Cardiac motion remains a challenge in the treatment of ventricular tachycardia with external beam ablation therapy. Current techniques involve expansion of the treatment area which can lead to unwanted collateral damage. Surrounding healthy tissue could be spared by gating the delivery of the beam to the cardiac cycle. In prior work, we assessed cardiac motion using in vivo fiducial markers and demonstrated that motion would be reduced if treatment were gated to half of the cardiac cycle, approximately corresponding to diastole. In the current work, we extend our prior analysis by quantitatively assessing the optimal gating window for motion reduction in the left ventricle. Motion was assessed in five porcine models with two fiducial clips per animal for a total of ten clips. The minimal cardiac motion occurred when the gating window started at 70% of the cardiac cycle. Without gating, three-dimensional cardiac motion was 7.0 ± 3.9 in x (left/right), 5.3 ± 2.5 in y (anterior/posterior), and 5.6 ± 2.3 in z (superior/inferior) mm. Using an optimal gating window, cardiac motion was 3.1 ± 1.8 in x (left/right), 2.5 ± 1.2 in y (anterior/posterior), and 3.1 ± 1.7 in z (superior/inferior) mm. The percentage reduction in motion with optimal gating was 51 ± 23 in x (left/right), 49 ± 21 in y (anterior/posterior), and 45 ± 24 % in z (superior/inferior). This work demonstrates that gating shows significant promise for reducing the effects of left ventricular motion when treating ventricular tachycardia with external beam ablation therapy.
External beam ablation therapy has the potential to treat cardiac arrhythmias non-invasively by targeting arrhythmogenic myocardial tissue; however, a challenge of treating cardiac tissue with beam ablation therapy is cardiac motion. Currently, cardiac motion is typically compensated by expansion of the target volume which can potentially lead to collateral damage of surrounding healthy tissue. This collateral damage could be minimized by gating the beam delivery to a portion of the cardiac cycle. In prior work, we evaluated cardiac motion using anatomic landmarks in multi-phase cardiac computed tomography volumes of swine hearts across the left atria and ventricles. Other work evaluated left atrial motion using implanted fiducial clips. In the current work, we extend this prior work by quantifying cardiac motion using gold standard implanted fiducial clips across all four chambers of the heart. Cardiac motion varied by chamber, ranging from 2.1 to 7.2 mm in the x direction, 7.2 to 8.1 mm in the y direction, and 3.1 to 9.7 mm in the z direction. In addition, we quantify the reduction in motion if delivery were gated to phases 40% to 90% of the cardiac cycle, which corresponds to treating across 50% of the cardiac cycle. Cardiac motion across 50% of the cardiac cycle ranged from 1.1 to 5.3 mm in the x direction, 4.5 to 5.2 mm in the y direction, and 1.2 to 7.8 mm in the z direction. Percentage reduction in motion for treating during 50% of the cardiac cycle ranged from 18% to 47% in the x direction, 31% to 43% in the y direction, and 11% to 61% in the z direction. These results demonstrate that a substantial improvement in target localization could be achieved by gating the beam to 50% of the cardiac cycle.
Proton beam therapy has the potential to non-invasively treat ventricular tachycardia (VT) by homogenizing infarct scar. It has been previously demonstrated that proton beam therapy can create lesions in healthy myocardial tissue, thereby suggesting a potential for treatment of VT. In prior work, we quantified the relationship between dose delivered to myocardial tissue with lesion formation identified with in vivo, delayed contrast-enhanced magnetic resonance imaging (DCE-MRI) scans. In the current work, we evaluate the relationship of delivered dose with lesions identified in high resolution, post-mortem DCE-MRI scans. Deformable registration is used to align the dose maps from the baseline planning CT scans to ex vivo scans following proton beam therapy in swine. The current study demonstrates that nearly 100% of tissue exposed to a dose of 30 Gy or higher developed into lesion and approximately 85% of the tissue in the 20-30 Gy interval developed into lesion. On the other hand, tissue exposed to doses of 10 Gy or less tended to remain healthy myocardium, with less than 10% of tissue in the 5-10 Gy range and almost no tissue in the 0-5 Gy range developing into lesion.
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