Author + information
- Peter Wenaweser, MD and
- Otto M. Hess, MD⁎ ()
- ↵⁎Department of Cardiology, Swiss Cardiovascular Center, University Hospital, CH-3010 Bern Switzerland
We thank Dr. Alfonso for his interest in our work (1). We agree with him that the phenomenon of “stent thrombosis” is a multifactoral process and that mechanical factors play an important role, especially in the setting of an acute stent thrombosis (within 24 h), whereas for subacute (1 to 30 days) or late stent thrombosis (>30 days) a more complex etiology has been postulated. In our case-control study no patient with an acute stent thrombosis was included (1). Platelet aggregation was assessed several months after stent thrombosis to avoid confounding factors such as platelet activation induced by thrombotic stent occlusion. Dr. Alfonso cites four issues in his letter. We address each one here.
First, we fully agree that an optimal angiographic result is a key factor in the prevention of stent thrombosis (2). In our study population two patients showed a suboptimal angiographic result (one had a distal residual dissection with Thrombolysis In Myocardial Infarction [TIMI] flow grade 2; another showed a no-reflow phenomenon).
Second, intravascular ultrasound was not routinely performed after stent implantation in our institution. Therefore, we cannot exclude stent underexpansion or stent malapposition.
Third, acute coronary syndromes have been previously identified as potential risk factors for stent thrombosis (2,3). In our study population, 83% of the patients in the stent thrombosis group suffered from an acute coronary syndrome at time of stent implantation, whereas only 43% of patients in the control group were affected (p < 0.001). This highlights the importance of activated platelets in the setting of an acute coronary syndrome and the role of an effective antithrombotic regimen in the prevention of stent thrombosis. Therefore, a resistance to antiplatelet therapy may represent an additional risk factor for stent thrombosis.
Fourth, all patients in our study population were on lifelong aspirin therapy; however, at the time of stent thrombosis 26% were off thienopyridine treatment. We agree that this may be another risk factor, although the rate of clopidogrel resistance was lowest in stent thrombosis patients. According to our protocol all patients were first examined under aspirin therapy alone, followed by a second measurement under aspirin and clopidogrel.
Finally, the etiology of stent thrombosis is multifaceted, and we agree that mechanical risk factors should be avoided. Nevertheless, the efficacy of our standard (dual) antiplatelet treatment might not be as good as wished for. A higher dose of clopidogrel or new antithrombotic drugs as alternative treatment in patients with resistance to antiplatelet therapy warrant further evaluation to prevent stent thrombosis and its high morbidity and mortality.
- American College of Cardiology Foundation
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