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Deep Venous Arterialization: How Does It Work?
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Peripheral artery disease (PAD) affects >230 million people worldwide, representing a global healthcare problem. The most severe clinical manifestation of PAD is chronic limb-threatening ischemia (CLTI), which affects ~11% of the patients with PAD, and its incidence continues to grow at a rapid pace. Revascularization remains the key treatment for CLTI to reduce the amputation rate and improve quality and quantity of life.
Although revascularisation options have substantially improved in recent years due to the advancement of endovascular techniques, ~20% of CLTI patients are still considered not suitable for any type of traditional revascularization due to severe unreconstructable arterial disease. These "no-option" patients are generally old, with type 2 diabetes and/or end-stage renal disease; however, it is not uncommon to observe younger patients with early CLTI onset due to type 1 diabetes or inflammatory disorders. Outcomes of patients with no-option CLTI are poor, with major amputation rates up to 46% at 1 year, low quality of life, and increased mortality rates. Thus, the need for alternative, effective treatment strategies in no-option CLTI patients is pressing.
Transcatheter arterialization of the deep veins (TADV) is a new promising technique for saving limbs of patients with no-option CLTI. The old and fascinating idea to divert blood flow from the diseased arterial system to the healthy vein system is now presented in a new totally percutaneous scenario, without surgical wounds, and in a standardized and reproducible procedure across centers and countries.
The procedure starts with a double approach: Arterial and venous catheters are introduced into the common femoral artery and lateral plantar vein, respectively, and then advanced to the desired crossing point, usually between the proximal posterior tibial artery and a paired posterior tibial vein. The re-entry needle is deployed from the arterial catheter so that it passes through the mesh loop of the parallel venous catheter. A guide is then advanced and externalized by access to the foot veins, which creates a crossing access from one side to the other. The arteriovenous junction is dilated with a balloon. Then, the coaxial cutting valvulotome is inserted in thrust and progresses in the tibial vein up to the middle of the foot, so as to render the venous valves incompetent.
After successful valvulotomy, balloon dilation of the tibial vein to the ankle prevents compression of the stent-graft that will be placed there. Self-expanding stents are deployed into the target vein from the proximal edge of the calcaneus to the junction point. The procedure concludes with placement of a tapered self-expanding stent across the arteriovenous junction point, and angiographic confirmation that adequate venous return of the foot has been achieved. Patients are prescribed dual antiplatelet or anticoagulant therapy for at least 3 months following the operation.
There is a fundamental difference between traditional revascularization procedures and TADV. After a successful bypass or angioplasty, the functional result of the procedure is immediately visible, angiographically and clinically, and the reestablishment of distal blood flow achieves a sudden relief of ischemia. That is not the same with TADV. At the end of the TADV procedure we generally observe a roundabout of blood in the foot without any blood flow reaching the tissues: the so-called vein "fortress" is locked by a multitude of small vein valves. In some cases, patient’s symptoms can worsen in the short-term, and pain control is a fundamental part of the post-procedural care.
TADV needs time for perfusing tissues, waiting for a remodeling process that relies on the residual biological adaptation capacity of the patient’s vascular system. In patients submitted to a new angiographic study months or years after the index TADV procedure, we have observed an impressive expansion of the arterialized venous system with new connections between vein and arteries able to recruit "hibernated" original arterial segments.
Moreover, while in the acute phase, the arterialized circuit has an extensive venous outflow responsible for a precocious steal of blood from the fortress, and reduction of the perfusion pressure in the plantar venous arch. After the positive remodeling process we observed a spontaneous self-pruning of these "non-tissue feeding" veins, leading to Doppler flow and distal pressure patterns typical of arteries. To be able to monitor, guide, and promote this process will be the main argument of research on TADV for the coming years.