A15-6 Spectral and time domain analyses of heart rate variability during head-upright tilt table testing in children with neurally mediated syncope
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.
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DIAGNOSED VASOVAGAL SYNCOPE
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
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.
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N E W INSIGHT INTO NEUROCARDIOGENIC BRAIN OXYGENATION AND ELECTROENCEPHALOGRAPHY
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
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.
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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
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.
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SPECTRAL AND TIME DOMAIN RATE VARIABILITY DURING TABLE TESTING IN CHILDREN MEDIATED SYNCOPE
ANALYSES OF HEART
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
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
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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
OF DESCRIPTORS HETEROGENEITY OF
P. Smetana, V Batchvarov, K. Hnatkova, A.J. Cam,
Hospital Medical School, London, United Kingdom
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
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
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
Conclusion Dyslipidemia and increased body weight may have a direct
effect on the studied ECG markers.
NON DIPPING HYPERTENSIVE
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