Ultra-high-frequency ECG volumetric and negative derivative epicardial ventricular electrical activation pattern.

From precordial ECG leads, the conventional determination of the negative derivative of the QRS complex (ND-ECG) assesses epicardial activation. Recently we showed that ultra-high-frequency electrocardiography (UHF-ECG) determines the activation of a larger volume of the ventricular wall. We aimed to combine these two methods to investigate the potential of volumetric and epicardial ventricular activation assessment and thereby determine the transmural activation sequence. We retrospectively analyzed 390 ECG records divided into three groups-healthy subjects with normal ECG, left bundle branch block (LBBB), and right bundle branch block (RBBB) patients. Then we created UHF-ECG and ND-ECG-derived depolarization maps and computed interventricular electrical dyssynchrony. Characteristic spatio-temporal differences were found between the volumetric UHF-ECG activation patterns and epicardial ND-ECG in the Normal, LBBB, and RBBB groups, despite the overall high correlations between both methods. Interventricular electrical dyssynchrony values assessed by the ND-ECG were consistently larger than values computed by the UHF-ECG method. Noninvasively obtained UHF-ECG and ND-ECG analyses describe different ventricular dyssynchrony and the general course of ventricular depolarization. Combining both methods based on standard 12-lead ECG electrode positions allows for a more detailed analysis of volumetric and epicardial ventricular electrical activation, including the assessment of the depolarization wave direction propagation in ventricles.

Bipolar anodal septal pacing with direct LBB capture preserves physiological ventricular activation better than unipolar left bundle branch pacing.

Background: Left bundle branch pacing (LBBP) produces delayed, unphysiological activation of the right ventricle. Using ultra-high-frequency electrocardiography (UHF-ECG), we explored how bipolar anodal septal pacing with direct LBB capture (aLBBP) affects the resultant ventricular depolarization pattern. Methods: In patients with bradycardia, His bundle pacing (HBP), unipolar nonselective LBBP (nsLBBP), aLBBP, and right ventricular septal pacing (RVSP) were performed. Timing of local ventricular activation, in leads V1-V8, was displayed using UHF-ECG, and electrical dyssynchrony (e-DYS) was calculated as the difference between the first and last activation. Durations of local depolarizations were determined as the width of the UHF-QRS complex at 50% of its amplitude. Results: aLBBP was feasible in 63 of 75 consecutive patients with successful nsLBBP. aLBBP significantly improved ventricular dyssynchrony (mean -9 ms; 95% CI (-12;-6) vs. -24 ms (-27;-21), ), p < 0.001) and shortened local depolarization durations in V1-V4 (mean differences -7 ms to -5 ms (-11;-1), p < 0.05) compared to nsLBBP. aLBBP resulted in e-DYS -9 ms (-12; -6) vs. e-DYS 10 ms (7;14), p < 0.001 during HBP. Local depolarization durations in V1-V2 during aLBBP were longer than HBP (differences 5-9 ms (1;14), p < 0.05, with local depolarization duration in V1 during aLBBP being the same as during RVSP (difference 2 ms (-2;6), p = 0.52). Conclusion: Although aLBBP improved ventricular synchrony and depolarization duration of the septum and RV compared to unipolar nsLBBP, the resultant ventricular depolarization was still less physiological than during HBP.

Arterial Aging Best Reflected in Pulse Wave Velocity Measured from Neck to Lower Limbs: A Whole-Body Multichannel Bioimpedance Study.

Pulse wave velocity is a commonly used parameter for evaluating arterial stiffness and the overall condition of the cardiovascular system. The main goal of this study was to establish a methodology to test and validate multichannel bioimpedance as a suitable method for whole-body evaluations of pulse waves. We set the proximal location over the left carotid artery and eight distal locations on both the upper and lower limbs. In this way, it was possible to simultaneously evaluate pulse wave velocity (PWV) in the upper and lower limbs and in the limbs via four extra PWV measurements. Data were acquired from a statistical group of 220 healthy subjects who were divided into three age groups. The data were then analysed. We found a significant dependency of aortic PWV on age in those values measured using the left carotid as the proximal. PWV values in the upper and lower limbs were found to have no significant dependency on age. In addition, the PWV in the left femoral artery shows comparable values to published already carotid-femoral values. Those findings prove the reliability of whole-body multichannel bioimpedance for pulse wave velocity evaluation and provide reference values for whole-body PWV measurement.

Left Ventricular Myocardial Septal Pacing in Close Proximity to LBB Does Not Prolong the Duration of the Left Ventricular Lateral Wall Depolarization Compared to LBB Pacing.

Background: Three different ventricular capture types are observed during left bundle branch pacing (LBBp). They are selective LBB pacing (sLBBp), non-selective LBB pacing (nsLBBp), and myocardial left septal pacing transiting from nsLBBp while decreasing the pacing output (LVSP). Study aimed to compare differences in ventricular depolarization between these captures using ultra-high-frequency electrocardiography (UHF-ECG). Methods: Using decremental pacing voltage output, we identified and studied nsLBBp, sLBBp, and LVSP in patients with bradycardia. Timing of ventricular activations in precordial leads was displayed using UHF-ECGs, and electrical dyssynchrony (e-DYS) was calculated as the difference between the first and last activation. The durations of local depolarizations (Vd) were determined as the width of the UHF-QRS complex at 50% of its amplitude. Results: In 57 consecutive patients, data were collected during nsLBBp (n = 57), LVSP (n = 34), and sLBBp (n = 23). Interventricular dyssynchrony (e-DYS) was significantly lower during LVSP -16 ms (-21; -11), than nsLBBp -24 ms (-28; -20) and sLBBp -31 ms (-36; -25). LVSP had the same V1d-V8d as nsLBBp and sLBBp except for V3d, which during LVSP was shorter than sLBBp; the mean difference -9 ms (-16; -1), p = 0.01. LVSP caused less interventricular dyssynchrony and the same or better local depolarization durations than nsLBBp and sLBBp irrespective of QRS morphology during spontaneous rhythm or paced QRS axis. Conclusions: In patients with bradycardia, LVSP in close proximity to LBB resulted in better interventricular synchrony than nsLBBp and sLBBp and did not significantly prolong depolarization of the left ventricular lateral wall.

3-Dimensional ventricular electrical activation pattern assessed from a novel high-frequency electrocardiographic imaging technique: principles and clinical importance.

The study introduces and validates a novel high-frequency (100-400 Hz bandwidth, 2 kHz sampling frequency) electrocardiographic imaging (HFECGI) technique that measures intramural ventricular electrical activation. Ex-vivo experiments and clinical measurements were employed. Ex-vivo, two pig hearts were suspended in a human-torso shaped tank using surface tank electrodes, epicardial electrode sock, and plunge electrodes. We compared conventional epicardial electrocardiographic imaging (ECGI) with intramural activation by HFECGI and verified with sock and plunge electrodes. Clinical importance of HFECGI measurements was performed on 14 patients with variable conduction abnormalities. From 3 × 4 needle and 108 sock electrodes, 256 torso or 184 body surface electrodes records, transmural activation times, sock epicardial activation times, ECGI-derived activation times, and high-frequency activation times were computed. The ex-vivo transmural measurements showed that HFECGI measures intramural electrical activation, and ECGI-HFECGI activation times differences indicate endo-to-epi or epi-to-endo conduction direction. HFECGI-derived volumetric dyssynchrony was significantly lower than epicardial ECGI dyssynchrony. HFECGI dyssynchrony was able to distinguish between intraventricular conduction disturbance and bundle branch block patients.

Left bundle branch pacing compared to left ventricular septal myocardial pacing increases interventricular dyssynchrony but accelerates left ventricular lateral wall depolarization.

BACKGROUND: Nonselective His-bundle pacing (nsHBp), nonselective left bundle branch pacing (nsLBBp), and left ventricular septal myocardial pacing (LVSP) are recognized as physiological pacing techniques. OBJECTIVE: The purpose of this study was to compare differences in ventricular depolarization between these techniques using ultra-high-frequency electrocardiography (UHF-ECG). METHODS: In patients with bradycardia, nsHBp, nsLBBp (confirmed concomitant left bundle branch [LBB] and myocardial capture), and LVSP (pacing in left ventricular [LV] septal position without proven LBB capture) were performed. Timings of ventricular activations in precordial leads were displayed using UHF-ECG, and electrical dyssynchrony (e-DYS) was calculated as the difference between the first and last activation. Duration of local depolarization (Vd) was determined as width of the UHF-QRS complex at 50% of its amplitude. RESULTS: In 68 patients, data were collected during nsLBBp (35), LVSP (96), and nsHBp (55). nsLBBp resulted in larger e-DYS than did LVSP and nsHBp [- 24 ms (-28;-19) vs -12 ms (-16;-9) vs 10 ms (7;14), respectively; P <.001]. nsLBBp produced similar values of Vd in leads V5-V8 (36-43 ms vs 38-43 ms; P = NS in all leads) but longer Vd in leads V1-V4 (47-59 ms vs 41-44 ms; P <.05) as nsHBp. LVSP caused prolonged Vd in leads V1-V8 compared to nsHBp and longer Vd in leads V5-V8 compared to nsLBBp (44-51 ms vs 36-43 ms; P <.05) regardless of R-wave peak time in lead V5 or QRS morphology in lead V1 present during LVSP. CONCLUSION: nslbbp preserves physiological LV depolarization but increases interventricular electrical dyssynchrony. LV lateral wall depolarization during LVSP is prolonged, but interventricular synchrony is preserved.

Ventricular activation pattern assessment during right ventricular pacing: Ultra-high-frequency ECG study.

BACKGROUND: Right ventricular (RV) pacing causes delayed activation of remote ventricular segments. We used the ultra-high-frequency ECG (UHF-ECG) to describe ventricular depolarization when pacing different RV locations. METHODS: In 51 patients, temporary pacing was performed at the RV septum (mSp); further subclassified as right ventricular inflow tract (RVIT) and right ventricular outflow tract (RVOT) for septal inflow and outflow positions (below or above the plane of His bundle in right anterior oblique), apex, anterior lateral wall, and at the basal RV septum with nonselective His bundle or RBB capture (nsHBorRBBp). The timings of UHF-ECG electrical activations were quantified as left ventricular lateral wall delay (LVLWd; V8 activation delay) and RV lateral wall delay (RVLWd; V1 activation delay). RESULTS: The LVLWd was shortest for nsHBorRBBp (11 ms [95% confidence interval = 5-17]), followed by the RVIT (19 ms [11-26]) and the RVOT (33 ms [27-40]; p < .01 between all of them), although the QRSd for the latter two were the same (153 ms (148-158) vs. 153 ms (148-158); p = .99). RV apical capture not only had a longer LVLWd (34 ms (26-43) compared to mSp (27 ms (20-34), p < .05), but its RVLWd (17 ms (9-25) was also the longest compared to other RV pacing sites (mean values for nsHBorRBBp, mSp, anterior and lateral wall captures being below 6 ms), p < .001 compared to each of them. CONCLUSION: RVIT pacing produces better ventricular synchrony compared to other RV pacing locations with myocardial capture. However, UHF-ECG ventricular dysynchrony seen during RVIT pacing is increased compared to concomitant capture of basal septal myocytes and His bundle or proximal right bundle branch.

Novel ultra-high-frequency electrocardiogram tool for the description of the ventricular depolarization pattern before and during cardiac resynchronization.

INTRODUCTION: The present study introduces a new ultra-high-frequency 14-lead electrocardiogram technique (UHF-ECG) for mapping ventricular depolarization patterns and calculation of novel dyssynchrony parameters that may improve the selection of patients and application of cardiac resynchronization therapy (CRT). METHODS: Components of the ECG in sixteen frequency bands within the 150 to 1000 Hz range were used to create ventricular depolarization maps. The maximum time difference between the UHF QRS complex centers of mass of leads V1 to V8 was defined as ventricular electrical dyssynchrony (e-DYS), and the duration at 50% of peak voltage amplitude in each lead was defined as the duration of local depolarization (Vd). Proof of principle measurements was performed in seven patients with left (left bundle branch block) and four patients with right bundle branch block (right bundle branch block) before and during CRT using biventricular and His-bundle pacing. RESULTS: The acquired activation maps reflect the activation sequence under the tested conditions. e-DYS decreased considerably more than QRS duration, during both biventricular pacing (-50% vs -8%) and His-bundle pacing (-77% vs -13%). While biventricular pacing slightly increased Vd, His-bundle pacing reduced Vd significantly (+11% vs -36%), indicating the contribution of the fast conduction system. Optimization of biventricular pacing by adjusting VV-interval showed a decrease of e-DYS from 102 to 36 ms with only a small Vd increase and QRS duration decrease. CONCLUSIONS: The UHF-ECG technique provides novel information about electrical activation of the ventricles from a standard ECG electrode setup, potentially improving the selection of patients for CRT and application of CRT.

The relationship between ECG predictors of cardiac resynchronization therapy benefit.

INTRODUCTION: Cardiac resynchronization therapy (CRT) is an effective treatment that reduces mortality and improves cardiac function in patients with left bundle branch block (LBBB). However, about 30% of patients passing the current criteria do not benefit or benefit only a little from CRT. Three predictors of benefit based on different ECG properties were compared: 1) "strict" left bundle branch block classification (SLBBB); 2) QRS area; 3) ventricular electrical delay (VED) which defines the septal-lateral conduction delay. These predictors have never been analyzed concurrently. We analyzed the relationship between them on a subset of 602 records from the MADIT-CRT trial. METHODS & RESULTS: SLBBB classification was performed by two experts; QRS area and VED were computed fully automatically. High-frequency QRS (HFQRS) maps were used to inspect conduction abnormalities. The correlation between SLBBB and other predictors was R = 0.613, 0.523 and 0.390 for VED, QRS area in Z lead, and QRS duration, respectively. Scatter plots were used to pick up disagreement between the predictors. The majority of SLBBB subjects- 295 of 330 (89%)-are supposed to respond positively to CRT according to the VED and QRS area, though 93 of 272 (34%) non-SLBBB should also benefit from CRT according to the VED and QRS area. CONCLUSION: SLBBB classification is limited by the proper setting of cut-off values. In addition, it is too "strict" and excludes patients that may benefit from CRT therapy. QRS area and VED are clearly defined parameters. They may be used to optimize biventricular stimulation. Detailed analysis of conduction irregularities with CRT optimization should be based on HFQRS maps.

Comparison of noninvasive pulse transit time determined from Doppler aortic flow and multichannel bioimpedance plethysmography.

The main goal of this study was to make a comparison of aortic flow timing obtained by PW Doppler in four aortic sections with timing of - dZ/dt max obtained by bioimpedance measurement in nine locations on the thorax and neck. This knowledge is essential for determination of which bioimpedance channel could be used as a proximal for evaluation of pulse wave velocity (PWV) from the beginning of the ascending aorta or another aortic section. Time intervals between the Doppler flow and bioimpedance information (- dZ/dt max) were compared. It was found that the channel located on the left part of the neck is the most suitable as a proximal bioimpedance channel which corresponds to the aortic arch. This match is obtained with regard to the value of the time difference as well as inter-subject stability. This channel can be used as a proximal for evaluation of pulse wave velocity from the aortic arch to the desired distal target place in the body when distance between measured parts is known. The data from 35 volunteers with adequate signal quality were analyzed. Graphical abstract ᅟ.

Ventricular Electrical Delay Measured From Body Surface ECGs Is Associated With Cardiac Resynchronization Therapy Response in Left Bundle Branch Block Patients From the MADIT-CRT Trial (Multicenter Automatic Defibrillator Implantation-Cardiac Resynchronization Therapy).

BACKGROUND: Although cardiac resynchronization therapy (CRT) is beneficial in heart failure patients with left bundle branch block, 30% of these patients do not respond to the therapy. Identifying these patients before implantation of the device is one of the current challenges in clinical cardiology. METHODS: We verified the diagnostic contribution and an optimized computerized approach to measuring ventricular electrical activation delay (VED) from body surface 12-lead ECGs. We applied the method to ECGs acquired before implantation (baseline) in the MADIT-CRT trial (Multicenter Automatic Defibrillator Implantation-Cardiac Resynchronization Therapy). VED values were dichotomized using its quartiles, and we tested the association of VED values with the MADIT-CRT primary end point of heart failure or death. Multivariate Cox proportional models were used to estimate the risk of study end points. In addition, the association between VED values and hemodynamic changes after CRT-D implantation was examined using 1-year follow-up echocardiograms. RESULTS: Our results showed that left bundle branch block patients with baseline VED <31.2 ms had a 35% risk of MADIT-CRT end points, whereas patients with VED ≥31.2 ms had a 14% risk (P<0.001). The hazard ratio for predicting primary end points in patients with low VED was 2.34 (95% confidence interval, 1.53-3.57; P<0.001). Higher VED values were also associated with beneficial hemodynamic changes. These strong VED associations were not found in the right bundle branch block and intraventricular conduction delay cohorts of the MADIT-CRT trial. CONCLUSIONS: Left bundle branch block patients with a high baseline VED value benefited most from CRT, whereas left bundle branch block patients with low VED did not show CRT benefits.

Ventricular dyssynchrony assessment using ultra-high frequency ECG technique.

PURPOSE: The aim of this proof-of-concept study is to introduce new high-dynamic ECG technique with potential to detect temporal-spatial distribution of ventricular electrical depolarization and to assess the level of ventricular dyssynchrony. METHODS: 5-kHz 12-lead ECG data was collected. The amplitude envelopes of the QRS were computed in an ultra-high frequency band of 500-1000 Hz and were averaged (UHFQRS). UHFQRS V lead maps were compiled, and numerical descriptor identifying ventricular dyssynchrony (UHFDYS) was detected. RESULTS: An electrical UHFQRS maps describe the ventricular dyssynchrony distribution in resolution of milliseconds and correlate with strain rate results obtained by speckle tracking echocardiography. The effect of biventricular stimulation is demonstrated by the UHFQRS morphology and by the UHFDYS descriptor in selected examples. CONCLUSIONS: UHFQRS offers a new and simple technique for assessing electrical activation patterns in ventricular dyssynchrony with a temporal-spatial resolution that cannot be obtained by processing standard surface ECG. The main clinical potential of UHFQRS lies in the identification of differences in electrical activation among CRT candidates and detection of improvements in electrical synchrony in patients with biventricular pacing.

Respiratory induced heart rate variability during slow mechanical ventilation : Marker to exclude brain death patients.

BACKGROUND: Respiratory induced heart rate variability (rHRV) was analysed in mechanically ventilated patients during two levels of sedation and brain death. Our aim was to determine whether rHRV can distinguish between different levels of sedation and especially between brain death and sedated patients. METHODS: In this study 30 critically ill and 23 brain death patients were included and four respiratory rates of 15, 12, 8 and 6 breaths per minute, each lasting 5 min were used. Two sedation levels, basal and deep, were performed in the critically ill patients. Heart rate and blood pressure changes induced by ventilation were subsequently detected and analysed. RESULTS: Significant differences were found in rHRV and rHRV adjusted for tidal volume (rHRV/VT) between critically ill and brain death patients during slow breathing at 6 or 8 breaths per minute. The rHRV at 6 breaths per minute was below 15 ms in all brain death subjects except one. The rHRV/VT was lower than 25 ms/l at both 6 and 8 breaths per minute in all brain death patients and simultaneously at 75% of non-brain death patients was higher (specificity 1, sensitivity 0.24). Differences in rHRV and rHRV/VTs between basal and deep sedation were not significant. CONCLUSIONS: The main clinical benefit of the study is the finding that rHRV and rHRV/VT during 6 and 8 breaths per minute can differentiate between critically ill and brain death patients. An rHRV/VT exceeding 25 ms/l reliably excludes brain death.

A multichannel bioimpedance monitor for full-body blood flow monitoring.

The design, properties, and possible diagnostic contribution of a multichannel bioimpedance monitor (MBM) with three independent current sources are presented in this paper. The simultaneous measurement of bioimpedance at 18 locations (the main part of the body, legs, arms, and neck) provides completely new information, on the basis of which more precise haemodynamic parameters can be obtained. The application of the MBM during various haemodynamic stages, such as resting in a supine position, tilting, exercise stress, and various respiration manoeuvres, is demonstrated. Statistical analysis on a group of 34 healthy volunteers is presented for demonstration of blood flow monitoring by using the proposed method.

The impact of sedation on pulse pressure variation.

OBJECTIVE: Pulse pressure variations (PPV) are mainly influenced by ventilation. The impact of sedation on PPV is not known. The aim of the study was to test the influence of sedation on pulse pressure variation in mechanically ventilated critically ill patients and to compare PPV in critically ill and brain dead patients. Beside the absolute value of PPV, the adjusted values of pulse pressure were used to eliminate influence of ventilation. DESIGN AND INTERVENTION: Mechanically ventilated patients received four different breath frequencies. At each frequency airway pressure was adjusted to keep the end-tidal CO2 stable. In critically ill patients the frequencies were applied at basal (bispectral index - BIS median 38) and deeper sedation (BIS 29). MAIN OUTCOME MEASURES: Simultaneous haemodynamic and respiratory data including oesophageal pressure were recorded, adjusted PPV were calculated as PPV/VT, PPV/dPair, PPV/dPes where VT is tidal volume, dPair and dPes are airway and oesophageal driving pressures. SETTING: University Hospital, ICU. PARTICIPANTS: 30 critically ill and 23 patients with a diagnosis of brain death. RESULTS: The pulse pressure variation did not change significantly during deep sedation compared to basal sedation (median 10.3 vs 10.9%) whereas PPV/dPair increased from 0.7 to 0.8%/cmH2O and PPV/dPes from 1.9%/cmH2O to 2.4%/cmH2O (p=0.04). Patients with a diagnosis of brain death had higher PPV and adjusted PPV than critically ill patients. CONCLUSION: Deeper sedation increases values of adjusted pulse pressure variation.

Measure of the QT-RR dynamic coupling in patients with the long QT syndrome.

BACKGROUND: The patients with the long QT syndrome type-1 (LQT-1) have an impaired adaptation of the QT interval to heart rate changes. Yet, the description of the dynamic QT-RR coupling in genotyped LQT-1 has never been thoroughly investigated. METHOD: We propose a method to model the dynamic QT-RR coupling by defining a transfer function characterizing the relationship between a QT interval and its previous RR intervals measured from ambulatory Holter recordings. Three parameters are used to characterize the QT-RR coupling: a fast gain (Gain(F) ), a slow gain (Gain(L) ), and a time constant (τ). We investigated the values of these parameters across genders, and in genotyped LQT-1 patients with normal QTc interval duration (QTc < 470 ms). RESULTS: The QT-RR dynamic profiles are significantly different between LQT-1 patients (97) and controls (154): LQT-1 have longer QTc interval (453 ± 35 vs. 384 ± 26 ms, P < 0.0001), and an increased dependency of the QT interval to previous RR changes revealed by a larger Gain(L) (0.22 ± 0.06 vs. 0.18 ± 0.07, P < 0.0001) and Gain(F) (0.05 ± 0.02 vs. 0.03 ± 0.01, P < 0.0001). Importantly, LQT-1 patients have a faster QT dynamic response to previous RR changes described by τ: 122 ± 44 vs. 172 ± 92 beats (P < 0.0001). This faster QT dynamic response of the QT-RR dynamic coupling remained in LQT-1 patients with QTc in a normal range (<430 ms). CONCLUSIONS: The measurement of QT-RR dynamic coupling could be used in patients suspected to carry a concealed form of the LQT-1 syndrome, or to provide insights into the types of arrhythmogenic triggers a patient may be prone to.

Use of a novel transfer function to reduce repolarization interval hysteresis.

BACKGROUND: Cardiac repolarization is assessed by the QT interval on the surface electrocardiogram and varies with the heart rate. Standard QT corrections (QTc) do not account for the lag in QT change following a change in heart rate (QT hysteresis). Our group has developed and tested a transfer function (TRF) model to assess the effectiveness of a dynamic model of QT/RR coupling in eliminating hysteresis. METHODS: We studied three groups: group I, healthy volunteers (n = 23, 41 ± 17 years); group II, hypertensive patients (n = 25, 45 ± 11 years); and group III, patients in a predominately paced rhythm (n = 5, 75 ± 6 years). To vary the heart rate, either exercise bicycling in the supine position (groups I and II) or manipulation of the pacemaker parameters (group III) was done. We then compared a dynamic TRF model with a model based on weighted averages of previous RR intervals. Two parameters were tested: root mean square (RMS) of the error signal between measured and computed QT and the elimination of hysteretic loops. RESULTS: TRF-based measurements eliminated hysteresis in 22/23 (95%) group I patients, 21/25 (84%) group II patients, and 4/5 (80%) group III patients. When hysteresis elimination was not complete, the QT drift that followed RR intervals was different before and after bicycling (100 ms). In these patients, the corresponding QT interval did not significantly change during this period. The TRF model was found superior to the other tested models with respect to both analyzed parameters (RMS and hysteresis elimination). CONCLUSION: The TRF model limited QT hysteresis in healthy, hypertensive, and pacemaker-dependent patients. In addition, an important finding of QT drift in patients with hypertension was identified. With further study in these and other diseased states, the TRF model may improve our ability to measure accurately cardiac repolarization and to determine arrhythmia risk.

Cardiac output measurement in patients with an implanted pacemaker.

In this paper we present a study of measuring the cardiac output at patients with implanted pacemakers. The cardiac output is measured with respect to the atrio-ventricular delay. We have scored the maximum relative cardiac output for each patient. For the measurement we have used a home made digital bioimpedance monitor for impedance cardiography. The result of 26 patients is presented in this study.

Dynamic coupling between heart rate and ventricular repolarisation.

A novel model for the coupling between ventricular repolarisation and heart rate (QT/RR) is presented. It is based upon a transfer function (TRF) formalism that describes the static and dynamic properties of this coupling, i.e., the behaviour after a sudden change in heart rate. Different TRF models were analysed by comparing their capability to describe experimental data collected from 19 healthy volunteers using several RR stimulation protocols: (i) rest with deep breathing at 0.1 Hz; (ii) tilt with controlled breathing at 0.1 and 0.33 Hz; and (iii) cycling. A search for the best TRF led to unambiguous identification of a three-parameter model as the most suitable descriptor of QT/RR coupling. Compared with established static models (linear or power-law), our model predictions are substantially closer to the experimental results, with errors approximately 50% smaller. The shape of the frequency and step responses of the TRF presented is essentially the same for all subjects and protocols. Moreover, each TRF may be uniquely identified by three parameters obtained from the step response, which are believed to be of physiological relevance: (i) gain for slow RR variability; (ii) gain for fast RR variability; and (iii) time during which QT attains 90% of its steady-state value. The TRF successfully describes the behaviour of the RR control following an abrupt change in RR interval, and its parameters may offer a tool for detecting pharmacologically induced changes, particularly those leading to increased arrhythmogenic risk.

Two-channel bioimpedance monitor for impedance cardiography.

In this paper we introduce our conception of a two-channel bioimpedance monitor for the impedance cardiography. We describe the design of a homemade device which is based on a direct digital synthesizer and a digital down converter. This solution enables us to obtain a high-quality bioimpedance signal, which can be used for computing the cardiac output beat per beat. It further enables us to analyze impedance phase changes beat per beat. Our device allows simultaneous measuring of complex impedance in two arbitrary directions on human/animal body without any interference between channels. The setting of the main parameters of the measurement like the amplitude and the frequency of the measurement current depends on the user.