A.L. de Jongh

Extracting isovolumes from three-dimensional torso geometry using PROLOG

Three-dimensional (3D) finite element torso models are widely used to simulate defibrillation field quantities, such as potential, gradient and current density. These quantities are computed at spatial nodes that comprise the torso model. These spatial nodes typically number between 10/sup 5/ and 10/sup 6/, which makes the comprehension of torso defibrillation simulation output difficult. Therefore, the objective of this study is to rapidly prototype software to extract a subset of the geometric model of the torso for visualization in which the nodal information associated with the geometry of the model meets a specified threshold value (e.g., minimum gradient). The data extraction software is implemented in PROLOG, which is used to correlate the coordinate, structural and nodal data of the torso model. A PROLOG-based environment has been developed and is used to rapidly design and test new methods for sorting, collecting and optimizing data extractions from defibrillation simulations in a human torso model for subsequent visualization.

Effects of cardiac anisotropy on modeling transvenous defibrillation in the human thorax

The objective of this study is to determine the effects of cardiac tissue anisotropy on transvenous defibrillation fields in a human torso model. The study is implemented with a physiologically realistic 3-D finite element model of the human thorax. The model computes potential and potential gradient distributions within the heart from a knowledge of defibrillation shock strength, defibrillation electrode location, and the relative conductivities of the interior thorax. Coil electrodes were placed in the right ventricular cavity and the superior vena cava. Results are compared between a model with an isotropic myocardium and a model with an anisotropic myocardium. Comparison of the potential and potential gradient distributions within the myocardium between the isotropic and anisotropic models yielded root mean square errors of 4.9% and 19.%, respectively, and correlation coefficients of 0.999 and 0.981, respectively. These results indicate that cardiac anisotropy and fiber orientation do not significantly affect transvenous defibrillation fields.

Determining the level of complexity required to model transvenous defibrillation fields

The objective of this study is to determine the level of complexity needed to model transvenous defibrillation fields in the heart. A physiologically realistic 3D finite element model is constructed from 90 transverse magnetic resonance images of the human thorax. Two models are developed: 1) a realistic torso and 2) a spherical torso surrounding the great vessels and heart. The defibrillation threshold (DFT) is calculated based on a potential gradient of 5 V/cm throughout 95% of the ventricular myocardium during a shock. Comparison of the realistic and spherical models shows that the DFT is altered by 21%, 18%, and 8% for RV-SVC, RV-CAN, and RV-SVC/CAN electrode configurations, respectively. These results indicate that for configurations producing more uniform defibrillation fields between the electrodes (RV-SVC/CAN), the complexity of the model can be greatly reduced by excluding the tissue structures external to the heart. The significance of this study is that realistic representation of the human thorax is needed in order to accurately predict DFTs.

Reducing mesh size for finite element modeling of transvenous defibrillation

The objective of this study is to determine if transvenous defibrillation simulations can be simplified by reducing the size of the volume conductor model. The study is implemented with a physiologically realistic 3-D finite element model of the human thorax. The model computes potential distributions within the heart from a knowledge of defibrillation shock strength, defibrillation electrode location, and the relative conductivities of the interior thorax. Results are compared between a model of the entire torso and a model consisting only of the heart surrounded by a spherical shell. Comparison of the potential distributions within the heart between the two models yielded a root mean square error of 13.696 and a correlation coefficient of 0.995. For the finite element solution, storage requirements were decreased by a factor of 4 and computational time was reduced by a factor of 15. These results indicate that for transvenous defibrillation simulations the size of the model can be greatly reduced by excluding the interior structures of the torso external to the heart. In addition, the results suggests that interior structures such as the lungs may not affect the potential distributions within the heart during transvenous defibrillation.

Left ventricular volume changes after defibrillation

A previous study has shown that the cross-sectional area of the left ventricular cavity (LV) increases immediately after defibrillation, suggesting that the defibrillation shock may cause relaxation. Since a single area slice may not reflect the entire myocardium, we wanted to test the relaxation hypothesis by evaluating volume. Ten to twenty defibrillation shocks were delivered in each of six dogs. A catheter was placed in the LV to measure intraventricular volume (IVV). Ultrasound images of the LV were recorded simultaneously with IVV. LV cavity area increased 13% (p<0.001) and IVV increased 4% (p<0.001) post-shock. Our results confirm that the heart is relaxing after defibrillation.

Ventricular wall thickness and volume during hemodynamic collapse produced by AC leakage current

Medical equipment can unintentionally allow the flow of power line current through the patient causing complete hemodynamic collapse without fibrillation. This study tests the hypothesis that static wall thickening accompanies AC induced collapse via an isovolumic state. In 3 dogs, we delivered AC current stimulation ranging from 10-160 Hz and 10-1000 /spl mu/A to the right ventricle. A steerable, quadripolar catheter was placed in the apex of the left ventricle and deflected towards the basal region to measure left ventricular volume. Two dimensional, short-axis ultrasound images of the LV endocardial walls were recorded to measure wall thickness. Our results indicate that wall thickness during collapse is significantly greater than during systole (/spl Delta/ thickness =11.7/spl plusmn/12 mm, p<0.001) and diastole (/spl Delta/ thickness=23.6/spl plusmn/13 mm, p<0.001). In addition, the volume of the left ventricle is significantly smaller during collapse than the average volume during normal sinus rhythm (/spl Delta/ impedance=0.152/spl plusmn/0.006 no units, p<0.001).

Ventricular fibrillation in rats with cardiac fibrosis

Previous studies have shown that administration of angiotensin II (Ang II) causes atrial and ventricular fibrosis in rats, as is found in patients with chronic heart failure. We hypothesize that fibrosis creates a substrate that promotes the induction of ventricular fibrillation (VF). Fourteen, eight-week old, Sprague-Dawley rats were studied. Eleven received a four-week treatment of Ang II (9 /spl mu/g/hr) from an implanted mini-pump. After treatment, the chest was opened, and 50 Hz stimulation at a strength of three times the pacing threshold was applied across the atria and ventricles for 2.5, 5, and 10 s. VF was more inducible in treated rats (6 of 11) than untreated rats (0 of 3, P < 0.05). Three of 12 VF episodes were sustained (> 10 s) while the remaining VF episodes were nonsustained (> 30 ms and < 10 s) after stimulation ended. Our results suggest that cardiac fibrosis induced by Ang II treatment creates a substrate for sustained VF.

Mechanical response of the left ventricle during AC induced hemodynamic collapse

Medical equipment can unintentionally allow the flow of small amounts of AC current through the patient causing hemodynamic collapse without fibrillation. This study examines the mechanical response of the left ventricle during AC induced hemodynamic collapse. Six dogs received 5 seconds of AC current stimulation ranging from 4-160 Hz and 10-1000 /spl mu/A to the right ventricle. A quadripolar catheter was placed in the apex of the left ventricle to measure left ventricular volume. Short-axis ultrasound images were recorded to measure left ventricular cross sectional area and wall thickness. Our results showed that the mean volume of the left ventricle during collapse was significantly smaller (p < 0.05) than the mean volume preceding collapse. Cross sectional area also decreased significantly and wall thickness increased. This suggests that the heart assumes a contracted, systole-like state during collapse.

Left ventricular geometry immediately following defibrillation-strength shocks

A previous 2D ultrasound study (R.A. Malkin et al., 2001) suggested that there is relaxation of the myocardium after defibrillation. However, that 2D study could not measure activity occurring within the first 33 ms following the shock. Thus, the objective of our study is to determine the left ventricular (LV) geometry during this period. Biphasic defibrillation shocks were delivered to seven dogs. 1D short-axis ultrasound images of the LV cavity were acquired, the boundary of the anterior and posterior endocardial walls was extracted and the distance between them computed from 32 ms before to 32 ms after the shock. The normalized mean pre- and post-shock slopes were 0.2 /spl plusmn/ 2.2 and 3.3 /spl plusmn/ 7.9 %/10 ms, respectively. The post-shock LV diameter slope is positive in the first 32 ms following both successful and unsuccessful defibrillation shocks (p<0.05). Therefore, our results confirm that the bulk of the myocardium is relaxing immediately after a defibrillation shock.

Optimizing dual threshold shocks with right- and left-ventricular electrodes: simulating defibrillation with a human thorax model

This research focuses on developing new implantable cardioverter defibrillator (ICD) dual lead configurations that reduce the defibrillation threshold (DFT) energy by delivering a second threshold shock in the area where the conventional shocks electric field is weakest. The objective of this study is to optimize electrode placements for lead systems including left-ventricular (LV) electrodes. A physiologically realistic 3D finite element model of the human thorax is employed to compute DFTs. The lead configurations investigated consist of a conventional lead system (TRIAD/sup TM/, Guidant Corporation) and additional LV shocking electrodes placed in the apical and basal portion of the posteriolateral coronary vein or directly within the TRIAD systems weak field region. The LV electrodes measure 50 mm in length and 1 mm in diameter. The computed DFT energy for the TRIAD is 6.2 J, falling within one standard deviation of the mean DFT reported in clinical studies using the TRIAD leads. LV leads located in the apical and basal portion of the posteriolateral coronary vein result in a DFT of 3.1 J, a 50% reduction from the TRIAD alone. LV leads placed in the anterior, middle, and posterior TRLAD weak field result in a DFT of 2.9 J, 2.7 J., and 3.5 J, respectively, corresponding to a 44-56% reduction in DFT from the TRIAD. The results indicate that an additional electrode placed in the proximity of the TRIAD weak field is just as effective in reducing DFTs as one placed directly within the weak field.