We showed direct transthoracic VSD repair to be feasible under real-time MRI guidance. MRI depicted the defect, the heart surface, and the chest wall in relation to each other for planning and execution of needle, guidewire, and catheter traversals into both right and left ventricular cavities. Real-time MRI also provided straightforward visualization of all steps of closure: device delivery, deployment, and release. Equally important, real-time MRI depicted structures in context in a way we find qualitatively superior to x-ray and ultrasound guidance of conventional nonsurgical structural heart procedures, because the heart, thorax, pleura, and pericardium are displayed instantaneously throughout.
Our closed-chest real-time MRI-guided transthoracic VSD repair approach offers an alternative for small children in whom percutaneous options are not possible (vascular access) or pose unnecessary risk of major adverse outcomes (arrhythmia, hemodynamic compromise, cardiac perforation, tamponade, death) (3
). It may avert cardiopulmonary bypass required in traditional VSD surgical repair or sternotomy required even in hybrid perventricular approaches.
In this preclinical experience with single “intentional” defects, all VSD closure procedures were successful. We did not encounter known complications of traditional (percutaneous, hybrid) VSD device closure, such as device embolization, residual shunt, atrioventricular valve distortion, ventricular dysfunction, or left ventricular free wall damage (2
). Nor did we observe damage to coronary, pleural, or intercostal arteries during percutaneous access (12
Even in this preliminary experience, procedure planning and conduct was completed in a little more than 1 h. This compares favorably with hybrid surgical (11
) and percutaneous (2
The marketed AGA medical VSD occluder and its matching delivery cable each have a small stainless steel microscrew hub that distorts MR images. In collaboration with the manufacturer, the microscrews were replaced with titanium to eliminate the steel susceptibility artifact.
We further customized the delivery cable as an active antenna device tuned to couple with the nitinol occluder in the partially and fully deployed positions. This novel approach to deliberate coupling significantly enhanced visibility and performance of the device.
We were able to close 9-F access port holes in the RV using a commercial vascular closure device, as has been described in case reports (14
). Our “permissive pericardial tamponade” technique facilitated appropriate deployment of the collagen sponge on the epicardial surface (8
), but failed without sequelae in 1 case. Two animals had small pericardial effusions, which we drained on day 2 and which did not recur. Similar pericardial collections are noted after “hybrid” VSD closure (11
). Gross pathology and histology at 1 month showed excellent healing of the access site and resorption of the copolymer anchor. By contrast, we have found this same collagen-based closure device to be unsuitable for closure of left ventricular access ports, and many operators report serious consequences of simple sheath withdrawal without surgical or device closure after transapical puncture for interventional procedures (15
). Custom epicardial closure solutions are under development using sutures, staples, and other approaches.
The chief procedural limitation in our experience was inadvertent loss of right ventricular access after VSD device delivery, which proved lethal in 2 animals. We found an alternative sheath solution that promises to mitigate this limitation, by providing a secure “lock” of the sheath tip inside the right ventricle when necessary. In addition, it can help to separate visceral and parietal pericardium during access port closure. Lower-profile intracameral retention sheaths are feasible.
The early nonrecurrent pericardial bleeding we experienced might be less important in clinical practice, where mitigation options include blood transfusion, reversal of anticoagulation (intentionally avoided in these experiments to “stress” hemostasis), temporary post-procedure pericardial drain catheters, and surgical repair if indicated.
We created a new animal model of VSD using percutaneous catheter techniques and MRI–x-ray co-registration. We had been unsuccessful using echocardiographic guidance because of poor acoustic windows. Before debulking myocardium using the excimer laser sheath extraction catheter, we had been unsuccessful in creating a sustained ventricular communication even using large conventional (up to 18 mm) or cutting (up to 6 mm) angioplasty balloons. Nevertheless, these naive animals suffered acute hemodynamic instability, accounting for significant procedural mortality during model creation. The acute physiology in this model resembled post-infarction, traumatic, and iatrogenic lesions. Our animal model challenged us to target, cross, and close small defects compared with technically easier larger chronic defects, in the range reported for hybrid (11
) and percutaneous (2
) closure. That said, we were not able to create apical VSD.
We showed that a real-time MRI-guided direct transthoracic procedure is feasible. Clinical translation would require further development of the titanium microscrews, assurance of no heating during MRI, and adjunctive catheter tools, such as an enhanced-conspicuity delivery sheath and “buddy” guidewires to enhance procedure safety.
Our transthoracic approach may be suitable for membranous (16
) and less common subarterial VSDs (13
). Related applications for complex congenital interventions include transventricular atretic pulmonary valve perforation and transatrial septal perforation/septostomy. With suitable devices, real-time MRI could facilitate percutaneous VSD repair in larger children.