Heparin-Coated Stent Placement for the Treatment of Stenoses in Small Coronary Arteries of Symptomatic Patients

Abstract

MD; for the heparin-COAted STents in small coronary arteries (COAST) Trial Investigators* Background-The role of stents, especially of heparin-coated stents for the treatment of stenoses in small coronary arteries, is still unclear. Therefore, we performed this prospective, randomized trial to evaluate the angiographic and clinical outcome after treatment of stenoses in small coronary arteries (2.0 to 2.6 mm) of symptomatic patients. Methods and Results-We randomly assigned 588 patients to angioplasty (nϭ195), bare stenting (nϭ196), or heparin-coated stenting (nϭ197). The primary end point was minimal lumen diameter (MLD) at 6 months. With comparable baseline parameters, the two stent arms showed a larger postinterventional MLD, larger acute gain, and smaller residual percent diameter stenosis, although a residual stenosis of 12Ϯ16% was achieved in the angioplasty arm, including a 27% crossover rate to stenting. Eighty percent of patients had follow-up angiography, which documented a borderline significantly larger MLD and smaller percent diameter stenosis for the two stent groups (1.34Ϯ0.48 mm and 42Ϯ20% after angioplasty, 1.47Ϯ0.48 mm and 36Ϯ20% after bare stenting, and 1.45Ϯ0.54 mm and 38Ϯ23% after heparin-coated stenting; Pϭ0.049 and Pϭ0.038, respectively), but restenosis rates were not different (32%, 25%, and 30%). Thrombotic events occurred in 1.0% after angioplasty and 0.5% after bare or heparin-coated stenting. Survival without myocardial infarction or target vessel revascularization at 250 days was 84.6% (angioplasty), 88.3% (bare stenting), and 88.3% (heparin-coated stenting; log-rank Pϭ0.39). Conclusion-Compared with angioplasty with provisional stenting, bare and heparin-coated stenting confer superior angiographic results and a nonsignificant 24% reduction in clinical events, with no difference between bare and heparin-coated stenting in the treatment of stenoses in small coronary arteries.

Heparin promotes platelet responsiveness by potentiating αIIbβ3-mediated outside-in signaling

“…50 Although heparin-coated stents were previously reported, 51 with some exception, 52 to reduce the incidence of subacute stent thrombosis compared with bare metal stents, a small percentage (Ͻ 1%) of patients experienced low levels of platelet activation leading to clinical thrombosis. Studies aimed at determining whether the molecular mechanisms of nonimmune platelet potentiation described herein contribute to the residual platelet deposition and thrombus formation observed on heparin-coated surfaces in vivo may be an interesting area of future investigation.…”

Ultrasound-Microbubble-Mediated NF-κB Decoy Transfection Attenuates Neointimal Formation after Arterial Injury in Mice

“…Restenosis, which is composed of neointimal formation after percutaneous coronary intervention, is still a clinically serious problem [1,2,3]. Because inflammation is an essential pathological feature of neointimal formation, NF-ĸB plays an important role in this process [4].…”

Fabrication of small-diameter vascular scaffolds by heparin-bonded P(LLA-CL) composite nanofibers to improve graft patency

“…8,9 Heparin is a polysaccharide anticoagulant with potent inhibitory effects on coagulation and a long history of safety and efficacy in the prevention and treatment of thrombosis. 10 Moreover, medical devices coated by heparin, such as vascular grafts 11 and coronary arterial stents, 12 have successfully enhanced the patency rate and improved patient outcomes. Therefore, vascular scaffolds incorporated with heparin may further improve graft patency.…”