A15-6 Spectral and time domain analyses of heart rate variability during head-upright tilt table testing in children with neurally mediated syncope

EP Europace, Dec 2003

Evrengul, H., Evrengul, H., Tavli, V., Dursunoglu, D.

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A15-6 Spectral and time domain analyses of heart rate variability during head-upright tilt table testing in children with neurally mediated syncope

I Al 0 B. Verheyden , F. Beckers, F. Kubben, K. Vandorpe, T. Reybrouck, H. Ector, A.E. Aubert. Dept 1 E. Szufladowicz', E. Kozluk', .I. Dobrogowska-Kunicka', A. Zbi& , R. Maniewskiz, F. Walczak' 2 J.L. Newton , P.T. Donaldson, SW. Parry , R.A. Kenny, C.M. Morris. Cardiovascular Investigation Unit, Royal Victoria Injirmary , Newcastle , & School 3 National Institute 4 H. Evrengul', H. Evrengulz, V T&i', D. Dursunogluz. 'DI: Behcet &Sick Children Is Hospital , Division 5 A. Musialik-Lydka , B. Sredniawa, T. Zielinska, P. Jarski, Z. Kalams, L. Polonski. I Department 6 Z. Szabo , M. Harangi, I. Lorincz, I. Seres, E. I&tom, Z. Karanyi, G. Paragh. 1st Dept 7 0. Takuya , S. Hirokazu, T. Katsuhiko, Y. Yee Gum, Y. Gang, H. Katerim , K. Yoshinmi, K. Takao, T. Term, M. Marek. Nippon Medical School , 1st Department ity) as an index of cerebrovascular resistance. Data are presented as m e a n & SD. Results: In the 13 tilt-positive patients (68%), EEG alterations during the prodromic and the syncopal phase were different a m o n g cardioinhibitory, mixed and vasodepressive types. No EEG alterations in tilt-negative patients. TCD demonstrated a significant PI increase at the onset of prodromic symptoms in comparison with baseline (2.01&0.94 vs. 0.77&0.20, p<O.OOl, paired-sample t-test). No TCD alterations in tilt-negative patients. Furthermore, the percentage change in PI with respect to baseline was signiiicantly higher in cardioinhibitory types (254&51%, 5 patients) than in mixed and vasodepressive ones (101&22%, 8 patients) @<O.OOl, independent-sample t-test). Conclusions: Our data show that the degree of cerebral vasoconshiction at the onset of prodromic symptoms changes with the positivity type of tilt test. W e suggest that the amount of sympathetic activation, (as hypothesized by Levine during graded Lower Body Negative Pressure in healthy humans), may cause the degree of cerebral vasoconshiction in N M S patients. Therefore the sympathetic modulation of cerebral vasoconshiction may be a turning point for the explanation of N M S pathophysiology. - I Al 5 3 ANGIOTENSIN-CONVERTING ENZYME INSERTION/DELETION POLYMORPHISM DIAGNOSED VASOVAGAL SYNCOPE AND TILT Vasovagal syncope (WS) is a common cause of syncope characterised by hypotension with or without bradycardia that results in cerebral hypoperfusion and resultant collapse with loss of consciousness. VVS is a disease that clusters in families and recent studies by OUTgroup suggest that VVS may have a significant heritable component (Xs:lOSO) (Newton et al., CAR 2003). Salt supplementation appears to improve orthostatic tolerance and increases baroreceptor sensitivity in patients with VVS and hence polymorphisms of the angiotensin-converting enzyme (ACE, DCPI) would be a plausible potential candidate for regulating some of the features of the disease. The aim of this study was to examine the frequency of the ACE insertion/deletion polymorphism in a large cohort of well-character&d patients with a definite diagnosis of VVS. DNA was collected prospectively from 165 unrelated patients attending the Cardiovascular Investigation Unit who had VVS diagnosed on the basis of an abnormal haemodymmic response during head up tilt in conjunction with symptom reproduction. Overall there was no significant difference in the distribution of the ACE insertion or deletion gene frequencies in cases compared to a large (>6000 subjects) national control population. Cases controls: This study suggests that polymorphisms of ACE alone are not associated with VVS. Further studies are planned to clarify the genotype/phenotype relationship in VVS and examine other candidate genes. I Al 5 4 N E W INSIGHT INTO NEUROCARDIOGENIC BRAIN OXYGENATION AND ELECTROENCEPHALOGRAPHY MONITORING SYNCOPE: Introduction: Near-infrared spectroscopy (NIRS) measure brain oxygenation (hemoglobin-HbO, Deoxygenated-Hb, total-HbT), eeg indicates disturbances of brain electrical activity. Aim of study: To present changes in NIRS and eeg during neurocardiogenic syncope (NS). Material and method: Study group 54 patients with history of syncope. 54 tilt tests (33 female, m e a n age 33 -1-18 years): Neurocardiogenic synape occurred in 42 pts. Control group 37 healthy volunteers (22 female, m e a n ag(30& 12). Neurocardiogenic syncope didn’t occurred in control group. Results: Control group- EEG didn’t change during tilt test in any patient. NIRS during m e a n time of 7 minutes after changing to up-right position we were observed in all pts. slow decrease of HbO curve with corresponding increase of Hb curve. This drop range between 10.15% (mean 11%) from the basal lines and stay stable to the end of the test. Study group In pts. with NS changes in NIRS proceed changes in blood pressure and heart rate (2,1&2,7 minutes). W e observed 3 types of curves: 1. Similar corresponding drop of HbO and HbT (10 pts); 2. Drop of HbO without decrease of HbT (5 pts); 3. Mixed (27 pts). Hb level increased 0,9&1,7 min. after HbO dropped. EEG in pts. with NS we observed slowing down of eeg activity (theta>delta) in 29 pts. with further suppression in 6 pts. No changes in eeg were in 7 pts. Conclusions: 1. During NS typical changes in brain NIRS monitoring proceed changes in heart rate, blood pressure and syncope. 2. Changes in eeg occur simultaneously with syncope. 3. The most deep changes in eeg are observed in cardiodepressive type of NS. 4. In some pts. changes in NIRS and eeg are present in prolong time after NS while pts. are already conscious and having normal heart rate and blood pressure. I Al 5 5 AUTONOMIC CARDIOVASCULAR RESPONSES TO ORTHOSTATIC STRESS IN VASO-VAGAL SYNCOPE PATIENTS: EFFECTS OF TILT TRAINING Introduction: The purpose of this pilot study is to evaluate the influence of tilt training in vasovagal syncope (VVS) patients on autonomic balance using indices of heart rate and blood pressure variability (HRV and BPV) and baroreflex sensitivity (BRS). Methods: 23 subjects (13 females and 10 males) consisting of a control group (N=lO, aged 23&5 ys), a patient group (N=5, aged 38&9 yrs) and a training group (N=S, aged 33&5 yrs) performed the Westminster tilt test protocol. The training group consisted of VVS-patients that were enrolled in a tilt-training program @ehveen 3 and 12 sessions). The tilt test was positive in 3 subjects from the training group and in all subjects of the patient group. Continuous ECG and blood pressure were recorded simultaneously. Low frequency (LF: 0.04-0.15 Hz) and high frequency (HF: 0.16-0.4 Hz) powers in heart rate and blood pressure were calculated for 3 tilt phases: supine rest (10 min), 10 minutes after tilt and 5 minutes recovery. BRS was assessedusing the sequencemethod. Results: Results did not show any difference between male and female subjects. Both HF and LF powers of HRV were higher in the control group compared to the patient group. In the control group LF power of BPV was increased after tilt compared to supine rest whereas in the patient group LF power of BPV remained unchanged. BRS tended to be higher at supine rest in the control group compared to the patient group (NS) and decreased signficandy after tilt only in the control group (P<O.O5). BRS in the training group tended to increase (NS) with increasing tilt sessions. Conclusion: Cardiac autonomic control and vammotor sympathetic reflex activity is suggested to be impaired in VVS-patients. Low BRS at supine rest is proposed to be a predictor of increased risk for VVS. Tilt training showed a general reconditioning of dynamic cardiovascular regulation in VVS-patients. I Al 5 6 SPECTRAL AND TIME DOMAIN RATE VARIABILITY DURING TABLE TESTING IN CHILDREN MEDIATED SYNCOPE ANALYSES OF HEART HEAD-UPRIGHT TILT WITH NEURALLY Denizli, Neurocardiac syncape (NS) is a common cause of syncope in children. The mechanism, though related to abnormalities in autonomic function, has not been fully elucidated, particularly in pediatric patients. This study assessedthe heart rate variability (HRV) response to head-upright tilt table test (HUT) in children with NS and normal volunteers. Spectral and time domain analysis of HRV was used to assesschanges in autonomic function in 27 children (9 male, m e a n age 12.3&1.6 years) with a history of at least one episode of syncope and positive passive HUT and 27 age-matched normal volunteers with negative passive HUT before and during postural tilt and to attempt to relate such changes to specific types of haemodynamic response to tilt. Frequency domain measurements of the high (HF) and low (LF) frequency bands and the ratio LF/ HF were derived from bolter recordings, computed by Fast Fourier Analysis for 5 min intervals. Time domain measurements of the SDNN, SDNNI, SDANN, RMSSD and triangular index were derived from 24 hours bolter recordings. There were no significant differences between clinical characteristics, time domain and basal frequency domain parameters of the groups. M e a n values of LF and LF/HF ratio were increased and HF was decreased signiiicantly in response to tilting in both patient and control groups. M e a n values of LF and LF/HF ratio were higher and HF was lower compared to controls immediately after tilting. LF and LF/HF ratio showed a statistically significant decrease and a significant increase in HF during syncope in patients. The three subgroups of patients had similar patterns of changes in autonomic activity. The results of this study show that syncopal patients have a different pattern of response to the tilting test although the basal autonomic function was similar compared to the controls. The syncopal patients have exaggerated response to the tilting B23 EUROPACE test. This exaggerated response may be activated to pathological reflexes of NS. The pathological mechanism leading to NS appears to be independent of the specific type of haemodynamic response to tilt testing Conclusion: Both TCRT and TWR show distinct rate dependence. In future studies using these descriptors, heart rate correction is needed to improve the risk stratiiication value. A16. REPOLARISATION ABNORMALITIES A N D RISK STRATIFICATION I Al 6 1 CAN NEW DESCRIPTORS OF VENTRICULAR REPOLARISATION DETECT THE HIGH-RISK PATIENTS WITH IMPLANTED CARDIOVERTER DEFIBRILLATOR IN THE PATIENTS WITH HEART DISEASES? QT dispersion (QTd) has been proposed to reflect the heterogeneity of ventricular repolaisation. However, it fails to stratify high-risk patients because of methodological limitations. QTd values are overlapping between control and cardiac patients. Recently, it has been proposed that T-wave morphology analysis (TMA) may quantify the irregularities of ventricular repolaisation based on singular value decomposition of standard 1ZLead electrocardiograms (ECGs). TMA has been reported to be a useful in risk stratiiication of patients with myocardial infarction and ischaemic heart disease. However, it remains to be elucidated whether it can detect groups at high arhythmic risk among other heart disease patients. The aim of this study was to distinguish arhythmic patients from patients with heart diseases by TMA indices. Methods: Patients with implanted cardioverter defibrillator (ICD, n=33, 57&16 years) and with heart diseases (HD, n=34, 65&10 years) were studied. Standard 1Zlead ECGs were recorded digitally. Three TMA descriptors, namely the total cosine R-to-T (TCRT), T-wave morphology dispersion (TMD), and percentage of the loop area (PL) were calculated by a custom written software package. TCRT describes the global angle between repolarisation and depolaisation wavefronts and TMD expresses the angle between all possible reconstruction T wave vector pairs. Results: TMD of ICD was significantly higher than that of HD (55.9&22 vs 40.5&29, P < 0.05). PL of ICD was significantly lower than that of HD. (0.497&0.15 vs 0.59&0.14, P < 0.05) There were no differences in TCRT between both groups. Conclusion: TMD and PL are useful descriptors to identify subjects at high mhythmic risk. RATE DEPENDENCE REPOLARISATION OF DESCRIPTORS HETEROGENEITY OF P. Smetana, V Batchvarov, K. Hnatkova, A.J. Cam, Hospital Medical School, London, United Kingdom M. Ma& St.George’s Objective: The total cosine of the angle between the ventricular depolarisation and repolaisation vectors (TCRT) reflects global repolarisation heterogeneity. The extent of non-dip&r contents within the T wave (TWR) is a measure of regional repolarisation heterogeneity. Both descriptors have been shown to provide independent risk stratiiication in cardiac patients. The predictive power of both TCRT and TWR might be influenced by heart rate. We therefore investigated the rate relationship of TCRT in 50 healthy young volunteers (25 0 Methods: During 24.hours recordings (SEER MC) a 10.second 1Zlead ECG was obtained every 30 seconds. Recordings were repeated after 1, 7, and 30 days and results in each subject were pooled together and grouped for women and men. Using customer written software TCRT and TWR values were calculated in each 10.second ECG sample and averaged over 50ms RR interval bands from 550 to 1150 ms in each subject and grouped for women and men. Results: Women had uniformly greater TCRT and TWR values than men over the entire range of investigated RR intervals. While TCRT in both sexes showed marked rate dependence with higher values at long RR intervals (550 ms vs 1150 ms: women: 0.46&0.31 vs 0.76&0.X3, p=9xlO ~7; men: 0.08&0.45 vs 0.49&0.35, p=9~10~~), rate dependence of TWR was more marked in women than in men, showing higher values at shorter RR intervals (540.550 ms vs 1140.1150 ms women: 0.29&0.14% vs 0.08&0.06%, p=2xlO ‘; men: 0.14&0.12% vs 0.04&0.02%, p=2x 10 15). Europace Supplements, Vol. 4, December 2003 THE EFFECT OF DYSLIPIDEMIA ON QT INTERVAL AND QT DISPERSION IN PATIENTS WITHOUT ISCHEMIC HEART DISEASE Background QT dispersion (QTd) is defined as the difference between the max. imum QT (QTmax) and the minimum QT duration. Our aim was to assess the effect of dyslipidemia on QTmax and QTd in patients with lipid abnormalities without myocardial &hernia and to make a comparison with healthy controls. Furthermore, the possible relationship between body mass index (BMI) and ECG parameters was examined. Methods Ninety-six patients with dyslipidemia (44 men and 52 women, mean age: 53&13 years) and 101 healthy subjects (58 women and 43 men, mean age: 46&16 years) were studied. Total cholesterol, HDL-cholesterol, LDL-cholesterol, triglyceride, apoA1, ape-B, lipoprotein-(a) levels and QTmax, QTd, corrected QTmax and corrected QTd were determined. Results A difference occurred between the two subgroups of patients regarding cholesterol [mmoliL] 7.5&1.92 vs. 4.17&0.68 (p<O.OOOl), LDL-C: 4X3&1.67 vs. 2.77&0.54 (p<O.OOOl), triglyceride: 3.68&1.76 vs. 1.08&0.65 @<O.OOOl) ape-B: 1.42&0.43 vs. 1.X3&0.34 @<O.OOOl), QTmax [msec]: 430&34 vs. 370&27 (p<O.OOOl), corrected QTmax: 470&41 vs. 402&36 @<O.OOOl). QT dispersion was 59&18 msec in patients and 34&14 in controls (p<O.OOOl), also corrected QT dispersion differed significantly: 65&20 vs 37&15 msec (p<O.OOOl). A positive correlation occurred between cholesterol and QTmax @<O.OOOl, r=0.5), corrected QTmax @<O.OOOl, r=0.47), QTd (p<O.OOOl, r=0.53) and corrected QTd (p<O.OOOl, r=0.54). Triglyceride showed a positive correlation with QTmax (p<O.OOOl, r=0.29), corrected QTmax @=O.OOOZr,=0.26), QTd (p<O.OOOl, r=0.27), corrected QTd (p<O.OOOl, r=0.54). A significant relationship appeared between LDL-C and QTmax @<O.OOOl, r=0.41), corrected QTmax @<O.OOOl, r=0.41), QTd (p<O.OOOl, r=0.45) and corrected QTd (p<O.OOOl, r=0.47). A positive correlation was found between HDL-C and QTmax @<O.Ol, r=0.16), ape-B and QTd (p<O.O5, r=0.14). BMI showed positive correlation with all the studied ECG markers (p<O.OOOl) and cholesterol (p<O.OOOl), triglyceride @<O.OOOl), LDL-C @<0.0001). Conclusion Dyslipidemia and increased body weight may have a direct effect on the studied ECG markers. NON DIPPING HYPERTENSIVE VENTRICULAR HYPERTROPHY SUBJECTS AND LEFT AND QT DISPERSION Subjects with event absent nighttime blood pressure fall are at higher risk of hypertensive organ damage. It has been reported recently that they could be at higher risk of malignant ventricular arrhythmias and sudden cardiac death, which increased QT dispersion is one of known factors. The aim of the study: to assessparameters derived from the 24h arterial blood pressure monitoring in hypertensive patients and to compare left ventricular hypertrophy and QT dispersion between hypertensive subjects with preserved (dippers) or absent (non-dippers) night blood pressure fall. Methods: The study population consisted of 73 pts (41F, 32M; aged 52&16) with essential hypertension. Ambulatory blood pressure (BP) monitoring was performed in all patients. Patients were classiiied as dippers (52 pts, 29F, aged 52&17) or non-dippers (21 pts, 12F, aged 50&10) according to the magnitude of nocturnal BP fall > or < 10% of diurnal values. Left ventricular hypertrophy was confirmed by ultrasonocardiography using left ventricular rims index (LVMI). QT dispersion was assessed based on 12.leads standard ECGs. Results: Dippers and non-dippers had similar 24h systolic BP (147,8&16,7 vs 148,8&10,2 mmHg; NS), 24h diastolic BP (91,8&14,9 vs 93,1&7,7 mmHg; NS), while nocturnal diastolic BP was smaller in dippers than in non-dippers (87,8&14,8 vs 93,0&7,7 mmHg; p=O,O26). LVMI was signiiicantly greater in non-dippers than in dippers (126,5&21,7 vs 107,0&14,3 g/m’ ; p=O,OOO4). QT dispersion was significantly greater in non-dippers: 51,4&11,5 ms than in dippers: 44,0&13,5 ms; p=O,O3. Conclusions: The lack of nocturnal blood pressure fall in hypertensive patients is a risk factor of left ventricular hypertmphy and as well as of sudden cardiac death.

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Evrengul, H., Evrengul, H., Tavli, V., Dursunoglu, D.. A15-6 Spectral and time domain analyses of heart rate variability during head-upright tilt table testing in children with neurally mediated syncope, EP Europace, 2003, B23-B24, DOI: 10.1016/S1099-5129(03)91590-X