Design in BME: challenges, issues, and opportunities.
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Biomedical subjects
Publications and source records attributed to Bruce H Kenknight.
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The goal of this study is to assess the predictive capacity of computational models of transvenous defibrillation by comparing the results of patient-specific simulations to clinical defibrillation thresholds (DFT). Nine patient-specific models of the thorax and in situ electrodes were created from segmented CT images taken after implantation of the cardioverter-defibrillator. The defibrillation field distribution was computed using the finite volume method. The DFTs were extracted from the calculated field distribution using the 95% critical mass criterion. The comparison between simulated and clinical DFT energy resulted in a rms difference of 12.4 J and a 0.05 correlation coefficient (cc). The model-predicted DFTs were well matched to the clinical values in four patients (rms = 1.5 J; cc = 0.84). For the remaining five patients the rms difference was 18.4 J with a cc = 0.85. These results suggest that computational models based soley on the critical mass criterion and a single value of the inexcitability threshold are not able to consistently predict DFTs for individual patients. However, inspection of the weak potential gradient field in all nine patients revealed a relationship between the degree of dispersion of the weak field and the clinical DFT, which may help identify high DFT patients.
Conventional transvenous defibrillation is performed with an ICD using a dual current pathway. The defibrillation energy is delivered from the RV electrode to the superior vena cava (SVC) electrode and the metallic case (CAN) of the ICD. Biventricular defibrillation uses an additional electrode placed in the LV free wall with sequential shocks to create an additional current vector. Clinical studies of biventricular defibrillation have reported a 45% reduction in mean defibrillation threshold (DFT) energy. The aim of the study was to use computational methods to examine the biventricular defibrillation fields together with their corresponding DFTs in a variety of patient derived models and to compare them to simulations of conventional defibrillation. A library of thoracic models derived from nine patients was used to solve for electric field distributions. The defibrillation waveform consisted of a LV --> SVC + CAN monophasic shock followed by a biphasic shock delivered via the RV --> SVC + CAN electrodes. When the initial voltage of the two shocks is the same, the simulations show that the biventricular configuration reduces the mean DFT by 46% (3.5 +/- 1.3 vs 5.5 +/- 2.7 J, P = 0.005). When the leading edge of the biphasic shock is equal to the trailing edge of the monophasic shock, there is no statistically significant difference in the mean DFT (4.9 +/- 1.9 vs 5.5 +/- 2.7 J, P > 0.05) with the DFT decreasing in some patients and increasing in others. These results suggest that patient-specific computational models may be able to identify those patients who would most benefit from a biventricular configuration.
This study tested the hypothesis that the DFT could be lowered by delivering a weak auxiliary shock in conjunction with a stronger primary shock with the auxiliary shock electrode near the cardiac region where the primary shock electric field is weakest. This hypothesis was tested by determining the DFTs with the auxiliary shock delivered from different locations within the great cardiac vein (GCV). In 15 dogs, catheters with defibrillation electrodes were placed transvenously in the RV apex, the SVC, and the GCV. An active can electrode and the SVC electrodes were electrically coupled to serve as a return electrode for the RV and GCV electrodes. DFTs were determined for a primary shock through the RV electrode with and without a subsequent auxiliary shock of lower amplitude through the GCV electrode. The leading edge voltage and current at DFT were significantly lowered by addition of the auxiliary shock (17% and 19% decreased, respectively), but energy was not changed. The animals were divided into three groups according to the location of the GCV electrode. The leading edge voltage, current, and total delivered energy at the DFT were significantly lower in animals with the GCV electrode near the apex (22%, 24%, and 13% reduction, respectively) compared with those where the GCV electrode was positioned away from apex (8%, 10% reduction and 18% increase, respectively, P < 0.001). Application of an auxiliary shock to the apical region, near the region where previous studies have indicated that the RV primary shock has its weakest effects, caused the greatest decrease in DFT.
INTRODUCTION: We recently developed an ambulatory canine model of spontaneous ventricular tachycardia (VT) and sudden cardiac death by creating myocardial infarction, complete AV block, and infusion of nerve growth factor to the left stellate ganglion. Whether or not T wave alternans is associated with the spontaneously occurring episodes of VT in our model was unclear. METHODS AND RESULTS: Through intracardiac electrograms obtained from an implantable cardioverter defibrillator, we manually measured T wave amplitudes prior to VT and while the dogs were at rest (baseline, no VT). Of the 79 VT episodes analyzed, 28 (35.4%) exhibited repolarization alternans. In contrast, only 3 (4.7%) of 64 baseline data cases displayed alternans (P < 0.0001). The magnitude of T wave alternans for dogs that died of sudden cardiac death, dogs that did not die suddenly, and for the total 28 episodes that exhibited repolarization alternans were 4.8 +/- 2.8 mm, 4.9 +/- 3.5 mm, and 4.9 +/- 3.3 mm, respectively (P = NS). We also found the sensitivity, specificity, positive predictive value, negative predictive value, and relative risk of repolarization alternans in predicting VT to be 35.4%, 95.3%, 90.3%, 54.5%, and 1.98, respectively. The ventricular rate prior to VT (65 +/- 11 beats/min) was significantly higher than that at rest (49 +/- 12 beats/min; P < 0.0001). CONCLUSION: T wave alternans often occurred immediately before the onset of VT in dogs with myocardial infarction, complete AV block, and nerve growth factor infusion to the left stellate ganglion. Increased sympathetic activity might be responsible for the occurrence of the T wave alternans.