CORRESPONDENCE: LETTER TO THE EDITOR
Pathophysiology of Stent Thrombosis: Platelet Activation, Mechanical Factors, or Both?
Fernando Alfonso, MD, PhD, FESC*
* Unidad de Hemodinámica, Servicio de Cardiolog& acute;a Intervencionista, Instituto Cardiovascular, Hospital Universitario "San Carlos", Ciudad Universitaria, Plaza de Cristo Rey, Madrid 28040, Spain (Email: falf{at}hotmail.com).
We read with great interest the elegant study of Wenaweser et al. (1) demonstrating impaired response to antiplatelet therapy in patients suffering stent thrombosis (ST). Notably, response to acetylsalicylic acid was impaired in these patients, and additional clopidogrel therapy failed to overcome the enhanced platelet aggregation as compared with that found in patients with uneventful coronary stenting or normal volunteers.
The relevance of antiplatelet therapy to prevent in this dreadful complication appears clear. However, the other potential major player in the field, namely a stent-related mechanical problem, was not adequately addressed by these investigators. Therefore, owing to the potential clinical implication of this study (1) additional information would be most useful. First, it would be important to know whether all patients presented an optimal angiographic result after the procedure or whether suboptimal results could be detected immediately after stenting. Information on vessel size and balloon/artery ratio would be of interest in this regard.
Second, we previously demonstrated that intravascular ultrasound is able to depict significant underlying mechanical problems in most patients with ST (stent underexpansion, malapposition, dissections, inflow/outflow stenoses) (2). Because these findings, which require specific therapy, are frequently undetected by angiography, a description of the ultrasonic data of these patients (if available) would be helpful. Third, information on the reason for initial stent implantation would be appreciated because it has been suggested that acute coronary syndromes (with the associated platelet hyperactivity) may be a predisposing factor for ST (2).
Moreover, detailing whether some episodes of ST were secondary to antiplatelet therapy withdrawal would also be of great interest.
Finally, considering the potentially catastrophic consequences of recurrent ST, it would be important to define precisely when clopidogrel therapy was discontinued in the study in order to evaluate platelet aggregation with aspirin alone. The potential benefit of a higher dose of clopidogrel has been suggested (3,4), and this strategy appears especially attractive for high-risk patients. Therefore, from a pragmatic standpoint, it will be critical to determine whether the relative inefficacy of a conventional clopidogrel regimen (1) can be overcome with higher doses (3,4). Eventually, unraveling the multifaceted etiology of ST is urgently required to prevent and successfully treat this challenging problem.
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1. Wenaweser P, Dörffler-Melly J, Imboden K, et al. Stent thrombosis is associated with an impaired response to antiplatelet therapy J Am Coll Cardiol 2005;45:1748-1752.[Abstract/Free Full Text]2. Alfonso F, Suarez A, Angiolillo DJ, et al. Findings of intravascular ultrasound during acute stent thrombosis Heart 2004;90:1455-1459.[Abstract/Free Full Text] 3. Gurbel PA, Bliden KP, Hiatt BL, O’Connor CM. Clopidogrel for coronary stentingresponse variability, drug resistance and the effect of pretreatment platelet reactivity. Circulation 2003;107:2908-2913.[Abstract/Free Full Text] 4. Kastrati A, Mehilli J, Schuhelen H, et al. A clinical trial of abciximab in elective percutaneous coronary intervention after pretreatment with clopidogrel N Engl J Med 2004;350:232-238.[Abstract/Free Full Text]
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F. Alfonso and D. J. Angiolillo
Platelet Function Assessment to Predict Outcomes After Coronary Interventions: Hype or Hope?
J. Am. Coll. Cardiol.,
November 7, 2006;
48(9):
1751 - 1754.
[Full Text]
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