Cardiac C-arm CT imaging delivers a tomographic region-of-interest reconstruction of the patient's heart during image guided catheter interventions. Due to the limited size of the flat detector a volume image is reconstructed, which is truncated in the cone-beam (along the patient axis) and the fan-beam (in the transaxial plane) direction. To practically address this local tomography problem correction methods, like projection extension, are available for first pass image reconstruction. For second pass correction methods, like metal artefact reduction, alternative correction schemes are required when the field of view is limited to a region-of-interest of the patient. In classical CT imaging metal artefacts are corrected by metal identification in a first volume reconstruction and generation of a corrected projection data set followed by a second reconstruction. This approach fails when the metal structures are located outside the reconstruction field of view. When a C-arm CT is performed during a cardiac intervention pacing leads and other cables are frequently positioned on the patients skin, which results in propagating streak artefacts in the reconstruction volume. A first pass approach to reduce this type of artefact is introduced and evaluated here. It makes use of the fact that the projected position of objects outside the reconstruction volume changes with the projection perspective. It is shown that projection based identification, tracking and removal of high contrast structures like cables, only detected in a subset of the projections, delivers a more consistent reconstruction volume with reduced artefact level. The method is quantitatively evaluated based on 50 simulations using cardiac CT data sets with variable cable positioning. These data sets are forward projected using a C-arm CT system geometry and generate artefacts comparable to those observed in clinical cardiac C-arm CT acquisitions. A C-arm CT simulation of every cardiac CT data set without cables served as a ground truth. The 3D root mean square deviation between the simulated data set with and without cables could be reduced for 96% of the simulated cases by an average of 37% (min -9%, max 73%) when using the first pass correction method. In addition, image quality improvement is demonstrated for clinical whole heart C-arm CT data sets when the cable removal algorithm was applied.
Objectives: This study hypothesized that P-wave morphology and timing under left atrial appendage (LAA) pacing change characteristically immediately upon anterior mitral line (AML) block. Background: Perimitral flutter commonly occurs following ablation of atrial fibrillation and can be cured by an AML. However, confirmation of bidirectional block can be challenging, especially in severely fibrotic atria. Methods: The study analyzed 129 consecutive patients (66 ± 8 years, 64% men) who developed perimitral flutter after atrial fibrillation ablation. We designed electrocardiography criteria in a retrospective cohort (n = 76) and analyzed them in a validation cohort (n = 53). Results: Bidirectional AML block was achieved in 110 (85%) patients. For ablation performed during LAA pacing without flutter (n = 52), we found a characteristic immediate V1 jump (increase in LAA stimulus to P-wave peak interval in lead V1) as a real-time marker of AML block (V1 jump ≥30 ms: sensitivity 95%, specificity 100%, positive predictive value 100%, negative predictive value 88%). As V1 jump is not applicable when block coincides with termination of flutter, absolute V1 delay was used as a criterion applicable in all cases (n = 129) with a delay of 203 ms indicating successful block (sensitivity 92%, specificity 84%, positive predictive value 90%, negative predictive value 87%). Furthermore, an initial negative P-wave portion in the inferior leads was observed, which was attenuated in case of additional cavotricuspid isthmus ablation. Computational P-wave simulations provide mechanistic confirmation of these findings for diverse ablation scenarios (pulmonary vein isolation ± AML ± roof line ± cavotricuspid isthmus ablation). Conclusions: V1 jump and V1 delay are novel real-time electrocardiography criteria allowing fast and straightforward assessment of AML block during ablation for perimitral flutter.
ECG imaging is an emerging technology for the reconstruction of cardiac electric activity from non-invasively measured body surface potential maps. In this case report, we present the first evaluation of transmurally imaged activation times against endocardially reconstructed isochrones for a case of sustained monomorphic ventricular tachycardia (VT). Computer models of the thorax and whole heart were produced from MR images. A recently published approach was applied to facilitate electrode localization in the catheter laboratory, which allows for the acquisition of body surface potential maps while performing non-contact mapping for the reconstruction of local activation times. ECG imaging was then realized using Tikhonov regularization with spatio-temporal smoothing as proposed by Huiskamp and Greensite and further with the spline-based approach by Erem et al. Activation times were computed from transmurally reconstructed transmembrane voltages. The results showed good qualitative agreement between the non-invasively and invasively reconstructed activation times. Also, low amplitudes in the imaged transmembrane voltages were found to correlate with volumes of scar and grey zone in delayed gadolinium enhancement cardiac MR. The study underlines the ability of ECG imaging to produce activation times of ventricular electric activity-and to represent effects of scar tissue in the imaged transmembrane voltages.
Background: Perimitral flutter commonly occurs following ablation of atrial fibrillation (AF) and can be cured by an anterior mitral line (AML). However, confirmation of bidirectional block can be challenging. Objective: We hypothesized that P-wave morphology and timing under left atrial appendage (LAA) pacing changes upon AML- block. Methods: We analyzed 129 consecutive patients (66±8 y, 64%male) who developed perimitral flutter after AF ablation. We designed ECG-criteria in a retrospective cohort (n=76) and analyzed them in a validation cohort (n=53). Results: Bidirectional AML-block was achieved in 110 patients (85%). For ablation performed during LAA-pacing without flutter (n=52), we found an immediate V1-jump (increase in LAA- stimulus to P-wave peak in lead V1) as a real-time marker of AML-block (V1-jump ≥30ms: sensitivity 95%, specificity 100%, PPV 100%, NPV 88%). Since V1-jump is not applicable when block coincides with termination of flutter, absolute V1-delay was used as a criterion applicable in all cases (n=129) with a delay of 203ms indicating block (sensitivity 92%, specificity 84%, PPV 90%, NPV 87%). Furthermore, an initial negative P-wave portion in the inferior leads was observed, which was attenuated in case of additional cavotricuspid isthmus (CTI) ablation. Computational P-wave simulations provide mechanistic confirmation of these findings for diverse ablation scenarios (pulmonary vein isolation±AML±roof-line±CTI ablation). Conclusion: V1-jump and V1-delay are novel real-time ECG- criteria allowing fast and straightforward assessment of AML- block during ablation for perimitral flutter.
Body surface potential mapping (BSPM) can be used to non- invasively measure the electrical activity of the heart using a dense set of thorax electrodes and a CT/MR scan of the thorax to solve the inverse problem of electrophysiology (ECGi). This technique now shows potential clinical value for the assessment and treatment of patients with arrhythmias. Co-localisation of the electrode positions and the CT/MR thorax scan is essential. This manuscript describes a method to perform the co-localisation using multiple biplane X-ray images. The electrodes are automatically detected and paired in the X-ray images. Then the 3D positions of the electrodes are computed and mapped onto the thorax surface derived from CT/MR. The proposed method is based on a multi-scale blob detection algorithm and the generalized Hough transform, which can automatically discriminate the leads used for BSPM from other ECG leads. The pairing method is based on epi-polar constraint matching and line pattern detection which assumes that BSPM electrodes are arranged in strips. The proposed methods are tested on a thorax phantom and two clinical cases. Results show an accuracy of 0.33 ± 0.20mm for detecting electrodes in the X-ray images and a success rate of 95.4%. The automatic pairing method achieves a 91.2% success rate.
Student Theses (4)
H. Chen. Simulated Electromechanical Heterogeneity in Human Left Ventricle. Institute of Biomedical Engineering, Universität Karlsruhe (TH). Diplomarbeit. 2005
After adjusting the parameters of the conductance or properties of late sodium current, transient outward current, slow component of delayed rectifier potassium current, sodium calcium exchange current, as well as the intracellular calcium release and uptake current, the heterogeneous action potential, calcium transient and tension development were re- constructed in Endo, M and Epi cell in human left ventricle. The morphology, amplitude and time courses showed good agreement with the experimental recordings. This modified model suggested that the different APs of the three types of myocytes are based on the different ion current density or ion channel properties. The simulation of the calcium tran- sient predicted that the heterogeneous calcium activities are based both on the different shape of APs and calcium related gene expressions. The mechanical function of Epi, M and Endo cells were described by a tension development model and the time to peak in the tension development curves could explain how the inhomogeneous electrophysiology leads to a more homogenized contraction in left ventricle.Limitations in the Modified ModelTheir are some limitations in the modified model, but the principle behavior of the model is in good agreement with the physiological measurement. Some of the limitations are inherited from the Iyer et al. model, and some are from the modification for the hetero- geneity.Limitation in Experimental DataTo formulate the ion currents in cardiac myocytes, the concrete experimental data must be known, like the current density at different clamped voltages, its frequency dependence and other properties. In cell models for human left ventricular myocytes, though, all the research tried to model the electrophysiology based on more recently experimental data in human ventricle, there were still some currents based on animal experiments, because no human data was available at the moment. For example, in the Iyer et al. model, the current-voltage relations of current INaK was adopted from a formulation given for guinea pig. For the same reason, in this simulation for electromechanical heterogeneity, some currents were adapted according to the canine ventricular experiments, like the adaptation of the INaCa scaling factor in midmyocardial cell, the current density through RyR channels in both Epi and M cells and so on. More data on human left ventricle are needed to accomplish the cell model.Many of the ion currents in the Iyer et al. model were based on voltage clamp experiments in which cloned human cardiac ion channels are heterologously expressed. Therefore, till now there is still no obvious evidence to prove that the cloned ion channels had exactly the same properties as the nature ones . Some modification in this work was also based on the gene expression experiment of the ion channels. More proofs of the relation between existing channel proteins and those who really function in cellular membrane were required to support such modification.Weak Influence of IKs on APDFig. 5.10 showed that IKs had a little influence on action potential duration, that the APD changed only about 24 ms when the total current was blocked. Bosch et al. reported a prolongation of about 140 ms in human ventricular cells when total IKs was blocked , which is much longer than the simulation. In the studies of the heterogeneity in ventricle, many experiments have proved that IKs was a very important component of ion currents, which prolonged APD in M cells.The low IKs current density or the influences of other ion currents occurred in repolari- zation might cause smaller effects of IKs on APD. Since the current density of IKr was set to match the experiment of Magyar et al., the conductance of IKs was doubled in the simulation to fit the ratio of IKs : IKr in the same experiment . Even though, the difference of APD in different position of the ventricle was still not as noticeable as in experiments.After the modification of late INa, IK1 and Iup in calcium handling, the APD changed more significantly. So APD in the Iyer et al. model might depend more on such currents and intracellular calcium concentration than IKs.Controversial Influence of INaCa on APDThe heterogeneous distribution of INaCa was firstly proposed by Zygmunt et al. in 2000, who have measured the whole cell current of INaCa in Endo, M and Epi cells in canine left ventricle . INaCa can be triggered both by release of calcium from SR or by rapid removal of external sodium. In their experiments, INaCa was largest in M cell and smallest in Endo cell under both conditions. As conclusion, they have drawn that larger INaCa might contribute to the prolongation of APD in M cell, though weaker IKs and larger late INa may play a more important role in this prolongation. The modification of INaCa in the Priebe-Beuckelmann model confirmed this determination and presented that larger INaCa prolonged the APD . In our simulation, largest INaCa in M cell and smallest INaCa in Endo cell were obtained by adjusting the conductance of INaCa, but the influence of the current to action potential duration was controversial compared to the report of Zygmunt et al.. Fig. 5.13 shows the INaCa current and the action potential of three types of cells after modifying the conductance of INaCa. M cell presents a larger INaCa but shorter APD. In further, more experimental data is needed to determine the influences of INaCa on APD accurately.Insignificant Difference of Time to Peak in Calcium TransientCompared with the experiments of Cordeiro et al., there are still some disagreements in the calcium activities and tension development in the simulation. The time to peak of calcium transients is shortest in Endo cell after the modification, but the experimental data shows that it is shortest in subepicardium. The relation of time to peak, as well as the duration of tension development in Endo and M cells is reversed as in the experiment.Lower Computational EfficiencyMost ion currents in the Iyer et al. model were described with Markov chain models, which sustain more variables and smaller calculation steps, compared with other models. In the Iyer et al. model there are 67 variables, whereas the Priebe-Beuckelmann model and the ten Tusscher et al. model consist of only 15 and 16 variables, respectively. This leads to a higher model complexity, namely lower computational efficiency, especially when tissue simulations were accomplished.PerspectivesAll the simulations till now were based on the single cell model. The simulation of the whole ventricular wall can be applied to reconstruct the cellular physiology in a tissue, the excitation propagation and contraction in the ventricular wall. With the simulation in the intact ventricular wall, a more realistic electrophysiology of the myocytes in different layers can be also obtained, because for the single cell model, the cells are always stimu- lated by a preset depolarizing current, while in nature heart they are mostly stimulated by the neighboring cells.The modified Iyer et al. model has directed the focus on the electromechanical hetero- geneity of human left ventricle and succeeded to reconstructed the APs, calcium transients and tension development of Endo, M and Epi cells. It can help to reconstruct the virtual heart with precise properties in different cell types of left ventricle. More research in hetero- geneity should be carried out on the basis of the results. Further more, it helps to study the basis and mechanisms of cardiac diseases like ventricular tachycardia.