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P Savard

Publications and source records attributed to P Savard.

At least 19 recordsLinked to original sources
PubMed1997

Risk stratification after myocardial infarction using signal-averaged electrocardiographic criteria adjusted for sex, age, and myocardial infarction location.

BACKGROUND: The objectives were to investigate the factors influencing signal-averaged ECGs (SAECGs) recorded in patients after myocardial infarction (MI) and to develop criteria for predicting arrhythmic events (AEs) that account for these factors. METHODS AND RESULTS: SAECGs were recorded 5 to 15 days after MI in 2461 patients without bundle-branch block. The duration (QRSd), terminal potential (VRMS), and terminal duration (LAS) of the filtered QRS were measured. During follow-up (17 +/- 8 months), AEs (arrhythmic death; ventricular tachycardia, VT; ventricular fibrillation, VF) occurred in 80 patients (3.3%). Receiver operating characteristic curves showed that QRSd discriminated patients with all types of AEs, but VRMS and LAS discriminated only VT patients; QRSd minus LAS also discriminated AE patients. Sex, age, and MI location significantly affected the SAECG; survivors without VT or VF were divided into subgroups (2 sex x 4 age x 2 MI), and QRSd values exceeding the 70th percentile in each subgroup predicted AEs with a sensitivity of 65.4%. An unadjusted QRSd criterion showed the same overall sensitivity and specificity but with less uniform values for each subgroup. A Cox model was constructed by use of multiple prognostic indicators, and in rank order, QRSd, previous MI, and Killip class were predictive of AEs. CONCLUSIONS: SAECG adjustments for sex, age, and MI location did not improve sensitivity and specificity but produced a more uniform predictive performance. The proposed criteria are based only on QRSd, because late potentials (VRMS and LAS) did not discriminate patients with sudden death. Duration of high-level activity during QRS (QRSd-LAS) can predict AEs, suggesting that the arrhythmogenic substate involves a large mass of myocardium.

Age Factors↗
PubMed1997

Spatial resolution and role of pacemapping during ablation of accessory pathways.

The objectives of this study were: (1) to evaluate quantitatively the spatial resolution of pacemapping; and (2) to assess the predictive value and role of pacemapping for the catheter ablation of overt APs. Sixty-three unipolar leads were used instead of the standard 12-lead ECG to acquire more information and assess the intrinsic accuracy of pacemapping. Spatial resolution was evaluated in 19 patients for whom data were recorded during bipolar ventricular pacing near the AV ring using the three electrode pairs of a quadripolar ablation catheter with a 5-mm interelectrode spacing. The predictive value was assessed in 27 patients with overt APs who underwent RF ablation; their data were recorded during pacing at the site of successful ablation and at one or two sites where RF energy delivery was ineffective. Data from different beats were compared visually by using body surface potential maps and quantitatively by computing average correlation coefficients (r). Reproducibility was high for paced beats (r = 0.98 +/- 0.02). Displacements of 5 mm of the pacing site could be detected with a sensitivity of 90% and a specificity of 87%. Correlation between pacing at successful ablation sites and preexcited sinus rhythm was low (r = 0.79 +/- 0.11) and the ablation outcome could be predicted with a negative prediction accuracy of 87% and a positive prediction accuracy of 49%. Despite an excellent spatial resolution, pacemapping is of limited value for the identification of successful AP ablation sites, probably because APs can be interrupted at some distance from their ventricular insertion point.

Adult↗
PubMed1996

Myocardial infarction patients in the 1990s--their risk factors, stratification and survival in Canada: the Canadian Assessment of Myocardial Infarction (CAMI) Study.

OBJECTIVES: This study sought to evaluate the in-hospital and postdischarge mortality of patients with an acute myocardial infarction in the 1990s. BACKGROUND: The widespread implementation of therapeutic interventions that modify the natural history of coronary artery disease has led to changes in the profile and survival of patients with an acute myocardial infarction. Although data exist for selected subsets of patients with an acute myocardial infarction, at this time there is little recent prospective information on all patients presenting with an acute myocardial infarction, particularly for survival after hospital discharge. METHODS: All patients < or = 75 years old presenting with an acute myocardial infarction between July 1, 1990 and June 30, 1992 at nine Canadian hospitals were prospectively evaluated and followed up for 1 year. From November 1991, patients of all ages were included. In two centers, recruitment continued until December 31, 1992. A total of 3,178 patients were recruited. RESULTS: The in-hospital mortality rate of patients < or = 75 years old was 8.4%, and that at 1 year after hospital discharge was 5.3%. For patients of all ages recruited after November 1, 1991, the in-hospital mortality rate was 9.9% and 7.1% for 1 year after hospital discharge. For patients < or = 75 years old, age carried an independent in-hospital but no post discharge risk. Female patients had a twofold greater risk of dying in hospital. After hospital discharge, only 1.7% of patients < or = 75 years old and 1.9% of patients of all ages died of a presumed arrhythmic death. Premature ventricular contractions had no independent prognostic value. The relatively low in-hospital (5.3%) and postdischarge (6.1%) reinfarction rate may have contributed to improved survival. A greater reinfarction rate in patients >75 years old (17.4% vs. 9.6%, p < 0.001) may have contributed to their poorer outcome. CONCLUSIONS: One-year mortality after acute myocardial infarction continues to decrease, and changes in the prognostic value of traditional methods of risk stratification have occurred.

Age Factors↗
PubMed1996

A computer heart model incorporating anisotropic propagation. III. Simulation of ectopic beats.

With the advent of catheter ablation procedures, it has become an important goal to predict noninvasively the site of origin of ventricular tachycardia. Site classifications based on the observed body surface potential maps (BSPMs) during ventricular endocardial pacing, as well as on the patterns of the QRS integrals of these maps, have been suggested. The goals of this study were to verify these maps and their QRS integral patterns via simulation using a computer heart model with realistic geometry and to determine whether the model could improve clinical understanding of these ectopic patterns. Simulation was achieved by initiating excitation of the heart model at different endocardial sites and their overlying epicardial counterparts. This excitation propagated in anisotropic fashion in the myocardium. Retrograde excitation of the model's His-Purkinje conduction system was necessary to obtain realistic activation durations. Simulated BSPMs, computed by placing the heart model inside a numerical torso model, and their QRS integrals were close to those observed clinically. Small differences in QRS integral map patterns and in the positions of the QRS integral map extrema were noted for endocardial sites in the left septal and anteroseptal regions. The simulated BSPMs during early QRS for an endocardial site and its epicardial counterpart tended to be mirror images about the zero isopotential contour, exchanging positive and negative map regions. The simulation results attest to the model's ability to reproduce accurately clinically recorded body surface potential distributions obtained following endocardial stimulation. The QRS integral maps from endocardial sites in the left septal and anteroseptal regions were the most labile, owing to considerable cancellation effects. Conventional BSPMs can be useful to help distinguish between endocardial and epicardial ectopic sites.

Anisotropy↗
PubMed1996

Mapping of septal ventricular tachycardia: clinical and experimental correlations.

In patients with chronic myocardial infarction, ventricular tachycardia originating in the interventricular septum may account for a significant number of arrhythmia recurrences after direct ablative operations. We used total computer-assisted cardiac mapping (epicardial sock, left and right ventricular endocardial balloon electrode arrays) to assess whether tachycardia originating in deep or right-sided layers of the interventricular septum is associated with a specific pattern of epicardial activation sequence. We performed these studies during operations in 18 patients and during experiments in 12 dogs in which a septal myocardial infarction was produced by ligating the anterior septal coronary artery. Intraseptal needle electrodes were plunged into the septum of all animal preparations to generate pace-mapping data and to obtain intraseptal recordings (six preparations) during reentrant ventricular tachycardia induced by programmed stimulation. In addition, pace-mapping data of infarcted canine heart preparations were compared with those of nine healthy heart preparations. In the clinical study, 31 ventricular tachycardias with a septal site of origin were analyzed. Twenty tachycardias displayed an epicardial breakthrough in the area of the interventricular groove, whereas 11 had an epicardial breakthrough in the right ventricular free wall. Biventricular endocardial mapping revealed that left septal endocardial activation preceded right septal activation in the former and that right septal activation occurred earlier in the latter. In the experimental study, 14 ventricular tachycardias (cycle length 146 +/- 34 msec) were induced by programmed stimulation in 11 infarcted heart preparations. Eight tachycardias displaying an epicardial breakthrough on the right ventricle were found to originate in the right ventricular septal subendocardial layers, whereas six tachycardias in which the epicardial breakthrough occurred on the anterior interventricular groove originated in the left ventricular septal subendocardial layers. The epicardial breakthrough preceded the left ventricular endocardial breakthrough in six tachycardias (85.7%) originating in intermediate or right ventricular septal layers, but in only one of five tachycardias originating in the left ventricular septal layers. In the pace-mapping study, the epicardial breakthrough shifted progressively from the right ventricular free wall toward the interventricular groove area in response to pacing from the right, intermediate, and left ventricular thirds of the basal septum. This relationship was similar for infarcted and noninfarcted hearts, although transseptal conduction time was prolonged in infarcted hearts (45 +/- 10 msec vs 33 +/- 7 msec, p < 0.01). Therefore the information integrated from the localization of the epicardial breakthrough and the relative timing between the epicardial and the left ventricular endocardial breakthroughs can be used to estimate the depth of the site of origin of septal ventricular tachycardias. This study confirms that a three-dimensional view of the substratum of ventricular tachycardia can be derived from simultaneous epicardial and left ventricular endocardial mapping and can provide a superior basis for therapeutic interventions.

Animals↗
PubMed1995

Differential regulation of Hox C6 in the appendages of adult urodeles and anurans.

Morphogenesis and pattern formation are biological processes that rely on the expression of positional determinants to divide the embryo into compartments. Hox genes are among the selector genes that direct the mechanism of positional information. Here we report the molecular structure and pattern of expression of a new Hox C6 transcript in the adult newt. Molecular analysis showed that the gene transcribes a long primary transcript in both limb and tail regeneration territories and subsequently uses maturation events to produce two RNAs that share the same DNA binding domain and differ in their 5' extremity. Both RNAs were found in the limb and showed a proximal-distal gradient of expression. The tail sample showed accumulation of only one Hox C6 transcript. These results suggest that both transcriptional and post-transcriptional regulations are involved in the appendage-specific expression of Hox C6 in the adult newt. Finally, the adult frog, which has lost its regeneration capacity, also post-transcriptionally regulates the expression of Hox C6 in its appendages.

Amino Acid Sequence↗
PubMed1995

Body surface potential distributions during idiopathic ventricular tachycardia.

BACKGROUND: The purpose of this report is to describe the body surface potential maps (BSPMs) during idiopathic ventricular tachycardia (VT) and to determine what differences exist between different idiopathic VT morphologies. METHODS AND RESULTS: We performed BSPMs during VT on 12 consecutive patients (3 women and 9 men; mean age, 42 +/- 13 years) presenting symptomatic idiopathic VT referred to our institution for electrophysiological study. Basal ECG, chest radiograph, and echocardiogram were normal in all patients. Clinical tachycardia showed left bundle branch block pattern (LBBB) in 9 patients, with sustained VT in 5 and nonsustained VT in 4, and right bundle branch block pattern (RBBB) in 3 with sustained VT. We found a unique pattern of BSPMs in each of the 9 patients during idiopathic LBBB VT configuration, whether sustained or nonsustained VT. This pattern appeared at the onset of the QRS and remained stable during the whole QRS complex. The area of minimal potential located in the upper anterior part of the torso was compatible with an origin of VT in the right ventricular outflow tract, as confirmed in 5 patients by successful radiofrequency ablation. We found an evolving pattern with two phases in each of the three RBBB VTs. The electrical axis during the initial part of the QRS could correspond to an endocardial-epicardial vector. The second phase, with a high voltage and area of minimal potential located in the inferior and anterior part of the torso, was compatible with a left ventricular apical origin that was confirmed by epicardial and endocardial mapping during cryosurgery in 1 patient. For all the VTs, the QRS isoarea maps showed the same pattern as the second phase of the QRS. CONCLUSIONS: Two different BSPM patterns were found. All LBBB VTs had the same stable pattern corresponding to an infundibular origin. All RBBB VTs had an evolving pattern that stabilized in the second part of the QRS complex corresponding to an apical origin.

Adult↗
PubMed1995

Three distinct patterns of ventricular activation in infarcted human hearts. An intraoperative cardiac mapping study during sinus rhythm.

BACKGROUND: Comprehensive data based on single-beat analysis of the ventricular activation sequence during sinus rhythm in infarcted hearts are currently not available. It was the aim of our study (1) to measure and analyze these activation sequences on the epicardial surface of the right and left ventricles and on the left ventricular endocardial surface, and (2) to correlate specific activation patterns with the surface ECG. METHODS AND RESULTS: Isochronal maps were computed from 127 endocardial and epicardial unipolar electrograms recorded simultaneously during sinus rhythm in 45 post-myocardial infarction patients operated on for recurrent ventricular tachycardia (age, 57 +/- 10 years [mean +/- SD], left ventricular ejection fraction, 29 +/- 9%). Patients with bundle-branch block, but not with intraventricular conduction defects, were excluded. Data such as the timing of initial and terminal activation, the number of breakthroughs, the total activation time, and the number of ventricular segments without activation were measured and analyzed according to location of the myocardial infarction. The global epicardial activation was characterized in all patients by a widespread initial breakthrough on the anterior right ventricle (16 +/- 8 milliseconds after QRS onset), which was followed by one or two other breakthroughs in 65% of patients. Subsequently, three characteristic epicardial patterns of the activation spread were found: (1) radial, from the right to the left ventricle, found in all patients with inferoposterior myocardial infarction; (2) counterclockwise rotation, in which posteroseptal crossing preceded the anteroseptal crossing, found in 38% of patients with anterior myocardial infarction; and (3) pincerlike encirclement, in which both septal crossings and/or breakthroughs occurred nearly simultaneously and merged at the left ventricular free wall (typical for apical involvement in anterior and combined myocardial infarction). The simultaneous presence of multiple major activation wave fronts typically found in patients with the pincerlike activation pattern was reflected on the surface ECG by multiphasic, notched QRS complexes. Activation delay was observed in 89% of patients, and terminal activation was topographically related to myocardial infarction in 94% of patients. Delayed activation exceeding the surface QRS was observed in 11% and 31% of cases on the endocardium and epicardium, respectively. CONCLUSIONS: These results offer a solid basis for a more precise interpretation of a wide range of electrophysiological data and provide a framework for future investigations of surface ECG reflections of endocardial and epicardial activation patterns recorded in patients with chronic myocardial infarction.

Electrocardiography↗
PubMed1995

Clinical applications of BSM.

Body surface mapping (BSM) has now become a feasible clinical technique, providing useful information applicable to the diagnosis of cardiac arrhythmias and their treatment by surgical and endocardial catheter ablation. In WPW patients, validation of preexcitation patterns has been obtained by computer simulation and by direct epicardial mapping at surgery. BSM pacemapping has subsequently been developed to be used during radiofrequency catheter ablation. This method has been evaluated prospectively and its predictive accuracy assessed. The recognition of two distinct BSM patterns in idiopathic ventricular tachycardia, has led to the application of successful pacemapping for radiofrequency catheter ablation. The use of a realistic tri-dimensional heart-torso computer model has shown that specific sites of endocardial stimulation are related to distinct thoracic map patterns.

Body Surface Potential Mapping↗
PubMed1995

Regional distribution of atrial electrical changes induced by stimulation of extracardiac and intracardiac neural elements.

UNLABELLED: Autonomic nerves and intrinsic cardiac neural elements are known to influence the electrophysiologic and dynamic properties of the heart. This study describes the regional distribution in the canine atria of electrophysiologic effects induced by stimulation of the right and left cervical vagosympathetic complexes, the right atrial ganglionated plexus, and the right and left stellate ganglia. Local atrial effects were determined from changes in QRST area of unipolar electrograms recorded from multiple sites with plaque electrodes sewn onto the atria in 16 anesthetized dogs. RESULTS: (1) Although being very consistent in any given preparation, atrial changes varied between animals when similar neural structures were stimulated. (2) Among the common features identified between preparations, consistent effects were induced by neural stimulation in the region of the sinus node, indicating that this atrial region is the most richly innervated. (3) All other regions of the atria could be affected by stimulation of either right-sided or left-sided efferent nerves. (4) Responses to right atrial ganglionated plexus stimulation after atropine administration indicated that the corresponding fat pad contains both sympathetic and parasympathetic neural elements. CONCLUSION: This study demonstrates that there is considerable overlapping of atrial innervation affecting all regions of the atria, as well as the sinus node region.

Animals↗
PubMed1995

On the detection of QRS variations in the ECG.

Detection of subtle beat-to-beat variations in the morphology of the ECG is complicated by the effects of alignment errors and respiration. A method of directly estimating the alignment error (trigger jitter) from an ECG is derived by relating the variance to the squared slope of the averaged QRS complex. Results based on recordings obtained from 12 normal subjects and alignment performed by the cross-correlation method showed that the alignment errors were dependent upon the choice of the alignment channel, with the best distribution of the errors occurring when alignment was based on the vector magnitude of the three orthogonal leads. The estimated average alignment errors ranged from 0.33-0.42 ms, which were near the optimal value of 0.29 ms based on the sampling rate of 1000 samples/s. It was shown that the effects of respiration could be reduced by normalizing the amplitude of the QRS complexes. It was also estimated that a significant proportion of the variation (0.54-0.67) in the normalized ECG's could be attributed to alignment errors and noise.

Adult↗
PubMed1995

Electrode polarity does not alter the initial ventricular activation sequence during pacing with extracardiac electrodes.

Ventricular epicardial mapping was performed in six closed-chest anesthetized dogs to investigate the cardiac electrical response to external pacing. A right thoracotomy was performed, complete AV block was produced by formaldehyde injected into the AV node and a sock electrode array, comprised of 127 unipolar electrodes, was placed over the ventricles. Isopotential and isochronal epicardial maps were generated by computer from the unipolar electrograms. Unipolar stimulation pulses were applied between pairs of different types of cutaneous (metal, carbon) and esophageal (metal) electrodes, and recordings were performed at maximum lung inflation. Isopotential maps recorded during the stimulation artifacts showed that the epicardial electrical field was little affected by the type of electrode but depended mostly on electrode position. A reproducible and relatively uniform apex-to-base potential gradient was regularly produced with anteroposterior and anteroesophageal electrode configurations. This uniform potential gradient induced ventricular activation sequences that showed interindividual differences. Thus, for each dog, the areas of initial activation observed on the isochronal maps during pacing tended to remain the same (i.e., apical, lateral, and anterior) despite changes in the stimulation protocol. Inverting the polarity of the electrodes did not appreciably change the site of origin of activation (81% remained the same) and activation never originated from the area showing the most negative potential during the stimulation artifact. In conclusion, since electrode polarity does not seem to alter the ventricular activation sequence during cardiac pacing with extracardiac electrodes, the standard nomenclature for cutaneous patches, which defines the negative electrode as the "active" electrode, may have to be revised.

Animals↗
PubMed1994

Forward problem of electrocardiography: construction of human torso models and field calculations using finite element method.

Finite element models of the human torso were constructed using anatomical data measured by serial computerised tomography scans in a subject. A first set of three models with a mesh resolution of 5517 nodes and 29810 elements included an homogeneous conductivity, lungs inhomogeneity, and heart, lungs and spinal region inhomogeneities. A second set comprised similar models with a mesh resolution of 12084 nodes and 67045 elements. A cylindrically shaped volume conductor was also constructed to evaluate the convergency and accuracy of the finite element solutions by comparison with the analytical solution. Forward simulations were performed using different excitation sites on the cardiac surface. The inclusion of conductivity inhomogeneities altered the maximum and minimum values of the body surface potentials, but did not substantially modify the pattern of the potential distributions. The greatest effect was due to the inclusion of the lungs. Increasing the mesh resolution from 5517 to 12084 nodes did not change noticeably the shape or amplitude of the simulated body surface potential maps. These models can readily be used for other bioelectromagnetic problems.

Electrocardiography↗
PubMed1994

Markedly different effects on ventricular remodeling result in a decrease in inducibility of ventricular arrhythmias.

OBJECTIVES: The purpose of this study was to determine whether the type and extent of ventricular remodeling after infarction influence inducibility of ventricular arrhythmias after infarction. BACKGROUND: Although serious ventricular arrhythmias after infarction are related to ventricular dysfunction, the relation between inducibility of ventricular arrhythmias and ventricular remodeling remains incompletely understood. METHODS: Rats that survived ligation of the left anterior descending coronary artery (n = 218) were randomized to receive placebo (saline solution) or captopril or propranolol therapy and were followed up for 5 weeks. Hemodynamic and neurohumoral blood measurements were obtained, and therapy was stopped. Two days later, susceptibility to ventricular arrhythmias was assessed by programmed electrical stimulation, and hearts were prepared for pathologic studies. RESULTS: Placebo-treated rats with a large myocardial infarction had ventricular dysfunction, marked neurohumoral activation, ventricular enlargement (endocardial circumference 16 +/- 3 [mean +/- SD] to 20 +/- 4 mm, p < 0.05) and increased cardiac fibrosis (volume density of collagen 2.3 +/- 0.8% to 5.6 +/- 2.4%, p < 0.05). In many rats this resulted in easily inducible ventricular arrhythmias (inducibility quotient 4.9 +/- 2.2). Captopril attenuated the development of ventricular dysfunction, neurohumoral activation, ventricular hypertrophy and dilation (endocardial circumference 18 +/- 3 mm) and cardiac fibrosis (3.1 +/- 0.8%, p < 0.05). These modifications were accompanied by decreased inducibility of ventricular arrhythmias (inducibility quotient 1.1 +/- 2.0, p < 0.05). Propranolol did not prevent ventricular dysfunction, had variable effects on neurohumoral activation and led to increased ventricular dilation (endocardial circumference 25 +/- 4 mm, p < 0.05) and cardiac fibrosis (7.7 +/- 1.2%, p < 0.05). Nevertheless, these morphologic changes led to decreased inducibility of ventricular arrhythmias (inducibility quotient 2.2 +/- 2.5%, p < 0.05). CONCLUSIONS: This study indicates that the inducibility of ventricular arrhythmias can be reduced as a result of markedly different effects on ventricular remodeling, indicating that the relation between ventricular remodeling, arrhythmias and survival is more complex than previously thought.

Animals↗
PubMed1994

QRS alterations in body surface potential distributions during percutaneous transluminal coronary angioplasty in single-vessel disease.

Body surface QRS potentials were recorded with 63 chest leads in 20 patients with proximal single-vessel disease located on either the left anterior descending coronary artery (n = 10), the right coronary artery (n = 6), or the left circumflex coronary artery (n = 4) before, during, and after percutaneous transluminal coronary angioplasty. In each case, three consecutive inflations of relatively short duration (37 +/- 14 seconds) were carried out. Electrical activity was displayed as unipolar electrograms and body surface potential maps. The total QRS complex duration decreased in 14 of the 20 patients. Focal conduction disturbances were observed in six cases; all six had left anterior descending coronary artery occlusion and two were also accompanied by a clear shortening of the right epicardial breakthrough time. In these two cases, an initial activation loss seemed to be characteristic, whereas in the other four cases, a rather diffuse slowing of intraventricular conduction, especially during the terminal portion of the QRS, could be observed. Individual and group mean isointegral difference body surface potential maps (during-minus-before dilation) were considered valuable for the interpretation of localized changes in intraventricular conduction during percutaneous transluminal coronary angioplasty, and their individual variations could, at least partly, be explained by the presence or absence of collateral circulation. Two different hypotheses are suggested to account for the QRS complex shortening observed during short-term myocardial ischemic injury: (1) coronary artery occlusion delayed activation of the portion of the septal region that is normally activated early during the QRS, and/or (2) coronary artery occlusion increased the speed of propagation within the ventricles. Both of these hypotheses are discussed in light of earlier clinical and experimental results.

Angioplasty, Balloon, Coronary↗
PubMed1994

Forward and inverse problems of electrocardiography: modeling and recovery of epicardial potentials in humans.

To assess the accuracy of solutions to the inverse problem of electrocardiography in man, epicardial potentials computed from thoracic potential distributions were compared to potentials measured directly over the surface of the heart during arrhythmia surgery. Three-dimensional finite element models of the thorax with different mesh resolutions and conductivity inhomogeneities were constructed from serial computerized tomography scans of a patient. These torso models were used to compute transfer matrices relating the epicardial potentials to the thoracic potentials. Potential distributions over the torso and the ventricles were measured with 63 leads in the same patient whose anatomical data was used to construct the torso models. To solve the inverse problem, different methods based on Tykhonov regularization or regularization- truncation were applied. The recovered epicardial potential distributions closely resembled the epicardial potential distributions measured early during ventricular preexcitation, but not the more complex distributions measured later during the QRS complex. Several problems encountered as the validation process is applied in man are also discussed.

Electrocardiography↗
PubMed1994

A finite element model for radiofrequency ablation of the myocardium.

A finite element model was developed to simulate the temperature distributions produced by radiofrequency catheter ablation. This model incorporated blood, myocardium and torso tissues. The Laplace equation was solved to determine the steady-state electric field. The heat generation in the tissues was then computed from the power density distribution and the bioheat equation was solved to determine the time-varying temperature distribution, taking into account the convective energy exchange at the blood-myocardium and torso-air interfaces. This model was used to predict the lesion depth and to evaluate the effects of electrode location, changes of the electrical and thermal conductivities, and the electrode radius on the thermally induced damage to the myocardium. Temperature distributions induced by radiofrequency ablation were found to be: i) not very sensitive to the reference electrode location, ii) more sensitive to electrical conductivity changes than to thermal conductivity changes, and iii) larger electrodes allow a current distribution at higher level of power with reducing the chance of impedance rise.

Arrhythmias, Cardiac↗