Comparison of Antiplatelet Effects of Aspirin, Ticlopidine, or Their Combination After Stent Implantation

Rupprecht, Hans J.; Darius, Harald; Borkowski, Ulrike; Voigtländer, Thomas; Nowak, Bernd; Genth, Sabine; Meyer, Jürgen

doi:10.1161/01.cir.97.11.1046

Cited by 107 publications

(43 citation statements)

References 28 publications

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“…The thienopyridine P2Y 12 receptor antagonists are the only antiplatelet drugs that are known to reduce CD62 expression (Rupprecht et al, 1998;Klinkhardt et al, 2000), whereas treatment with GPIIb/IIIa inhibitors (Fredrickson et al, 2000;Klinkhardt et al, 2000), or aspirin (Rinder et al, 1993;Fredrickson et al, 2000;Klinkhardt et al, 2000) did not. We could demonstrate a significant decrease in the platelet activation marker CD62 and the secretion product PDGF after 6 …”

Section: Discussionmentioning

confidence: 99%

“…Moreover, it remains to be determined whether changes in CD62 expression induced by either drugs or diseases are paralleled by changes in the secretion of granule-derived products. Therefore, the aim of the present study was to characterize the relationship between platelet activation status (translocation of CD62) and PDGF secretion from ␣-granules in response to different concentrations of thrombin-receptor activating peptide (TRAP), and to determine whether such a relationship is maintained under antiplatelet drugs for which it is known that they either reduce CD62 expression (namely, the thienopyridine clopidogrel) (Rupprecht et al, 1998;Klinkhardt et al, 2000) or do not influence CD62 expression (namely the GPIIb/IIIa-inhibitor abciximab) (Fredrickson et al, 2000;Graff et al, 2001), or in clinical conditions that are associated with platelet hyper-reactivity (e.g., diabetes).…”

mentioning

confidence: 99%

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Close Relationship between the Platelet Activation Marker CD62 and the Granular Release of Platelet-Derived Growth Factor

Graff

Klinkhardt²,

Schini‐Kerth³

et al. 2002

The Journal of Pharmacology and Experimental Therapeutics

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The expression of CD62 on the surface of platelets is considered to be an indicator of platelet degranulation and secretion. We characterized the relationship between CD62 expression and platelet-derived growth factor (PDGF) AB and PDGF BB secretion in response to thrombin-receptor activating peptide (TRAP). The principal findings were 1) expression of CD62 as a constituent of platelet ␣-granule membrane and secretion of PDGF, an important ingredient of ␣-granules, can be stimulated by TRAP-induced activation in a dose-dependent fashion; 2) the activation marker and secretion product are closely correlated with each other; and 3) changes in the CD62 expression induced by a drug, namely clopidogrel, or by a disease, namely diabetes, are paralleled by changes in PDGF secretion. Although CD62 is perceived as an activation marker of platelets indicating enhanced aggregability and secretion of ␣-granular content, the proof that the CD62 status and its modifications reflect directly the actual secretion of the most important platelet mitogen, PDGF, has so far not been given. This ex vivo-in vitro study shows that at least for the activation pathway provided by the PAR-1 receptor for which TRAP is the selective agonist, CD62 expression on platelets could be a surrogate for their secretory activity.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Close Relationship between the Platelet Activation Marker CD62 and the Granular Release of Platelet-Derived Growth Factor

Graff

Klinkhardt²,

Schini‐Kerth³

et al. 2002

The Journal of Pharmacology and Experimental Therapeutics

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“…Ticlopidine has been established as one of the effective agents for antiplatelet therapy after stent implantation. 20,21) On the other hand, cilostazol, an antiplatelet agent with a cyclic AMP-mediated vasodilating action, has also been used to induce an attenuation of in-stent restenosis. The effect of cilostazol was reported to be comparable 17) or even superior 18,19) to that of ticlopidine on in-stent restenosis.…”

Section: Effect Of Basal Antiplatelet Treatmentmentioning

confidence: 99%

Effects of Angiotensin-Converting Enzyme Inhibitors or an Angiotensin Receptor Blocker in Combination With Aspirin and Cilostazol on In-stent Restenosis

et al. 2006

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SUMMARYIt remains to be determined whether adding an angiotensin-converting enzyme inhibitor (ACEI) or an angiotensin II receptor blocker (ARB) to antiplatelet therapy has a therapeutic benefit on in-stent restenosis.After successful coronary stenting, 165 patients (167 lesions) were randomly assigned to a basal (aspirin 162 mg + cilostazol 200 mg/day), ACEI (basal treatment + quinapril 10 mg or perindopril 4 mg/day), or ARB (basal treatment + losartan 50 mg/day) treatment group. Quantitative coronary angiography was performed before, immediately following, and 6 months after stenting. Follow-up coronary angiography was completed in 126 patients (128 lesions). Restenosis rates tended to be higher (12, 26, and 12% for the basal, ACEI, and ARB groups, respectively), and target lesion revascularization rates were higher in the ACEI group than in the other groups (9, 23,* and 5%, respectively, *P < 0.05 versus basal group). Moreover, late lumen loss was higher in the ACEI group than in the basal group (0.60 ± 0.55, 0.98 ± 0.61* and 0.73 ± 0.64 mm in the basal, ACEI, and ARB groups, respectively).The combinations of an ACEI or ARB with aspirin and cilostazol are ineffective for the prevention of in-stent restenosis, and an ACEI may even promote intimal proliferation after stent implantation. (Int Heart J 2006; 47: 173-184)

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“…Several experimental studies support the synergy of dual therapy with an ADP antagonist and aspirin. [37][38][39][40][41][42][43] The combination of aspirin plus an ADP antagonist decreases fibrinogen binding and platelet aggregation significantly more than either agent alone. The present study shows that long-term therapy with clopidogrel is superior to aspirin in patients who have had previous cardiac surgery, without an increase in bleeding risks.…”

Section: Dual Therapy With Clopidogrel and Aspirinmentioning

confidence: 99%

Superiority of Clopidogrel Versus Aspirin in Patients With Prior Cardiac Surgery

et al. 2001

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Background-After coronary artery bypass surgery, patients have a high cumulative rate of graft closure and recurrent ischemic events. We sought to determine whether antiplatelet therapy with clopidogrel would be more effective than aspirin, the accepted standard, in these patients. Methods and Results-The event rates for all-cause mortality, vascular death, myocardial infarction, stroke, and rehospitalization were determined for the 1480 patients with a history of cardiac surgery randomized to either clopidogrel or aspirin in a trial of 19 185 patients.

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Comparison of Antiplatelet Effects of Aspirin, Ticlopidine, or Their Combination After Stent Implantation

Abstract: Our results demonstrate synergistic and accelerated platelet inhibitory effects of ticlopidine plus aspirin in patients after stent implantation compared with a monotherapy with either ticlopidine or aspirin alone.

Cited by 107 publications

References 28 publications

Close Relationship between the Platelet Activation Marker CD62 and the Granular Release of Platelet-Derived Growth Factor

Close Relationship between the Platelet Activation Marker CD62 and the Granular Release of Platelet-Derived Growth Factor

Effects of Angiotensin-Converting Enzyme Inhibitors or an Angiotensin Receptor Blocker in Combination With Aspirin and Cilostazol on In-stent Restenosis

Superiority of Clopidogrel Versus Aspirin in Patients With Prior Cardiac Surgery

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