg/mL and 3.78 +/- 0.88 microg/mL (p < 0.001). Baseline values for QT/QTc intervals were 376.4 +/- 59.2/429.5 +/- 57.3 msec. At subtherapeutic and therapeutic SQCs, mean QT/QTc intervals were 403.6 +/- 59.9/450.5 +/- 38.5 msec and 439.1 +/- 48.9/472.4 +/- 44.6 msec, respectively. Mean QT dispersion was 47 +/- 16.2 msec at baseline, 98.2 +/- 27.5 msec at subtherapeutic SQC, and 70.9 +/- 33.9 msec at therapeutic SQCs (p = 0.001 for overall analysis; p < 0.001 for baseline vs. subtherapeutic concentrations; p = NS for therapeutic vs. subtherapeutic in post hoc comparison). CONCLUSIONS: Despite QT interval lengthening with increasing SQCs, QT dispersion was numerically greatest at subtherapeutic SQCs. Further study is required to determine the value of QT dispersion as a tool for identifying proarrhythmic risk with drugs that prolong the QT interval.     

Evaluation of Autonomic Influences on QT Dispersion Using the Head-Up Tilt Test in Healthy Subjects

Our objective was to examine the autonomic influence on QT interval dispersion using the head-up tilt test in healthy subjects. RR and QT intervals, heart rate variability, and plasma norepinephrine concentration were measured in the supine position and tilting to 70 degrees for 20 minutes using a footboard support in 15 healthy male volunteers (mean age +/- SD: 28.0 +/- 4.5 years). The rate-corrected QT interval (QTc) was calculated using Bazett's formula, and QT and QTc dispersions were defined as the maximum minus minimum values for the QT and QTc, respectively, from the 12-lead ECG. Spectral analysis of the heart rate variability generated values for the low- and high-frequency powers (LF and HF) and their ratio (LF/HF). Compared with values obtained in the supine position, tilting significantly increased QT (P < 0.05) and QTc dispersion (P < 0.01), the LF/HF ratio (P < 0.0001), and plasma norepinephrine concentration (P < 0.0001), and significantly decreased HF (P < 0.0001). QTc dispersion was positively correlated with the LF/HF ratio and plasma norepinephrine concentration, and negatively correlated with HF. These results suggest that head-up tilt testing increases QT dispersion by increasing sympathetic tone and/or decreasing vagal tone in healthy subjects.     

Spatial distribution of repolarization times in patients with coronary artery disease

The potential clinical value of QT dispersion (QTd), a measure of the interlead range of QT interval duration in the surface 12-lead ECG, remains ambiguous. The aim of the study was the temporal and spatial analysis of the QT interval in healthy subjects and in patients with coronary artery disease (CAD) using magnetocardiography (MCG) and surface ECG. Standard 12-lead ECG and 37-channel MCG were performed in 20 healthy subjects, 23 patients with CAD without prior myocardial infarction (MI), 31 MI patients and 11 MI patients with ventricular tachycardia (VT). QTd was increased in CAD without MI compared to normals (ECG 46.1 +/- 6.0 vs 42.8 +/- 5.0, P < 0.05; MCG 66.8 +/- 20.3 vs 49.7 +/- 10.8, P < 0.01) and in VT compared to MI (ECG 66.8 +/- 16.5 vs 51.9 +/- 16.6, P < 0.05; MCG 93.6 +/- 29.6 vs 66.8 +/- 20.8, P < 0.005). In MCG, spatial distribution of QT intervals in patient groups differed from those in healthy subjects in three ways: (1) greater dispersion, (2) greater local variability, and (3) a change in overall pattern. This was quantified on the basis of smoothness indexes (SI). Normalized SI was higher in CAD without MI compared to normals (3.8 +/- 1.1 vs 2.7 +/- 0.6, P < 0.001) and in VT compared to MI (6.4 +/- 1.6 vs 4.2 +/- 1.4, P < 0.0005). For the normal-CAD comparison a sensitivity of 74% and a specificity of 80% was obtained, for MI-VT, 100% and 77%, respectively. The results suggest that examining the spatial interlead variability in multichannel MCG may aid in the initial identification of CAD patients with unimpaired left ventricular function and the identification of post-MI patients with augmented risk for VT.     

Continuous positive airway pressure treatment improves the QT rate dependence adaptation of obstructive sleep apnea patients

BACKGROUND: QT rate dependence is one of the major properties of ventricular repolarization, with its circadian and autonomic modulations. The alteration of cardiac autonomic tone occurring in obstructive sleep apnea syndrome (OSAS) patients could explain the altered rate-dependent adaptation of the myocardial repolarization. Thus, we postulated that dynamic alterations in QT interval adaptation could be ameliorated in OSAS patients under continuous positive airway pressure (CPAP) treatment. To assess ventricular repolarization features in patients with OSAS, we compared QT parameters and their dynamicities along RR intervals from 24-hour ECG. METHODS: The study groups consisted of 38 consecutive OSAS patients and 38 healthy age-matched subjects. The syndrome was confirmed for OSAS patients according to standard polysomnographic criteria (apnea plus hypopnea index: 56.9 +/- 28.4/h). A second polysomnography synchronized with 24-hour ECG Holter and realized under efficient CPAP therapy confirmed the control of sleep-related breathing disorder. RESULTS: QT length related to heart rate was found significantly altered in patients with OSAS compared with controls (QTend/RR slope: -0.126 +/- 0.031 vs -0.173 +/- 0.038; P < 0.01). This flattened relationship was significantly improved with the treatment of the OSAS (-0.151 +/- 0.051; P < 0.01 vs pretreatment status). There was no significant impact of CPAP therapy on ventricular ectopic activity as well as on static repolarization parameters (QT, RT, QTc, RTc) measured separately over daytime and nighttime. CONCLUSIONS: The prognostic implications of such findings and the protective role of CPAP treatment to prevent sudden cardiac death in OSAS need to be evaluated.     

Prolongation of the QT interval in heart failure occurs at low but not at high heart rates

Abnormal left ventricular structure and function as in, for example, left ventricular hypertrophy or chronic heart failure, is associated with sudden cardiac death and, when the ejection fraction is depressed, with prolongation of the QT interval. The dependence on heart rate of QT interval prolongation in these conditions, and the relationship of any abnormalities either to deranged autonomic nervous system function or to an adverse prognosis, has not been well studied. We therefore investigated (1) the dependence on heart rate of the QT interval, and (2) the relationship between both QT interval and the QT/heart rate slope and markers of adverse prognosis in these two conditions. The QT interval was measured at rest and during exercise in 34 subjects with heart failure, 16 subjects with left ventricular hypertrophy and 16 age-matched controls with normal left ventricular structure and function. QTc (corrected QT) intervals at rest were significantly longer in heart failure patients (471+/-10 ms) than in controls (421+/-6 ms) or in subjects with hypertrophy (420+/-6 ms) (P<0.05). At peak exercise, despite the attainment of similar heart rates, the QT intervals no longer differed from each other, being 281+/-7 ms for controls, 296+/-11 ms in hypertrophy and 303+/-10 ms in heart failure (no significant difference). The QT/heart rate slope was significantly increased in heart failure [2.3+/-0.1 ms.(beats/min)(-1)] compared with controls [1.55+/-0.06 ms.(beats/min)(-1)] and hypertrophy [1. 66+/-0.1 ms.(beats/min)(-1)] (P<0.001). In left ventricular hypertrophy, despite animal data suggesting that QT interval prolongation should occur, no abnormalities were found in QT intervals at rest or during exercise. The QT/heart rate slope did not relate to any markers for an adverse prognosis, except that of prolongation of QT interval. Long QT intervals were associated principally with impairment of left ventricular systolic function. Our data emphasize the dynamic nature of the QT interval abnormalities found in heart failure.     

QT interval dispersion and autonomic modulation in subjects with anxiety

This study was designed to assess Q-T interval dispersion as a marker of electrical instability in subjects with anxiety. Recent observations have shown that the presence of anxiety symptoms increases the risk of sudden death. The Kawachi anxiety questionnaire identified 29 subjects (male/female ratio 13:16) who scored 0, 22 subjects (male/female ratio 14:8) who scored 1, and 37 subjects (male/female ratio 13:24) who scored 2 or more. In all subjects we measured electrocardiographic interlead QT dispersion and autonomic function through spectral analysis of R-R interval and blood pressure variabilities and left ventricular mass. Compared with subjects who scored 0, those reporting 2 or more symptoms showed increased heart rate-corrected QT dispersion (54.9+/-1.7 ms vs. 34.9+/-3.2 ms, P<.001), sympathetic modulation (normal logarithm low-frequency power/high-frequency power 0.59+/-0.1 vs. 0.12+/-0.04, P<.05), and left ventricular mass (120.7+/-3.5 g/m2 vs. 97.9+/-2.8 g/m2, P<.001). Probably because it augments sympathetic activity, anxiety causes left ventricular mass to increase and, like hypertension, increases heart rate-corrected Q-T interval dispersion. The consequent electrical instability could be the substrate responsible for inducing fatal ventricular arrhythmias.     

Effects of Postmyocardial Infarction Scar Size, Cardiac Function, and Severity of Coronary Artery Disease on QT Interval Dispersion as a Risk Factor for Complex Ventricular Arrhythmia

The aim of the study was to determine the relation between QT dispersion and ventricular arrhythmia after myocardial infarction, as well as the effects of postinfarction scar size, cardiac function, and severity of coronary artery disease on QT dispersion. Three hundred three patients, 3 months after myocardial infarction, and a group of 21 healthy subjects were evaluated. QT dispersion was the difference between maximal and minimal QT interval in 12-ECG leads. Postinfarction scar size was determined by Selvester's QRS scoring system. Cardiac function was evaluated by echocardiography and exercise stress test, and the severity of coronary artery disease by the number and degree of coronary artery stenoses. QT dispersion increased significantly in relation to the severity of arrhythmia (< 50 premature ventricular complexes vs ventricular tachycardia; 61.6 [± 12.3] vs 84.8 [± 16.4] ms, P < 0. 001). QT dispersion > 80 ms was associated with ventricular tachycardia with the sensitivity of 68% and specificity of 88%. QT dispersion also increased significantly, dependent on the postinfarction scar size (0% vs ± 33% of left ventricular myocardium; 61.8 [± 16.4] vs 74.7 [± 16] ms, P < 0. 001), as well as in the case of significantly impaired cardiac function. Although QT dispersion increased with the number of diseased vessels and the degree of stenoses, the differences were not significant (P > 0. 05). In conclusion, QT dispersion is a risk marker of complex ventricular arrhythmia in the chronic stage of myocardial infarction. Multiple regression analysis indicates that only the postinfarction scar size has an independent effect on QT dispersion (R²= 0. 39, P < 0. 05).