Acute Treatment of No Reflow Raises Important Questions

Hello, and welcome to the August 2019 edition of Vascular Disease Management. I have chosen to comment on Dr Luai Alhazmi and colleagues’ case report on “No Reflow in Below-the-Knee Vessels After Percutaneous Revascularization of the Superficial Femoral Artery.”

This case report concerns a patient who had previously undergone percutaneous transluminal angioplasty and stenting of a superficial femoral artery (SFA). The patient had developed a recurrent SFA occlusion with “no reflow” in the below-the-knee vessels following subintimal recanalization and repeat stenting of the SFA. The sluggish flow was successfully treated with intra-arterial administration of nitroglycerin and adenosine via a microcatheter, with delivery in the popliteal artery. The authors discussed possible etiologies of the no-reflow phenomenon post arterial intervention.

I have chosen to comment on this report because no reflow is a common phenomenon in peripheral interventional procedures. There are obviously acute outcome sequelae, but there is poor understanding of the long-term consequences of no reflow. 

Preventing no reflow is obviously preferable to treating no reflow after it has occurred. Adequately monitored anticoagulation during intervention and during use of antiplatelet therapies is important in preventing no reflow. Additionally, careful, frequent aspiration and flushing of long sheaths is required to lessen the risk of inadvertent flushing of thrombus into treatment areas. Use of distal protection devices can prevent embolization of thrombus and atherosclerotic debris, but these tools are not universally effective at capturing all debris and are associated with significant cost. Distal protection devices often have suboptimal device delivery performance, particularly when .035-inch compatible devices are required. Administration of vasodilators and careful attention to distal wire position during procedures may help to prevent arterial spasm. Prevention is universally important, but prevention is especially essential in high-risk cases in which there is suspected fresh thrombus or high thrombus burden. Prevention is also important in procedures that have a documented known risk of embolization due to large particulate debris.

Acute outcomes are of paramount importance, and in extreme cases, may determine limb viability. In this case, vasodilators resulted in improved flow, but in many cases, vasodilators do not result in improved flow. Occasional repeat vasodilator therapy may be successful but may sometimes fail. Determining the level of flow interruption is crucial in these cases in which there may be no flow in the entire vessel. Lack of flow can be discerned by placement of a catheter into the distal vasculature and by performing angiography after administration of vasodilators. If distal angiography shows adequate distal flow, then the catheter can be partially withdrawn, and angiography can be repeated sequentially after vasodilator administration. This technique typically allows discovery of the exact site resulting in no reflow, particularly with large particulate debris or unrecognized dissection, and allows specific, tailored therapy where proximal injection is inadequate. Aspiration thrombectomy, rheolytic therapy, thrombolytic therapy, and use of glycoprotein IIb/IIIa antiplatelet infusions may restore flow.

Unfortunately, we do not have any data about long-term outcomes in no-reflow cases that were successfully treated acutely. Do these individuals have similar long-term patency to other individuals who had good flow initially? Is there attrition of the distal vessels over time? Is limb salvage success affected? Are mortality rates increased? Is long-term administration of anticoagulants in full or attenuated doses helpful in preventing subsequent events? These are important questions that must be answered if we are to improve interventional outcomes.