3. Key Questions
1) Is patent haemostasis effective in ACS populations?
Cardiology Department, Royal Infirmary of Edinburgh
Sanmartin et
al. 2007
PROPHET
2008
RACOMAP
2009
4. Key Questions
Cardiology Department, Royal Infirmary of Edinburgh
Prothrombotic
state
Greater
pharmacotherapy
Larger sheaths
May favour patent
haemostasis
May disfavour
patent haemostasis
5. Key Questions
2. Would an end-of-case ACT be a more powerful
predictor of RAO than heparin dose alone?
Cardiology Department, Royal Infirmary of Edinburgh
Aykan et al. 2014 Hahalis et al. 2015
Degirmencioglu et al. 2015
Bernat et al. 2010 Spaulding et al. 1996
Low Dose vs. High Dose Heparin
12. Summary
In NSTEMI adopting a technique of patent haemostasis
reduces early RAO by 70%
End-of-case ACT does not predict RAO
- OR 1.0 (95% CI 0.99 to 1.01)
Cardiology Department, Royal Infirmary of Edinburgh
13. Conclusions
Arterial stasis following radial sheath removal is the
primary determinant of RAO
Patent haemostasis is highly effective in reducing early
RAO in both elective and ACS patients
Cardiology Department, Royal Infirmary of Edinburgh
14. Considerations
No association between the end-of-case ACT and RAO
irrespective of the treatment group:
• OR 0.997 [0.985-1.009] for patent haemostasis
• OR 1.004 [0.996-1.012] for standard care
Cardiology Department, Royal Infirmary of Edinburgh
Editor's Notes
We have known for a long time that patent haemostasis substantially reduces the incidence of RAO in patients undergoing elective TRA BUT whether similar benefits apply to inpatients undergoing TRA for ACS was largely unknown.
On the one hand ACS is a pro-inflammatory and prothrombotic state. RAO is a thrombotic process so, compared to standard radial compression, patent haemostasis may be of greater efficacy in ACS patients
On the other hand, ACS patients are managed with more intensive antiplatelet and anticoagulant pharmcacotherapy which may A) affect the feasibility of applying patent haemostasis to these patients because of the lower compression pressures required to achieve patency (THIS WAS CERTAINLY A CONCERN IN OUR INSTITUTION) and B) reduce the risk of developing RAO as a consequence of occlusive compression.
How these factors balanced out was unknown.
The second key question was “would and end of case ACT…...”
I think everyone accepts that heparin reduces the risk of RAO but the optimal dose is unclear with some studies showing 5000 units is superior to 2500 units while other studeis showed no statistical difference.
At the time of radial sheath removal the antithrombotic protection from an earlier bolus of heparin will vary considerably due to a number of factors including patient weight, renal function and procedural duration. ACT is a functional assessment of clotting status and we hypothesised that an end of case ACT may therefore prove to be a more powerful predictor of RAO. If so, this could potentially allow prospective action to be taken.
We enrolled 300 consecutive inpatients undergoing coronary angiography for NSTEMI into two sequential cohorts. Every patient had a 6fr radial sheath. The first cohort were managed with standard radial care in our institution – which is 13ml of air inserted into the TR band with gradual deflation over the next 3 hours on the ward. The second cohort were managed identically except for their radial artery care which was patent haemostasis guided by plethysmography.
All patients had an ACT immediately prior to sheath removal and all patients had radial patency assessed the following day.