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A computer heart model incorporating anisotropic propagation. II. Simulations of conduction block.

This study describes the simulation of the more common types of conduction blocks with a computer model of the heart incorporating anisotropic propagation. The rationale was to test the model as to its ability to simulate these blocks by physiologically justifiable adjustments of the conduction system alone. The complete blocks were generated by simply blocking conduction totally at selected sites in the proximal conduction system, and the incomplete blocks by slowing down the conduction velocity in the proximal system. Also simulated were the left fascicular blocks and the bilateral blocks. All simulated electrocardiograms, vectorcardiograms, body surface potential maps, and epicardial isochrones for these blocks were similar to clinically observed data, with the exception of the left posterior hemiblock, which was slightly atypical. This could be because such blocks are usually accompanied by other cardiac pathologies not included in our simulations. The model also supports van Dam's observation that during left bundle branch block the passage of activation from right to left occurs via slow myocardial activation with no evidence of a local delay due to a septal barrier. Finally, the model suggests that a left bundle branch block with a normal frontal plane QRS axis may simply represent a case of an incomplete left bundle block, whereas one that exhibits a left axis QRS deviation in the frontal plane represents a more severe complete left bundle branch block.

Anisotropy↗

Electrical current paths in acute pericarditis.

The electrocardiographic changes accompanying pericarditis consist of ST elevation in most of the leads of the 12-lead electrocardiogram. The source of this ST elevation is thought to be local inflammatory changes in the epicardium underlying the inflamed pericardium. The current from this area of ST elevation must return to some unaffected region of the heart and this should be associated with a region of ST depression. This current path from the external epicardial surface has been postulated to flow back into the endocardium through the great vessels and atria. To test this hypothesis, 18 patients with pericarditis were studied by body surface potential mapping and inverse epicardial potential distributions were computed. The resultant maps were compared to those of normal people and patients with acute anterior infraction. Epicardial maps from patients with pericarditis showed a region of current flow into the heart over the great vessels and atria in all 18 patients. This pattern was not seen in normal patients or infarction patients and was consistent with the mechanism resulting in ST elevation in pericarditis being one of current flowing from the epicardium out into the thorax and back into the heart through the great vessels and atria.

Acute Disease↗

Detection of acute ischemia from the EASI-derived 12-lead electrocardiogram and from the 12-lead electrocardiogram acquired in clinical practice.

ST-segment measurements in the standard 12-lead electrocardiogram (ECG) of patients with acute coronary syndromes are crucial for these patients' management. Our objective was to determine whether the 12-lead ECG derived from the 3-lead EASI system can attain a level of diagnostic performance similar to that of the Mason-Likar (ML) 12-lead ECG acquired in clinical practice (CP) by paramedics and emergency department technicians. Using 120-lead body surface potential maps recorded before and during balloon inflation angioplasty from 88 patients (divided into "responders" and "nonresponders"), and electrode placement data from 60 applications of precordial leads in CP, we generated for the "nonischemic" and "ischemic" states of each patient the following lead sets: the ML 12-lead ECG, the EASI-derived 12-lead ECG, and 60 sets of 12-lead CP ECGs. We extracted ST deviations at J + 60 milliseconds, summed them for all 12 leads of each lead set to obtain SigmaST, and, by using the bootstrap method, determined the mean sensitivity and specificity for recognizing the "ischemic" state at various thresholds of SigmaST. Results were displayed as receiver operating characteristics, and the area under these curves (AUC) +/- SE was used as the measure of diagnostic performance. AUC +/- SE for all patients were ML ECG, 0.66 +/- 0.03; EASI ECG, 0.64 +/- 0.03; and CP ECG, 0.67 +/- 0.03. Corresponding results for responders only were 0.81 +/- 0.04 for ML ECG, 0.78 +/- 0.04 for EASI ECG, and 0.81 +/- 0.04 for CP ECG. The differences between the AUCs for the different lead sets were not significant (P > .05). Thus, the EASI-derived 12-lead ECG is as good for detecting acute ischemia as is the 12-lead ECG acquired in CP.

Electrocardiography↗

Persistent changes in the body surface electrocardiogram following successful coronary angioplasty.

One hundred twenty-lead body surface potential maps (BSPMs) were recorded immediately before and 24 hours after coronary angioplasty (PTCA) in 24 patients with symptomatic coronary artery disease (single-vessel in 21 and two-vessel in 3). All PTCAs were uncomplicated and successful. The modified Gensini score decreased in every patient and the mean score fell from 43 +/- 36 to 21 +/- 28 (p less than 0.001). Resting spatial patterns of QRS, ST-segment, and T wave integral distributions over the torso surface were unchanged from before to after PTCA. Quantitative temporal subtraction maps, however, revealed a large precordial area of decreased T wave integral values after PTCA. The sum (sigma) positive T wave integrals fell from 20,501 +/- 10,544 microV.s before PTCA to 17,647 +/- 10,310 microV.s after PTCA (p less than 0.02). In contrast, the sigma positive QRS (10,115 +/- 4,848 microV.s before PTCA vs. 9,656 +/- 4,556 microV.s after PTCA) and the sigma negative ST integrals (-2,489 +/- 1,467 microV.s before PTCA vs. -2,359 +/- 1,505 microV.s after PTCA) were unchanged (NS). Thus, successful PTCA does not produce any persistent change in depolarization or early repolarization electrocardiographic variables but is associated with a decrease in late repolarization potentials that persists for at least 24 hours after the procedure. The pathophysiology of this persistent change is speculative, but myocardial ischemia during the PTCA procedure is a likely possibility. The clinical significance, including predictive value for subsequent stenosis, and the natural history of T wave effect remain incompletely defined. These data suggest that measures to decrease myocardial ischemia during PTCA are warranted.

Adult↗

Variation in the precordial QRS transition zone in normal subjects.

From body surface potential map data for 51 normal young men (with QRS axis between 0 and 90 degrees) both the spatial QRS area vector and the isoarea map of the QRS were obtained. Acting on Grant's assumption that the transition zone defined a plane perpendicular to the spatial QRS vector, we determined the angular shift in altitude and azimuth required to move the spatial vector of each individual to the position of the group mean. We then shifted the precordial map of the transition zone of each individual with the same angular correction. These resulting transition zone boundaries clustered much closer to each other, but did not move into absolute coincidence. We interpreted the nearness-to-fit to be an estimate of the degree to which the precordial QRS configurations conformed to a common simple vector or dipolar pattern.

Adult↗

Effect of electrode positioning on ECG interpretation by computer.

The aim of this study was to assess the variability in automated electrocardiogram (ECG) interpretation due to electrode positioning variations. Such variations were simulated by using a set of 746 body surface potential mappings from apparently healthy individuals and patients with myocardial infarction or left ventricular hypertrophy. Four types of electrode position changes were simulated, and the effect on ECG measurements and diagnostic classifications was determined by a computer program. At most 6% of the cases showed important changes in classification for longitudinal shifts. Transversal shifts causes less than 1.5% of important changes. An expert cardiologist, who analyzed a subset of 80 cases, agreed with the computer in 38 of 40 cases in which it made no change. In the 40 cases with large diagnostic changes, the cardiologist made no change in 18 cases. The effect of electrode position changes on ECG classification by an expert cardiologist was about half of the effect determined by computerized ECG classification. The effects on classification are significant; therefore, correct placement of chest electrodes remains mandatory.

Clinical Competence↗

Electrocardiographic and ventriculographic recovery patterns in Q wave myocardial infarction.

To further define the capacity for recovery after acute phase electrical and mechanical injury in patients with Q wave myocardial infarction who were treated with standard measures, 120 lead body surface potential maps and radionuclide angiograms were recorded at day 5 before discharge and month 6 after infarction in 23 patients with a first infarction (12 anterior and 11 inferior by standard 12 lead electrocardiographic criteria). In addition to assessment of spatial changes in electrocardiographic and wall motion patterns, five quantitative variables were evaluated: minimal Q zone integral, sigma Q wave integral, maximal ST integral, left ventricular ejection fraction and left ventricular wall motion abnormality score. From day 5 to month 6 after infarction, the only change in the inferior infarction group was a gain in sigma Q wave (-91 +/- 40 mu V X s X 10(2) to -68 +/- 24 mu V X s X 10(2); p less than 0.05). In contrast, all variables improved over the same time period in the anterior infarction group: Q zone minimum, -34 +/- 20 to -24 +/- 13 mu V X s (p less than 0.05); sigma Q wave, -160 +/- 122 X 10(2) to -120 +/- 90 mu V X s X 10(2) (p less than 0.05); ST maximum, 44 +/- 19 to 18 +/- 9 mu V X s (p less than 0.01); ejection fraction, 54 +/- 7 to 63 +/- 17% (p less than 0.05); and wall motion score, 6 +/- 3 to 3 +/- 3 (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗

Electrophysiological basis of QT dispersion measurements.

Dispersion of ventricular repolarization is a now widely used term describing nonhomogeneous recovery of excitability or heterogeneity of ventricular repolarization. It is usually expressed as the difference or the range of various repolarization measurements obtained from a heart. Experimentally, an increased dispersion of ventricular repolarization was found to be tightly associated with increased propensity for ventricular arrhythmias, and, therefore, is considered an important arrhythmogenic mechanism. Noninvasively, this arrhythmogenic substrate was approached using multilead body surface potential mapping, but also QT interval dispersion (QTd) and similar electrocardiogram (ECG) variables from the 12-lead surface ECG. Standard QTd from the ECG correlates significantly with dispersion of repolarization measured from the myocardium. A causal relationship is, however, still unclear, and there are 2 main hypotheses to explain the electrophysiological basis of QTd. The local hypothesis explaining QTd with spatial differences in action potential duration mirrored in the various QT intervals competes with the global hypothesis explaining the variation in surface ECG measurements with different projections of a common T-wave vector. Notwithstanding the final explanation for QTd, and particularly for technical reasons, new markers like advanced T-wave loop variables may best reflect the abnormal repolarization substrate on the surface ECG.

Arrhythmias, Cardiac↗

A novel approach for the averaging of magnetocardiographically recorded heart beats.

Performing signal averaging in an efficient and correct way is indispensable since it is a prerequisite for a broad variety of magnetocardiographic (MCG) analysis methods. One of the most common procedures for performing the signal averaging to increase the signal-to-noise ratio (SNR) in magnetocardiography, as well as in electrocardiography (ECG), is done by means of spatial or temporal techniques. In this paper, an improvement of the temporal averaging method is presented. In order to obtain an accurate signal detection, temporal alignment methods and objective classification criteria are developed. The processing technique based on hierarchical clustering is introduced to take into account the non-stationarity of the noise and, to some extent, the biological variability of the signals reaching the optimum SNR. The method implemented is especially designed to run fast and does not require any interaction from the operator. The averaging procedure described in this work is applied to the averaging of MCG data as an example, but with its intrinsic properties it can also be applied to the averaging of ECG recording, averaging of body-surface-potential mapping (BSPM) and averaging of magnetoencephalographic (MEG) or electroencephalographic (EEG) signals.

Algorithms↗

Effect of physical training on ventricular repolarization in type 1 long QT syndrome: a pilot study in asymptomatic carriers of the G589D KCNQ1 mutation.

AIMS: High-intensity physical exercise and competitive sports have been traditionally avoided in long QT syndrome. However, endurance training increases vagal activity and thus may improve cardiac electrical stability in healthy subjects. We hypothesized that controlled submaximal endurance training would not adversely affect ventricular repolarization in asymptomatic carriers of a KCNQ1 gene mutation of type 1 long QT syndrome (LQT1). METHODS AND RESULTS: Previously, sedentary carriers of a missense mutation of KCNQ1 gene (LQT1, n=7) and healthy controls (n=8) exercised on a bicycle ergometer 3-4 times a week, 30 min a day at 60-75% of maximal heart rate (HR) for a maximum of 3 months. Body surface potential mapping (BSPM) was recorded and QT intervals were determined automatically from 14 channels over the left chest area. Maximal work capacity increased by 4+/-1% in LQT1 and by 14+/-2% in controls (both P<0.05), and left ventricular (LV) mass by 8+/-1% and 9+/-1%, respectively (P<0.05). Resting corrected QT interval shortened by 10+/-1% (P<0.05) and QT interval dispersion by 25+/-9% (P<0.05) in LQT1, but not significantly in controls. QT intervals at specified HRs during workload and recovery phases were not changed in either group. CONCLUSION: In this pilot study of asymptomatic carriers of a KNCQ1 gene mutation, submaximal endurance training did not harmfully affect arrhythmia risk markers. Confirmatory studies in a broader spectrum of LQT1 genotypes are needed before any generalization can be made.

Adult↗

A possible mechanism for pacemaker-induced T-wave changes.

The genesis and the significance of pacemaker-induced T-wave changes remain unclear. Changes in body surface potential mapping (BSM) were observed and compared with resting thallium-201 myocardial scintigraphy (T1-SC) findings before, during and after ventricular pacing (VP) in 10 patients with various bradyarrhythmias. All studies were performed with the patients taking no medication. In all patients, isoarea QRST maps showed a characteristic abnormal dipolar pattern with positive values distributed over the upper chest and negative values over the lower chest during VP at a physiological rate for 14 days or more. These abnormalities were preserved almost completely after pacing was terminated; and coincided with deep T-wave inversions in leads II, III, aVF and V4-6. In three patients, BSM performed before VP showed normal QRST isoarea maps with positive values distributed over the left lower chest. All patients in whom resting T1-SC was performed during chronic VP showed transient perfusion defects in the posteroinferior (seven cases) or inferolateral (one case) left ventricular wall. In three patients, T1-SC was performed before VP and showed a normal distribution. Both the pacing-induced perfusion defects and the T-wave abnormalities remained unchanged 2 h after ceasing VP, were attenuated 7 days later and disappeared within a month. These findings suggest that chronic ventricular pacing may produce myocardial ischaemia, and that it persists for a certain period after the cessation of pacing, resulting in post-pacing T-wave inversion.

Adult↗

Thermistor guided radiofrequency ablation of atrial insertion sites in patients with accessory pathways.

Radiofrequency ablation has gained acceptance in the treatment of patients with symptomatic Wolff-Parkinson-White syndrome. The purpose of this study was to characterize the relation between temperature and other electroconductive parameters in patients undergoing atrial insertion accessory pathway ablation utilizing a thermistor equipped catheter. The mean temperature and power at sites of atrial insertion ablation are lower than has been previously associated with creation of radiofrequency lesions in the ventricle. While high cavitary blood flow in the atrium may result in cooling, the thinner atrial tissue may require less energy to achieve adequate heating than ventricular myocardium.

Adolescent↗

Diagnosis of right ventricular involvement in chronic inferior myocardial infarction by means of body surface QRS changes.

ST segment elevation in right precordial leads is thought to be good predictor of right ventricular involvement in patients with acute inferior myocardial infarction. This view, however, is rapidly disappearing. Therefore, using QRS changes in body surface potential maps in the chronic phase, we have attempted to differentiate patients with or without right ventricular involvement. Thirty patients with chronic inferior myocardial infarction (2 or more months after onset) were studied, in whom 87 unipolar ECGs and right ventriculograms were recorded. The patients were then divided into three groups depending on the locations of their abnormal QRS potentials (-2SD area) exceeding the normal range (mean -2SD). In group A, the -2SD area was located predominantly on the right inferior chest, in group B on the left inferior chest, and in group N on both the right and left inferior chests equally. The results showed that group A had a lower right ventricular ejection fraction (RVEF) compared with group B (A, 40 +/- 7%; B, 53 +/- 10%; p less than .001), while there was no difference in left ventricular ejection fraction between the two groups (49 +/- 11% and 49 +/- 11%, respectively). Moreover, right ventricular asynergy occurred in 14 of the 18 patients (78%) of group A but in only one of the 10 patients (10%) of group B. Group N was presumed to be intermediate between groups A and B.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Genetically defined therapy of inherited long-QT syndrome. Correction of abnormal repolarization by potassium.

BACKGROUND: Many members of families with inherited long-QT (LQT) syndrome have mutations in HERG, a gene encoding a cardiac potassium channel that is modulated by extracellular potassium. We hypothesized that an increase in serum potassium would normalize repolarization in these patients. METHODS AND RESULTS: We studied seven subjects with chromosome 7-linked LQT syndrome and five normal control subjects. Repolarization was measured by ECG and body surface potential mapping during sinus rhythm, exercise, and atrial pacing, before and after serum potassium increase. Potassium administration improved repolarization in the LQT syndrome. At baseline, LQT subjects differed from control subjects: resting corrected QT interval (QTc, 627 +/- 90 versus 425 +/- 25 ms, P = .0007), QTc dispersion (133 +/- 62 versus 36 +/- 9 ms, P = .009), QT/RR slope (0.35 +/- 0.08 versus 0.24 +/- 0.07, P = .04), and global root-mean-square QT interval (RMS-QTc; 525 +/- 68 versus 393 +/- 22, P = .002). All LQT subjects had biphasic or notched T waves. After administration of potassium, the LQT group had a 24% reduction in resting QTc interval (from 617 +/- 92 to 469 +/- 23 ms, P = .004) compared with a 4% reduction among control subjects (from 425 +/- 25 to 410 +/- 45 ms, P > .05). The reduction was significantly greater in LQT subjects (P = .018). QT dispersion became normal in LQT subjects and did not change in control subjects. The slope of the relation between QT interval and cycle length (QT/RR slope) decreased toward normal. T-wave morphology improved in six of seven LQT subjects. The LQT group had a greater reduction in RMS-QTc than control subjects (P = .04). CONCLUSIONS: An increase in serum potassium corrects abnormalities of repolarization duration, T-wave morphology, QT/ RR slope, and QT dispersion in patients with chromosome 7-linked LQT.

Adult↗

A study on the transmural conduction velocity of activation front in the left ventricle of RBBB patients.

To investigate the effect of ventricular hypertrophy on the conduction velocity, the transmural conduction velocity was obtained from the findings of echocardiographic, and body surface potential mapping examinations on 20 RBBB patients. The transmural conduction velocity was linearly correlated with the ventricular septal thickness and the greater the thickness, the faster was the conduction velocity. There was no statistically significant difference in the duration of the left ventricular activation obtained from the mapping examinations as well as in the time of onset of intrinsicoid deflection in V5 between the group of left ventricular hypertrophy and that of non-hypertrophy. There was a good linear correlation between the imaginary distance covered by the activation front which proceeded in the direction from endocardium to epicardium during the left ventricular activation and the ventricular septal thickness. These findings were explicable from the faster conduction velocity in the hypertrophied ventricle. The increase in the conduction velocity in the hypertrophy group would be due to cable characteristics of hypertrophied cardiac cells and also due to increase in the number of multiple intercalated discs in the hypertrophied ventricle. It was concluded that the conduction velocity would be an important information to interpret the ECGs in ventricular hypertrophy as well as to estimate the pathological state of the heart.

Bundle-Branch Block↗

Transmural conduction velosity index in healthy schoolchildren.

Transmural conduction velosity index (TCVI) was obtained in 174 healthy children. TCVI was defined as the echocardiographically determined interventricular septal thickness (IVST) divided by the ventricular activation time (VAT) measured by body surface potential mapping. TCVI ranged from 14 to 49 cm/sec and was highly correlated with IVST (r = 0.75, TCVI = 3.25 X IVST + 0.56). It was concluded that the left ventricular hypertrophy with muscular thickness does cause the greater conduction velosity in healthy children.

Adolescent↗

The missing link between cardiovascular rhythm control and myocardial cell modeling.

Cardiac arrhythmia is currently investigated from two different points of view. One considers ECG bio-signal analysis and investigates heart rate variability, baroreflex control, heart rate turbulence, alternans phenomena, etc. The other involves building computer models of the heart based on ion channels, bio-domain models and forward calculations to finally reach ECG and body surface potential maps. Both approaches aim to support the cardiologist in better understanding of arrhythmia, improving diagnosis and reliable risk stratification, and optimizing therapy. This article summarizes recent results and aims to trigger new research to bridge the different views.

Biological Clocks↗

Age and sex differences in the P-wave signal-averaged electrocardiogram in a Japanese study population.

Normal P wave signal-averaged electrocardiogram (SAE) values were determined in 120 healthy Japanese adults (56 men, 64 women), aged 44.5+/-10.2 years (mean+/-SD). The P wave trigger method was used with a Fukuda FDX6500 recorder. We used bipolar Frank leads (X,Y,Z), and recordings were made with forward and backward digital Butterworth filters [40 Hz (18 dB / oct) - 300 Hz (12 dB / oct)]. The recordings were taken for the following five parameters: forward and backward filtered P wave duration [fPd (F); tPd (B)]; bidirectionally corrected fPd [tPd (C)]; and 20 ms of the terminal portions of voltage at forward and backward filtering (RMS20). Overall, fPd (F) was 117.8-136.4 ms, fPd (B) 116.4-134.4 ms, fPd (C) 97.4-115.2 ms, RMS20 (F) 1.6-3.6 microV, and RMS20 (B) was 2.2-5.4 microV. Between the sexes, there were significant differences in fPd (F) (p<0.001) and fPd (B) (p<0.01) and in RMS20 (F) (p<0.05) and RMS20 (B) (p<0.05). Weak positive correlations were observed between fPd (F) and body surface area, fPd (F) and age, fPd (B) and body surface area, fPd (B) and age, fPd (C) and body surface area, and fPd (C) and age. There was no evident correlation, however, between either forward or backward RMS20 and body surface area or between forward or backward RMS20 and age. Differences in the normal P wave values between the sexes and age groups were evaluated in this study.

Adult↗