Risk for Tirofiban-induced thrombocytopenia in patients undergoing percutaneous coronary intervention for ST-segment elevation myocardial infarction

Stephan Rühle (Bremen)1, A. Fach (Bremen)1, R. Osteresch (Bremen)1, J. Schmucker (Bremen)2, L. A. Mata Marín (Bremen)1, H. Kerniss (Bremen)1, D. Garstka (Bremen)1, R. Hambrecht (Bremen)1, H. Wienbergen (Bremen)1

1Bremer Institut für Herz- und Kreislaufforschung (BIHKF) Bremen, Deutschland; 2Klinikum Bremen-Mitte Klinik für Innere Medizin III Bremen, Deutschland



The glycoprotein (GP) IIb/IIIa inhibitor tirofiban is approved to reduce thrombotic cardiovascular events in patients undergoing percutaneous coronary intervention (PCI), especially in patients presenting with acute coronary syndrome (ACS). Severe thrombocytopenia (ST) is a rare but potential severe complication. However, data on short- and long-term outcome are rare, some authors observed poor prognosis and higher mortality; most scientific publications are based on case-reports. Aim of this study was to examine short- and long-term mortality and bleeding complications in patients with acquired ST < 50/nl due to receiving tirofiban for therapy of ST-segment elevation myocardial infarction (STEMI).



We analyzed all patients included in the monocentric Bremen STEMI-registry (BSR) between 2006 and 2022 hospitalized for STEMI (n=12347), receiving invasive coronary angiography and tirofiban. Patients with normal platelet count at admission were divided in 2 groups (no or mild thrombocytopenia ≥ 50/nl [NT] versus severe thrombocytopenia < 50/nl [ST] after receiving tirofiban). Patients with heparin-induced thrombocytopenia (HIT) were excluded. The 2 groups then were compared to find out short- and long-term mortality, bleeding complications as well as risk factors for developing ST. 



5420 patients (43,9%) received tirofiban during/after PCI for STEMI. 69 patients (0,02%) developed acute ST < 50/nl. They all received tirofiban via prolonged intravenous infusion (mean time 23,6 ± 6,2 hours), no infusion was stopped prematurely.  In the NT-group infusion-duration was shorter (mean time 15,2 ± 6 hours; p < 0,01); infusion was stopped prematurely in n=214 cases (4,1%) particularly because of bleeding complications (97,2%). 

In-hospital mortality was 7,3% in the NT-group (n=393) and 1,4% in the ST-group (n=1; p <0,01). 1-year mortality did not differ between the two groups (175 [3,3%] versus 0 patients; p 0,4). Severe bleeding complications (BARC 3 and 5) occurred in 3,5% in the NT-group (n=185), leading to death in 18 cases (9,7% of cases with severe bleeding). In the ST-group no severe bleeding complications were observed (p 0,03).

While most patient characteristics did not differ between groups, patients in NT more often had cardiogenic shock (n=708 [13,2%] versus n=4 [5,8%]; p 0,01), mean creatinine-levels at admission were slightly lower (1 ± 1,4 versus 1,1 ± 0,2 mg/dl; p <0,01), and they had higher ejection fractions after revascularization (48 ± 19,6 versus 46,8 ± 23%; p <0,01; see Table). 



Real world data from the BSR confirm that tirofiban-caused severe thrombocytopenia in the therapy of STEMI is rare (0,02%). The risk may be higher with prolonged infusion. Interestingly, in our collective ST was not related to higher in-hospital or 1-year mortality nor to severe bleeding complications, indicating that tirofiban can be used safely in this collective. However, if tirofiban is used, utmost attention should be paid to bleeding complications (3,5%) independent of platelet count. 

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