Showing papers by "Marek Malik published in 2002"

Relation between QT and RR intervals is highly individual among healthy subjects: implications for heart rate correction of the QT interval

Abstract: Objective: To compare the QT/RR relation in healthy subjects in order to investigate the differences in optimum heart rate correction of the QT interval. Methods: 50 healthy volunteers (25 women, mean age 33.6 (9.5) years, range 19–59 years) took part. Each subject underwent serial 12 lead electrocardiographic monitoring over 24 hours with a 10 second ECG obtained every two minutes. QT intervals and heart rates were measured automatically. In each subject, the QT/RR relation was modelled using six generic regressions, including a linear model (QT = β + α × RR), a hyperbolic model (QT = β + α/RR), and a parabolic model (QT = β × RRα). For each model, the parallelism and identity of the regression lines in separate subjects were statistically tested. Results: The patterns of the QT/RR relation were very different among subjects. Regardless of the generic form of the regression model, highly significant differences were found not only between the regression lines but also between their slopes. For instance, with the linear model, the individual slope (parameter α) of any subject differed highly significantly (p < 0.000001) from the linear slope of no fewer than 21 (median 32) other subjects. The linear regression line of 20 subjects differed significantly (p < 0.000001) from the linear regression lines of each other subject. Conversion of the QT/RR regressions to QTc heart rate correction also showed substantial intersubject differences. Optimisation of the formula QTc = QT/RRα led to individual values of α ranging from 0.234 to 0.486. Conclusion: The QT/RR relation exhibits a very substantial intersubject variability in healthy volunteers. The hypothesis underlying each prospective heart rate correction formula that a “physiological” QT/RR relation exists that can be mathematically described and applied to all people is incorrect. Any general heart rate correction formula can be used only for very approximate clinical assessment of the QTc interval over a narrow window of resting heart rates. For detailed precise studies of the QTc interval (for example, drug induced QT interval prolongation), the individual QT/RR relation has to be taken into account.

Heart rate turbulence-based predictors of fatal and nonfatal cardiac arrest (The autonomic tone and reflexes after myocardial infarction substudy)

Abstract: A previous report on heart rate (HR) turbulence showed its value in postinfarction risk stratification. The present study determines the predictive value of HR turbulence in a low-risk population after acute myocardial infarction and provides insight into its pathophysiologic correlates. With use of the database of the The Autonomic Tone and Reflexes After Myocardial Infarction (ATRAMI) study, data were obtained from 1,212 survivors with a mean duration of follow-up of 20.3 months. The a priori end point was defined as the combination of fatal cardiac arrest and nonfatal cardiac arrest. HR turbulence characterized by turbulence onset (TO) and turbulence slope (TS) was calculated and correlated with baroreflex sensitivity (BRS) and the SD of the normal-to-normal RR intervals (SDNN). A composite index of cardiac autonomic function was assessed by combining HR turbulence (TO and TS), BRS, and SDNN. Both TO and TS correlated moderately but significantly with BRS and SDNN (r = 0.26 to 0.44, p <0.001 for all correlations). On Cox's univariate regression analysis, the RRs for abnormal values of TO, TS, and the combination of abnormal TO and TS were 1.86 (95% confidence interval [CI] 0.96 to 3.61, p = 0.065), 4.08 (95% CI 2.11 to 7.89, p <0.0001), and 6.87 (95% CI 3.06 to 15.45, p <0.0001), respectively. The composite autonomic index (combined TO, TS, BRS, and SDNN) was the strongest risk predictor: for all 4 abnormal factors, RR 16.79 (95% CI 6.01 to 46.89, p <0.0001). On multivariate analysis, abnormal TO and TS, and left ventricular ejection fraction remained as independent predictors: RRs 4.07 (95% CI 1.70 to 9.77, p = 0.0017) and 3.53 (95% CI 1.76 to 7.06, p = 0.0004), respectively. In a separate model, the composite autonomic index was the strongest multivariate risk predictor: RR 8.67 (95% CI 2.72 to 7.65, p = 0.0003) for all abnormal factors, and adjusted for left ventricular ejection fraction. Thus, this study confirms the independent value of HR turbulence in predicting fatal cardiac arrest and nonfatal cardiac arrest in a low-risk post-acute myocardial infarction population. By combining HR turbulence, BRS, and SDNN, a comprehensive assessment of cardiac autonomic reflexes and modulation can be obtained.

QT-RR relationship in healthy subjects exhibits substantial intersubject variability and high intrasubject stability.

Abstract: Recently, it was demonstrated that the QT-RR relationship pattern varies significantly among healthy individuals. We compared the intra- and interindividual variations of the QT-RR relationship. Tw...

Analysis of T-Wave Morphology From the 12-Lead Electrocardiogram for Prediction of Long-Term Prognosis in Male US Veterans

Abstract: Background— The aim of the present study was to assess the prognostic value of novel repolarization descriptors from the 12-lead ECG in a large cohort of US veterans. Methods and Results— Male US veterans (n=813) with cardiovascular disease had digital 12-lead ECGs recorded at the VA Medical Center, Washington, DC, between 1984 and 1991. The patient series was retrospectively compiled in 1991; follow-up was prospectively assessed until 2000. Novel ECG variables characterizing repolarization and the T-wave loop were automatically analyzed. Of 772 patients with technically analyzable data, 252 patients (32.6%) died after a mean follow-up of 10.4±3.8 years. Direct comparison between dead and alive patients showed that the so-called T-wave residua (the absolute and relative amount of nondipolar contents within the T wave) predicted mortality (111 900±164 700 versus 85 600±144 800 between dead and alive patients, P<0.0002; and 0.43±0.62% versus 0.33±0.56%, P<0.0005 for the absolute and relative T-wave residuum...

The imprecision in heart rate correction may lead to artificial observations of drug induced QT interval changes

Abstract: MALIK, M.: The Imprecision in Heart Rate Correction May Lead to Artificial Observations of Drug Induced QT Interval Changes. Because of the known limitations of the Bazett and other heart rate correction formulas, it has been proposed that studies of drug induced QT interval changes should use several different heart rate correction formulas and that the consistency of findings by a majority of such formulas should be considered as valid. The aim of this article was to show that such an approach is inappropriate. Using the database of the EMIAT trial, data of QT and RR intervals were taken from electrocardiograms of the first postrandomization visit of 1,402 patients. Of these, 309 were on amiodarone and β-blockers, 395 on amiodarone and off β-blockers, 318 on β-blockers and off amiodarone, and 380 off amiodarone and off β-blockers. An investigation of drug induced QT interval changes was modeled by evaluating the corrected QT (QTc) interval differences between patients on and off amiodarone, and on and off β-blockers. A set of 31 previously published heart rate correction formulas was used. In addition to calculating the QTc difference between on and off drug for each formula, the success of heart rate correction was judged by computing correlation coefficients between QTc and RR intervals (ideally corrected QTc values should be independent of heart rate). The difference between on and off drug QT intervals was also evaluated by logarithmic regression models between uncorrected QT and RR intervals in data taken from patients on and off treatment. The QTc interval prolongation on amiodarone was confirmed by all heart rate correction formulas but the extent of the prolongation differed from formula to formula and ranged from 13.6 to 30.9 ms. Of the 31 formulas, 3 reported QTc interval shortening on β-blockers (up to −11.8 ms) and 28 reported QTc interval prolongation (up to + 16.8 ms). The distribution of the results provided by the different formulas suggested that β-blocker treatment led to a QTc interval prolongation by approximately 7 ms (e.g., + 7.4 ms by the Fridericia formula, P = 0.002). The on treatment QTc changes obtained by different formulas were closely correlated to their correction success. Formulas that provided QTc intervals almost independent of the RR intervals estimated ≈ 20 ms QTc prolongation on amiodarone and no QTc change on β-blockers. QT/RR regression analysis confirmed that while amiodarone led to substantial QT prolongation, there was no change of QT interval on β-blockers beyond the change in heart rate. The study showed that the concept of “majority voting” by different heart rate correction formulas is inappropriate and may lead to erroneous conclusions.

Sex differences in repolarization homogeneity and its circadian pattern.

Abstract: The reason for sex differences in arrhythmic risk remains unclear. Heterogeneity of ventricular repolarization is directly linked to arrhythmogenesis; thus we investigated repolarization homogeneity and its circadian pattern in men and women. During 24-h Holter recordings in 60 healthy subjects (27 males), a 12-lead electrocardiogram (ECG) was obtained every 30 s. RR and QT intervals, and, after singular-value decomposition, two characteristics of repolarization homogeneity were calculated in each ECG. Corrected QT (QTc) values were obtained using an individually optimized heart rate (HR) correction formula. All values were averaged over 10-min time bands from 0000 to 2400. There were substantial sex differences in both global repolarization homogeneity (measured by the total cosine of the angle between QRS and T wave vectors) and regional homogeneity of repolarization (quantified independently by the relative T wave residuum). Whereas women throughout the 24 h followed more closely the pattern of inverse sequence between depolarization and repolarization, they also showed much higher localized repolarization heterogeneity than men. In both women and men, repolarization irregularity was greatest during morning hours. A sex difference was also observed for HR and QTc interval; however, the circadian patterns of the repolarization homogeneity descriptors were different from those of HR and QTc intervals.

Heart rate variability in critical care medicine.

Abstract: The autonomic nervous system plays an integral role in homeostasis. Autonomic modulation can frequently be altered in critically ill patients. Assessment of heart rate variability (HRV) is based on analysis of consecutive normal R-R intervals and may provide quantitative information on the modulation of cardiac vagal and sympathetic nerve input. The hypothesis that depressed HRV may occur over a broad range of critical illness and injury and may be inversely correlated with disease severity and outcome has been tested in the last decade. In this article, we review recent literature concerning assessment of HRV in patients with critical illness or injury, as well as the potential clinical implications and limitations of HRV assessment in this area.

Individual patterns of QT/RR relationship.

Abstract: In clinical practice, an imprecision introduced by ad hoc selected heart rate correction formula of the QTinterval is unlikely to lead to erroneous conclusions if all borderline cases are carefully considered. On thecontrary, in clinical investigations (e.g., studies of drug effects) the over- or undercorrection of QTcmay lead to significant and systematic bias with both false positive and false negative findings. None of the previously published “global” heart rate correction formulae has been universallysuccessful because the QT/RR relationship is different between different subjects and a formula that correctsthe QT interval for heart rate acceptably in one individual may be very misleading in another individual.Moreover, it has been recently established that the QT/RR patterns not only exhibit a substantialinter-subject variability but also a high intra-subject stability. Thus, in precise investigations, individualQT/RR relationship should be first established in each subject and subsequently translated into individualheart rate correction formula.

Mechanisms involved in heart rate turbulence.

Abstract: Proper understanding of the mechanisms involved in heart rate turbulence (HRT) may offer anexplanation of why it is such a potent postinfarction risk stratifier. This article reviews the physiologicalbackground of ventriculophasic sinus arrhythmia—a phenomenon which shares some underlying physiologicalfeatures with HRT including cardiac autonomic regulation. It is now believed that HRT is principally triggeredby a transient loss of vagal efferent activity in response to the missed baroreflex afferent input due toventricular premature beat-induced haemodynamically inefficient ventricular contraction. Studies are summarizedwhich support more or less directly this hypothesis. The physiology of early acceleration and late decelerationof heart rate after a ventricular premature beat is discussed. Qualitatively different but otherwisequantitatively uniform postectopic dynamics of systolic blood pressure after ventricular premature beats isdemonstrated in subjects with normal and abnormal left ventricular function. It is concluded that the slope oflate deceleration of heart rate after ventricular premature beats can serve as a reasonable surrogate forbaroreflex sensitivity.

Fractal correlation properties of R-R interval dynamics in asymptomatic relatives of patients with dilated cardiomyopathy☆

Abstract: Background and aim: asymptomatic relatives of patients with familial dilated cardiomyopathy who have left ventricular enlargement [LVE] are at risk for progression to dilated cardiomyopathy. A novel index of the fractal correlation properties of heart rate variability (HRV), the short-term scaling component (∝1) in detrended fluctuation analysis, is a promising prognostic tool in left ventricular dysfunction. The aim of this study was to compare values of ∝1 and conventional HRV indices in LVE relatives with dilated cardiomyopathy patients and normal controls. Methods: time-domain and spectral HRV measures, and the short-term scaling component (∝1) were assessed from 24-h Holter recordings from 22 LVE relatives (left ventricular end-diastolic dimension >112% predicted, normal fractional shortening), 24 dilated cardiomyopathy patients and 14 controls. Results: the time domain index SDNN was lower in dilated cardiomyopathy patients [101.8(±44.0)] than in LVE relatives [161.7(±53.9)] or controls [152.9(±51.4)], P - 0.01. Similarly, triangular index and spectral measures were reduced in dilated cardiomyopathy patients but not in LVE relatives or controls. In contrast, the short term scaling component (∝1) in detrended fluctuation analysis was reduced in both dilated cardiomyopathy patients [1.06(±0.33)] and in LVE relatives [1.15 (±0.20)], compared with controls [1.32(±0.16)], P - 0.01. Among DCM patients the short-term scaling component (∝1) was significantly associated with echocardiographic deterioration during follow-up (3.7±2.1 year) (P - 0.004). Conclusion: the short-term scaling component (∝1) is reduced in asymptomatic relatives of dilated cardiomyopathy patients who have LVE.

Assessment of noise in digital electrocardiograms.

Abstract: BATCHVAROV, V., et al.: Assessment of Noise in Digital Electrocardiograms. Technically related noise in 12-lead ECGs recorded with ambulatory recorders has never been systematically compared with that in ECGs recorded with conventional ECGs. This study compared serial 10-second ECGs obtained in ten healthy men, age 22–45 years, who were recorded in the supine resting position using a (1) MAC VU recorder, (2) digital ambulatory SEER MC recorder with a Multi-Link detachable ECG cable, and (3) digital ambulatory SEER MC recorder with a light ambulatory ECG cable. In each ECG, averaged sinus rhythm cycles of the entire recording were realigned with the native signal and subtracted. The resulting “residuum” was quantified by computing its standard deviation and root mean square of successive differences (RMSSD). While the RMSSD residuum values were significantly lower with the MAC VU recorder (6.27 ± 0.98 μV) than with the SEER MC recorder with either ECG cables (7.29 ± 1.31 and 7.17 ± 1.31 μV, P < 0.003 and p < 0.02), the difference was practically negligible and there was no detectable difference in the standard deviation residuum values. The study concludes that valid ECG investigations of serial ECG testing may be conducted using the ambulatory SEER MC recorders providing the biological sources of ECG noise are controlled. The available technology for noise assessment suggests that studies involving advanced analysis of serial ECGs (e.g., of drug related changes), should incorporate objective characterisation of ECG quality.

Practical use of T wave morphology assessment.

Abstract: QT dispersion (QTd) has not proven to be a useful marker derived from the 12-leadelectrocardiogram (ECG) for stratification of patients at risk for sudden cardiac death. To overcomeits methodological shortcomings, novel ECG variables of T wave morphology have been proposed. The total cosineR-to-T (TCRT), T wave morphology dispersion, T wave loop dispersion, normalized T wave loop area, aswell as absolute and relative T wave residuum evaluating non-dipolar ECG signal contents were evaluated in twoclinical studies involving post myocardial infarction (MI) patients and US veterans with cardiovasculardisease.

Effects of supratherapeutic doses of ebastine and terfenadine on the QT interval.

Abstract: Sir, Drs Gillen et al. recently reported [1] that at supratherapeutic doses, ebastine caused increase in heart rate and that, dependent on the method used for heart rate correction of QT interval, it led either to small but statistically significant, or minute and nonsig­nificant prolongation of the QTc interval. The use of Bazett and/or Fridericia formulae for QT interval correction is well placed in clinical practice because the relative magnitude of the errors due to under-or over-correction of the QT interval is unlikely to lead to incorrect clinical decision. However, in order to investigate drug related QTc interval changes in the presence of drug-induced heart rate change, the appropriateness and precision of the method used for correcting the QT interval for heart rate is essential. If the QTc interval is under-or over-corrected, the heart rate changes are projected into the QTc interval data and the analysis of the study becomes potentially meaningless with the possibility of both false positive and false negative findings. There are ways of judging the success of heart rate correction. Perhaps the simplest test is to investigate the correlation coefficient between the RR and QTc interval in the electrocardiograms obtained in drug-free stage. While a correlation coefficient of 0 does not guarantee that the QTc and RR interval data are truly independent, a value different from 0 shows that the heart rate correction formula used to obtain the QTc values has not been successful in removing the dependency of QT interval on heart rate. Drs Gillen et al. rightly say that a large number of heart rate correction formulae have previously been proposed. However, as their multiplicity implies, none of these formulae has found truly universal acceptance. The reasons for such a lack of a universally acceptable heart rate correction have become understood only recently. It has been observed that the QT/RR interval relationship is both different in different subjects and stable in the same individual over time [2, 3]. The intersubject variability of the QT/RR relationship means that a heart rate correction formula that correctly works in one individual, that is, provides QTc values that are independent of heart rate, will not necessarily be the optimum in another individual. Thus, to obtain truly heart rate-independent QTc values, individual characteristics of the QT/RR relationship need to be taken into account. This effectively means that the individual QT/RR pattern needs to be translated into an individual heart rate correction formula [4]. It is not for the first time that the study reported by Drs Gillen et al. has been analysed and published. I had the possibility of analysing the very same data set of this study and I have previously published the results obtained when using the technology of individual heart rate corrections [5]. Briefly, in the drug-free data of the study published by Dr Gillen et al., the heart rate correction formula QTc = QT/RRα has been optimized for each study participant, obtaining different values of the coefficient α for each individual. In these analyses, I have observed that while the coefficient of Fridericia's formula α = 0.33 was within the range of individually optimized coefficients (it was still significantly overcorrecting for some and under-correcting for other subjects), the coefficient of Bazett's formula α = 0.5 was well outside this range (Figure 1). Figure 1 The drug-free RR/QT interval data of each subject of the study reported by Drs Gillen et al.[1] were used to calculate heart rate corrected QTc intervals using the formula QTc = QT/RRα, ranging the values of α from ... The analyses based on the individually optimized heart rate corrections showed that in the study reported by Dr Gillen et al. ebastine did not in fact cause any QTc interval prolongation. The changes of the QTc interval on placebo, ebastine 60 mg daily ebastine 100 mg daily, and terfenadine 360 mg daily were −2. 76 ± 5. 51 ms, −3. 15 ± 9. 17 ms, −2. 61 ± 9. 55 ms, and 12. 43 ± 15. 25 ms, respectively [5].

Is there a physiologic QT/RR relationship?

Abstract: Investigations of the relationship between speciŽ c parts of the cardiac cycle and heart rate are not new. Well before the invention of electrocardiography, studies have reported the portion of the cardiac cycle taken by systole as measured from radial sphygmographic tracings and mechanical apexograms.* Whereas Donders2 suggested in 1865 that the duration of cardiac systole was almost constant and heart rate independent, Garrod3 concluded in 1870 that the duration of systole changes with the cube root of cardiac period. Later, when using mechanical cardiograph rather than sphygmograph, Garrod4 proposed that the duration of systole is related to the square root of the cardiac cycle. After the introduction of electrocardiography, these investigations eventually turned to the proportion between the QT and RR intervals, and the disputes about the proper formula to describe the QT/RR relationship have continued ever since. Theoretically, the task of describing the QT/RR relationship does not appear to be too complicated. In principle, it seems sufŽ cient to accumulate enough data points of corresponding QT and RR intervals, subject these data to a curve-Ž tting regression procedure, and use known mathematical tools that should provide not only the mathematical form of the relationship but also the corresponding numerical parameters. Unfortunately, the problem is far from this simple. Although regression analysis of QT/RR data has been performed many times, the reported results are highly variable. Frequently, perhaps because of the mathematical simplicity, QT interval has been related to different exponents of RR interval, i.e., it has been postulated that QT is a Ž xed proportion of RR (with RR interval measured in seconds). The most known study by Bazett,5 which suggested a 5 0.5, involved ECGs of 12 normal children aged 1 day to 11 years, 50 ECGs of 37 normal men aged from “boy” to 38 years, 32 ECGs of 20 normal women aged 20 to 53 years, and 16 ECGs of 3 healthy men who exercised. Compared with other investigations, Bazett’s study was actually a methodologic exception because it was purely observational and did not involve any regression modeling. A more detailed analysis of the data used by Bazett shows that had Bazett used regression analysis, he would have obtained the result of approximately a 5 0.4.6 Contemporary to Bazett’s work, the study by Fridericia7 used a detailed mathematical evaluation of 50 ECGs of 28 men and boys and 22 women and girls and concluded that the optimum parameter of a 5 0.3558 may be approximated by a 5 1/3. However, in a study of 200 “quite healthy” Japanese subjects (135 men) aged 18 to 64 years, Mayeda8 found a 5 0.604, whereas Yoshinaga et al.9 suggested a 5 0.31 based on data from 12,543 ECGs of Japanese children and adolescents. Simonson et al.1 0 investigated ECGs of 649 men and 311 women and concluded that a 5 0.32, with an age-related increase of QT by about 3 msec every 10 years. In a study involving heart rate changes by atrial pacing, atropine, isoproterenol, exercise, and recovery, Kawataki et al.1 1 concluded that a 5 0.25; Boudolas et al.12 proposed a 5 0.398 in men and a 5 0.384 5 women; Hodges13 reported a 5 0.38. The inconsistencies among the individual Ž ndings are substantial. The differences between the smallest (0.25) and largest (0.604) values of previously reported a values lead to discrepancies around 25 msec when the heart rate changes only between 55 and 65 beats/min! Similar inconsistencies also exist among studies investigating other types of QT/RR relationship. The slope b of linear relationship between QT and RR intervals was investigated by Schlamowitz,14 who reported b 5 0.205 based on data from 650 healthy soldiers aged 18 to 44 years. Simonson et al.1 0 found b 5 0.14, Larsen and Skulason1 5 proposed b 5 0.125, whereas from the data of the Framingham study (2,239 men and 2,779 women), Sagie et al.16 observed b 5 0.154 applicable to both sexes. There is one major methodologic problem with all of these studies. The investigations were performed most frequently to propose a heart rate correction formula, i.e., to establish a rule that allows conversion of a pair of QT and RR durations into a standardized QTc value corresponding to a “basal” RR interval of 1 second. That is, answering the question of how long would this QT interval be if the RR interval were 1 second, in a very similar way to the correction of, say, atmospheric pressure for altitude (what would this measured pressure be if the measurement were performed at sea level).1 7 The design of such a universal heart rate correction formula is based on the assumption that the investigated QT/RR data are representative of a “physiologic” QT/RR relationship that is the same in every healthy subject or at least in a same subject of a well-deŽ ned group (e.g., in healthy men). Unfortunately, as reported recently, it appears that such a common “physiologic” QT/RR relationship does not exist because the QT/RR patterns exhibit remarkable interindividual differences.1 8 ,19 For instance, Figure 1 shows QT and RR interval data carefully measured on serial stationary electrocardiograms of two healthy male subjects. It is obvious that the QT/RR pattern is rather  at in one patient but is much steeper in the other patient. Specifically, when the RR interval changes from 750 to 950 msec, J Cardiovasc Electrophysiol, Vol. 13, pp. 1219-1221, December 2002.

Comparison between Ventricular gradient and a new descriptor of the wavefront direction of Ventricular activation and recovery

Abstract: Background: Total R T cosine (TCRT) is a new descriptor of repolarization heterogeneity that quantifies the deviation between the directions of ventricular depolarization and repolarization. It revives the old concept of ventricular gradient (VG). Hypothesis: Our goal was to examine whether TCRT and VG contain nonredundant information by comparing their reaction to autonomic tests, namely, postural changes and Valsalva maneuver. Methods: Digital 12-lead electrocardiograms were recorded in 16 patients with cardiovascular syndrome X (SX, chest pain, exercise-induced ST-depression, normal coronary arteries, 3 men, age 60 ± 9 years) and 40 healthy volunteers (31 men, age 33 ± 7 years) during postural changes and Valsalva maneuver. The angle (VGA) [°] and magnitude (VGM) [ms.mV] of VG in reconstructed XYZ leads and TCRT (average cosine of the angles between the QRS and T vectors in mathematically reconstructed three-dimensional space) were calculated. Results: (mean ± standard of the mean): In healthy subjects, VGM and TCRT decreased, whereas VGA increased in the sitting and standing compared with supine position (TCRT: 0.61 ± 0.05, 0.47 ± 0.06, 0.29 ± 0.08, supine, sitting, and standing, p < 0.05) and during phase II Valsalva (TCRT: 0.47 ± 0.06 vs. 0.61 ± 0.05, p < 0.01 in supine, 0.24 ± 0.08 vs. 0.37 ± 0.07, p < 0.01 in standing). In patients with SX, VGM decreased in the standing position, VGA did not change significantly, while TCRT decreased only in patients without T-wave abnormalities (n = 9) (TCRT in standing and supine: 0.55 ± 0.09 vs. 0.68 ± 0.08, p < 0.05). VGM increased during Valsalva in patients with SX. Total R T cosine correlated strongly with VGA (r = –0.84, p< 0.00001) and, unlike VGM, did not correlate with heart rate. Conclusions: Ventricular gradient and TCRT contain non-redundant information. In healthy subjects, they react sensitively to autonomic provocation. In patients with SX, their reaction is attenuated, which suggests disturbance of the autonomic control of repolarization.

Non-invasive Wedensky modulation within the QRS complex.

Abstract: To investigate non-invasively induced Wedensky modulation, 2 ms pulses of 5, 20 and 40 mA were delivered between precordial and subscapular patches synchronously with the QRS complex. Wavelet vector magnitude was obtained for averaged modulated and non-modulated complexes. The surface area of a 3D-envelope of their difference (WSR) was compared in 59 patients with an uncomplicated follow-up after myocardial infarction (MI) (42 men, 64.3±9.1 years), in 30 patients with ischaemic heart disease and a history of ventricular tachycardia/fibrillation (VT/VF) (29 men, 63.1±9.8 years), and in 53 healthy subjects (control) (22 men, 56.6±10.1 years). Reproducibility of the assessment was tested by computing relative errors in a sub-population of 30 VT/VF patients and 47 controls. Wedensky modulation parameters differed significantly between control, MI and VT/VF subjects. In 10 ms post-modulation windows, the following WSR values were obtained: controls: 1184±496 (5 mA), 1553±838 (20 mA) and 2092±1488 (40 mA); VT/VF: 861±412 (5 mA), 1134±636 (20 mA) and 1320±1036 (40 mA); MI: 1305±885 (5 mA) and 1779±1169 (20 mA). With all modulating energies used, the VT/VF patients differed significantly from both the controls and MI patients; control patients against VT/VF patients: p<0.004 (5 mA), p<0.01 (20 mA) and p<0.001 (40 mA); VT/VF patients against MI patients: p<0.02 (5 mA), p<0.01 (20 mA); control patients against MI patients: all p=NS. The reproducibility assessment showed an acceptable stability of Wedensky modulation parameters. This study demonstrated that wavelet decomposition detects non-invasive Wedensky modulation within the QRS complex, and VT/VF patients are less sensitive to Wedensky modulation than control and MI patients.

Nitroglycerin induced syncope occurs in subjects with delayed phase shift of baroreflex action.

Abstract: MELENOVSKY, V., et al.: Nitroglycerin Induced Syncope Occurs in Subjects with Delayed Phase Shift of Baroreflex Action. Nitroglycerin (NTG) administration occasionally leads to syncope due to severe hypotension and bradycardia. This reaction resembles neurocardiogenic syncope but it may occur when the patient is in the supine position. To address the possible role of prevailing autonomic tone and baroreflex control in precipitation of NTG induced syncope, continuous noninvasive blood pressure and an ECG were taken shortly before NTG application in the supine position. Frequency-domain measures of heart rate variability (HRV) and noninvasive indices of baroreflex were compared between subjects who did (n = 6) and did not (n = 41) develop syncope after NTG. Both groups differed only in the phase shift (PCR) between oscillations of blood pressure and heart rate during controlled respiration (0.1 Hz). PCR was significantly delayed in subjects who developed syncope than in controls (−99.3 ± 14.1 vs −65.5 ± 27.0 degrees, P = 0.002). Thus, subjects with prolonged PCR are prone to NTG induced syncope because of increased lagging and, consequently, less stable baroreflex control.