In this issue of Cardiovascular Revascularization Medicine , Sanghvi et al. report a randomized comparison of two compression devices to achieve hemostasis after transradial angiography and intervention (TRA) [ ]. This is a contemporary study, using “right-sized” equipment (i.e., as small as possible), appropriate dose of anticoagulant (70U/kg heparin), the de facto standard-of care (patent hemostasis) with a short and fast compression device removal protocol [ ]. Current “best practices” were followed and resulted in excellent outcomes [ ]. Both devices performed well, with low radial artery occlusion (RAO) rates and minimal bleeding complications.

One would then wonder, why is this study important in 2018? And what does a study showing little or no difference between two different closure devices teach us?

There are two key questions that arise from this manuscript:

• 1.
  

  Are the current best practices enough, and do we need more work to further reduce or eliminate RAO?

  
  
• 2.
  

  Should non-occlusive radial artery injury be routinely included as an outcome measure of after TRA?

While there is extensive research in preventing RAO, non-occlusive radial artery injury remains currently under-researched and clearly needs to be addressed both clinically and technologically [ , ].

Regarding RAO, studies like Sanghvi’s further underline our contemporary understanding of hemostasis. It is not the device, but rather “best practices” that influence the rates of RAO. The small differences observed in this study relating to hematomas may be due to chance alone. To support this contention, a recent study showing excellent results in RAO rates with manual compression is exactly in line with the Sanghvi trial [ ]. Both manual and mechanical compression delivered similar outcomes. Of note, Sanghvi noted that re-bleeding was associated with higher rates of RAO. After re-bleeding, hemostasis management changes – re-application of the compression device is at higher pressure and longer compression times – both of which cause more RAO.

So … what are the next steps? What will it take to get to RAO rates to 0%? With the aforementioned considerations, it is clear that we need a better mousetrap. Promising results have been obtained with ulnar compression [ ]. Perhaps, new sheath designs with optimization of anticoagulation may be needed to fully eliminate RAO [ ].

This study also underlines what the meaningful endpoint is when we study RAO. 24-h RAO? [ ] One-week RAO? One-month RAO? [ , ] It is clear from multiple studies that early RAO resolves and that 1-month rates are significantly lower. Sanghvi’s study confirms this and corroborates that 1-month RAO should be used as a minimal standard when assessing the outcome of different interventions.

This brings us to the second question. What else is going on in the hand and forearm after TRA?

We all have seen patients in clinic after TRA who complained about forearm “discomfort.” It is quite plausible that this constellation of symptoms is due to “non-occlusive radial artery injury.” [ ]

There is clearly development of intimal thickening after TRA that limits re-accessing the radial artery [ ]. Sheathless systems do not seem to reduce this injury [ ]. Along with objective evidence of intima-media thickening, we are still struggling with these other outcome measures how to assess the impact of TRA on hand and forearm function. Is it pain after angiography? [ ] Hand-strength? [ ] Physiologic changes in hand function? [ ] There is little doubt that we do have to improve our understanding of the effects of TRA on the hand and forearm function.

As TRA became the prevailing access site around the world, we do have to resolve these two remaining questions. Future studies need to focus on both RAO and non-occlusive radial artery injury as two important endpoints when assessing the impact of TRA.