Aortic stenosis is the most common primary valve disease in high-income countries with
increasing importance. Throughout the last 15 years, transcatheter aortic valve implantation
(TAVI) has become an alternative to surgical aortic valve replacement, the former standard of
care. Nowadays, the use of TAVI in elderly patients at increased surgical risk is favored.
There is still an important lack of evidence concerning the optimal antithrombotic strategy
post TAVI. Recently, it has been shown that the prevalence of subclinical leaflet thrombosis
after intervention has been underestimated and may be present in around 15 % up to 40%
(PORTICO IDE trial) of transcatheter valves. One study demonstrated that transient ischemic
attacks are significantly increased in these patients.
European guidelines are undecided towards the length of the dual antiplatelet therapy (DAPT)
after TAVI and recommend optional treatment durations between 3 to 6 months. The optimal
duration of DAPT is not known, although DAPT duration is associated with an increased
bleeding risk. The most recent update of AHA guidelines for valvular heart disease state that
oral anticoagulation with a VKA (INR of 2.5) may be reasonable for at least 3 months after
TAVI in patients at low risk of bleeding. Without favoring one over the other recommendation,
the current AHA guidelines also maintain the prior statement (from 2014) that clopidogrel 75
mg daily may be reasonable for the first 6 months after TAVI in addition to life-long
aspirin, which is in accordance with the European Guideline recommendation. On the other
hand, the GALILEO trial has recently been stopped as patients receiving rivaroxaban after
TAVI (no prior atrial fibrillation) had a higher mortality and thromboembolic events as well
as higher bleeding event rates.
The TEG(R) 6S analyzer is a point-of-care system evaluating a patient's individual hemostasis
profile by thrombelastography (TEG(R)), a potentially superior tool compared to conventional
platelet function testing. The TEG(R) system has been able to predict thrombotic
complications in different clinical contexts.
In classic coronary interventional cardiology, the strength of adenosine diphosphate
(ADP)-induced and thrombin-induced platelet-fibrin clots were found to be indicators of
long-term poststenting ischemic events. As the pathophysiologic mechanism of subclinical
leaflet thrombosis has not been examined in detail, the investigators hypothesize that
several TEG(R) assays may provide insight in finding predictive TEG(R) markers. Furthermore,
as the onset of subclinical leaflet thrombosis is not clear and may possibly increase over
time, the design with subsequent TEG(R) analyses at 3 timepoints (0, 3, 6 months) will help
to hopefully identify predictors that may become evident at later time points.
It is intriguing to hypothesize that the better predictive marker may be found using the
Global Hemostasis Assay. This is relevant as leaflet thrombosis develops despite dual
antiplatelet therapy and anticoagulation has been shown to fully resolve subclinical leaflet
thrombosis. The Global Hemostasis Assay may deliver prediction beyond platelet function,
which may improve antithrombotic therapy post TAVI. Finding a predictive TEG marker
(examining Platelet Mapping and Global Hemostasis together) holds the promise for future
individualized clinical decision-making by identifying individual risk.
Taken together, we hope that individual TEG based stratification of patients at risk for
subclinical leaflet thrombosis or other events may allow individual clinical decision-making.