Outcomes of Stent Thrombosis and Restenosis During Extended Follow-Up of Patients Treated With Bare-Metal Coronary Stents

Abstract

Background-Concern regarding risk of late thrombosis after "off-label" treatment with drug-eluting stents has prompted increased use of bare-metal stents (BMS) in current practice. The sequelae of late BMS failures, however, have been poorly characterized. Methods and Results-We performed a retrospective study of 4503 consecutive patients treated with at least 1 BMS and dual antiplatelet therapy between 1994 and 2000. The cumulative incidence of stent thrombosis was 0.5% at 30 days (95% CI, 0.3% to 0.7%), 0.8% at 1 year (95% CI, 0.6% to 1.1%), and 2.0% at 10 years (95% CI, 1.5% to 2.5%

Compartmentation and compartment-specific regulation of PDE5 by protein kinase G allows selective cGMP-mediated regulation of platelet functions

“…Indeed, although it is generally acknowledged that drugs such as aspirin and the thienopyridines can effectively reduce thrombosis in ACS, they are significantly less effective at inhibiting the strong platelet activations associated with thrombolysis or in-stent thrombosis (7,8); the latter represent a significant cause of acute myocardial infarctions and sudden cardiac death (2)(3)(4)(5). In this context, recent attention has shifted to using selective PDE5 inhibitors such as sildenafil citrate (Viagra) for prevention of thrombosis (10,11).…”

“…Arterial occlusions contribute to the pathogenesis of acute coronary syndromes (ACS) (1), a spectrum of conditions including unstable angina and myocardial infarctions. Although drug-eluting stents have largely mitigated the problem of in-stent restenosis after percutaneous coronary interventions, in-stent thrombosis, which can occur anytime after stenting, often presents catastrophically triggering death or acute myocardial infarctions (2)(3)(4)(5)(6). Although anti-platelet agents, including aspirin or thienopyridines, can reduce thrombosis in ACS or at stents, their weak potencies rarely eliminate platelet-mediated re-occlusions in response to strong platelet activation signals, including those associated with thrombolysis (7,8).…”

A Case of Very Late Bare-Metal Coronary Stent Thrombosis Two Weeks after Aspirin Discontinuation, Histopathologic Thrombus Findings and Clinical Considerations

“…Therefore, the expansion of neovascularization to neointima may play a key role in atherosclerotic progression and surrounding tissue instability. In the clinical setting, neointimal growth presenting with later in-stent restenosis is significantly associated with adverse cardiac events [12], confirming the vulnerability of such complex plaques (Figure 2). …”

Very late thrombosis of a bare metal stent despite ongoing aspirin therapy after 10 years of implantation

“…In a report of Doyle et al, the incidence of stent thrombosis associated with BMS is 2% at 10 years and predictors of BMS thrombosis were; ulcerated lesions, vein graft intervention, prior myocardial infarction, prior coronary artery bypass graft operation, prior cerebrovascular accident, prior congestive heart failure and presence of peripheral vascular disease [5]. Generalized vascular inflammation may be the culprit pathophysiological mechanism.…”