Increased clot strength following transcatheter aortic valve replacement
Authors: Hesselbarth D , D'orazio M , Ciccarone G , Gjermeni D , Juelch C , Rilinger J , Pottgiesser T , Von Zur Muehlen C , Duerschmied D , Westermann D , Olivier C B 
Published: November 2023

Background

Patients treated with transcatheter aortic valve replacement (TAVR) are at high risk for bleeding and ischemic events. Thrombelastography (TEG) parameters are associated with thromboembolic and bleeding risk. TEG may be used to risk-stratify TAVR patients. The variability of TEG over time and the association of TEG parameters with antithrombotic medication in these patients has not been studied.

Aim

To assess the changes in platelet function and global hemostasis between periprocedural and long-term measurement in patients undergoing TAVR.

Methods

We performed a prospective, single center cohort study and included patients after TAVR. TEG was performed during the index hospitalization (T0) and 6 (± 2) months after TAVR (T1). TEG was used to determine the maximum blood clot strength as maximum amplitude (MA) after stimulation with kaolin + tissue factor (CRT) and kaolin + heparinase (CKH). Platelet count and thromboplastin time (INR) were determined as conventional coagulation parameters. At time of the measurements, patients were treated with acetylsalicylic acid (ASA), dual antiplatelet therapy (DAPT), oral anticoagulation (OAC) or a combination of these medications. We compared TEG parameters, thrombocytes and INR between measurements T0 and T1 and stratified patients according to the antithrombotic regimen.

Results

From December 2021 to April 2022, 64 patients were enrolled and measured after TAVR: T0 at median on day 4 (min. 2, max.17) and T1 at a median of 6 months (min. 4 max. 8). The median age was 81 years (interquartile range IQR 78-83) and 28 (47%) patients were male. 59 of 64 patients had no change in indication for anticoagulation between measurements T0 and T1, thus taking either OAC (28 of 59) or antiplatelet (AP) without OAC (31 of 59) at measurements T0 and T1. MA was higher in patients at T0 compared with T1 and was observed independently of antithrombotic therapy. OAC: [MA-CRT 66.5mm (IQR 64.5-69.1mm) vs. 63.8mm (IQR 59.7-66.0mm); p&lt;0.0001] and [MA-CKH 64.5mm (61.3-68.0mm) vs. 60.1mm (56.4-64.7mm); p&lt;0.0001)]. AP: [MA-CRT 66.8mm (IQR 63.75-69.9mm) vs 64.2mm (IQR 60.7.7-66.1mm); p&lt;0.0001] and [MA-CKH 64.5mm (61.3-68.0mm) vs 60.1mm (56.4-64.7mm); p&lt;0.0001]. Platelet count (Tc) was not significantly different at T0 vs. T1 in patients with OAC and those with AP. [Tc (OAC) 162.5103/µl (IQR 131.2-223.2 103/µl) vs.178tsd/µl (IQR 152-209.75103/µl); p=0.29] and [Tc (AP) 181tsd/µl (IQR 128-243103/µl) vs. 202tsd/µl (IQR 175-247103/µl), respectively; p=0.056, Figure 1].

Conclusion

Compared with long-term measurements, clot strength measured during the index hospitalization after TAVR was significantly increased. The increased clot strength was independent of baseline antithrombotic therapy. Whether this corresponds to an early procoagulant state that favors the occurrence of valvular thrombosis or cardiovascular events needs to be investigated in prospective studies.