Polymer-free Biolimus A9-coated stents in the treatment of de novo coronary lesions with short DAPT: 9-month angiographic and clinical follow-up of the prospective, multicenter BioFreedom USA clinical trial.

BACKGROUND: BioFreedom is a polymer- and carrier-free drug-coated stent that delivers Biolimus A9 to the vessel wall. Our purpose was to evaluate the efficacy and safety of this DCS in patients with short-duration dual antiplatelet therapy. METHODS: The BioFreedom US IDE feasibility trial was a single-arm, open-label, prospective study of patients requiring stenting of de novo lesions. Patients received 3 months of DAPT, repeat angiography at 9 months, and clinical follow-up at multiple intervals. A subgroup also underwent intravascular ultrasound (IVUS) interrogation. The primary safety end point was major adverse cardiac events, defined as a composite of cardiac death, myocardial infarction, target lesion revascularization, or stent thrombosis. The primary efficacy end point, in-stent late lumen loss at 9 months, was compared with a historical control from a first-generation paclitaxel-eluting stent. RESULTS: A total of 72 patients from 10 sites received BioFreedom DCS implanted in 83 de novo lesions. At 9 months, the incidence of composite MACE was 8.4%, and TLR was 1.5%. Short DAPT was safe without occurrence of stent thrombosis. The primary end point of LLL was 0.32±0.53 mm. Paired IVUS analyses comparing postprocedural with 9-month measurements showed low in-stent neointimal volume obstruction (5.39±5.28%) and low neointimal hyperplasia (7.43±8.04 mm3). CONCLUSIONS: This study's angiography and IVUS assessments demonstrated that the BioFreedom DCS has anti-restenotic efficacy similar to first-generation DES. In the absence of concerning safety signals, this DCS should be considered effective and safe for patients who require a shorter duration of DAPT.

Elastinolytic matrix metalloproteinases and their inhibitors as therapeutic targets in atherosclerotic plaque instability.

Atherosclerosis is a dynamic pathologic process involving interactions between many cell types and chemical mediators. There is increased evidence in the literature that matrix metalloproteinases, especially those with elastolytic activity, are associated with atherosclerotic plaque instability. Results of recent studies also suggest that the balance between matrix metalloproteinases and their inhibitors contributes to the extracellular matrix integrity, and an imbalance could be a predeterminate of both cerebral and cardiac ischemic events. Significant evidence demonstrates that the balance between elastolytic matrix metalloproteinases and their inhibitors are involved in the atherosclerotic process. Studies investigating pharmacologic therapies that inhibit matrix metalloproteinases or increase their natural inhibitor levels suggest an antiatherosclerotic and potential plaque-stabilizing benefit. Carefully designed clinical trials must be completed to better understand the functions and interactions of these enzymes with the goal of developing selective therapies to prevent the progression and complications of atherosclerosis.