We find that a commercial collagen-based vascular closure device can achieve temporary hemostasis for closure of a direct transthoracic myocardial access port, but that it provides insufficiently durable hemostasis. Failure to deploy the epicardial plug component inside the pericardial space may lead to ineffective hemostasis. MRI provided insight into a mitigation approach: temporary (“permissive”) pericardial tamponade effectively separates the visceral and parietal pericardial layers to allow the hemostatic collagen sponge to reach the epicardial surface.
Percutaneous transthoracic left ventricular access will be useful for a spectrum of interventional procedures including trans-apical aortic valve replacement (7
), treating prosthetic paravalvular leak (5
), investigational mitral valve repair (4
), and left ventricular radiofrequency ablation of ventricular arrhythmias (6
). These share a need for a large, rigid, or other geometrically constrained access port to deliver equipment to a target. Current practice requires direct surgical exposure, and placing apical sutures under direct visualization by a skilled surgeon prior to left ventricular puncture (13
In our experiments, early hemostasis probably reflects the ability of the swollen Angio-Seal collagen sponge to suppress bleeding along the left ventricle puncture site. Nevertheless, bloody pericardial fluid re-accumulated after only a few days, likely reflecting slow continuous ooze. We believe the following failure modes may have contributed to this process. First, the myocardial hole may have been tethered open by the foot or suture, analogous to what we observed when the sponge deployed outside the pericardium. Second, repeated high pressure myocardial contraction creates a different device environment from the intended peri-vascular position of the device. For example myocardial contraction may displace the collagen sponge otherwise retained by friction. Accordingly, it is possible the device underwent mechanical failure or rapid biodegradation.
We do not believe other potential failure modes contributed to late hemostatic failure in this experiment, such as exit or erosion of the rigid 10mm foot through the puncture tract, non-orthogonal or other maldeployment of the foot along an endocardial trabeculation, or cardiac ejection of the device.
A more robust closure system might include some of the following features. We find a separate pericardial catheter valuable to separate the pericardial layers but also as an emergency drain. A closure bailout mechanism, such as a guidewire, probably should remain until hemostasis is assured. Direct imaging guidance, unconstrained by ribs and imaging windows, is invaluable in assuring procedure success. An enhanced closure device itself may incorporate features such as a hemostatic material inside the myocardial channel, enhanced occlusive hoods for the endocardial or epicardial surfaces, features to protect left ventricular structures from injury or entrapment, and alternative closure mechanisms such as sutures or staples. Finally, we have learned that avoiding parietal pericardial entrapment is probably important for hemostasis, at least in a “naïve” pericardium.
Our findings are limited in that we use a device designed for vascular and not myocardial closure, and we test in an animal model with different thoracic anatomy from humans. Animals remained fully anticoagulated during deployment of the closure device, in order to test this procedure in a stressed condition. We are aware that anticoagulation reversal prior to puncture site closure could potentially improve device effectiveness. An additional limitation is the use of an 8 Fr Angio-Seal to close a site larger than 8 Fr. The 8 Fr Angio-Seal device has been shown to be effective for closure of 10 Fr and even some 12 Fr vascular punctures (15
). Left ventricular mural elasticity is greater than femoral artery elasticity, and should accommodate a smaller closure device. Nevertheless our experience has provided insight into requirements for successful engineering of a tailored left ventricular closure device.