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Background There is limited comparative clinical data regarding the safety and efficacy profile of paclitaxel delivery via balloon versus stent-polymer matrix. In this study, we aimed to compare the clinical and angiographic results of two different methods of paclitaxel delivery among patients undergoing percutaneous coronary intervention (PCI) for single de novo coronary lesions. Methods A total of 202 patients undergoing PCI due to symptomatic heart disease and at least one significant coronary artery lesion were prospectively enrolled in a multicenter non-inferiority trial. Eligible patients were randomized to a revascularization with either a paclitaxel eluting stent (PES = Coroflex Please, B.Braun) or a bare metal stent (BMS) followed by a paclitaxel coated balloon (PCB) dilation (BMS = Coroflex + PCB = Sequent Please, B.Braun). Clinical follow-up was obtained at 9 months in all patients, whereas angiographic in a subset of 94 (46.5%) patients. Results The baseline characteristics were well balanced between groups. At 9 months, the primary endpoint of in-stent late lumen loss in BMS + PCB was comparable and non-inferior to PES (0.21 ± 0.5 vs. 0.30 ± 0.7 mm, respectively. Pnon-inf < 0.05). At 9 months, the incidence of MACE (7.0 vs. 6.9%, HR = 1, 95%CI: 0.3-2.8; P = 0.99), comprising the occurrence of myocardial infarction (4.9 vs. 3.0%, HR = 1.62, 95%CI: 0.4-6.5; P = 0.32), target lesion revascularization (6.9 vs. 5.0%, HR = 1.42, 95%CI: 0.4-4.4; p = 0.54) and stent thrombosis (4.9 vs. 3.0%, HR = 2.01, 95%CI: 0.5-7.4; P = 0.74) was comparable between BMS + PCB and PES, respectively. In the BMS + PCB group, thrombosis tended to occur within 30 days (3.9 vs. 1.0%; P = 0.38). Conclusions Paclitaxel delivery via drug coated balloon or polymer-stent matrix achieved comparable angiographic and clinical results among patients with de novo coronary lesions. BMS + PCB revascularization was associated with a higher rate of stent thrombosis when compared to newer generation drug eluting stents, therefore, should be recommended as a bail-out for PCB alone angioplasty. [ABSTRACT FROM AUTHOR]

It is generally thought that an increase in collagen may be responsible for increased vascular stiffness with age. We confirmed this in a rodent model of aging where the protein level of both collagen type 1 and type 3, measured by western blotting, increased by 4-fold in the aorta of old versus young rats (P<0.01). We also analyzed the effects of aging on the thoracic aorta in young (6.6±0.5 yr) vs. old (21.2±0.2 yr) monkeys (Macaca fascicularis). Pressure strain elastic modulus and stiffness index measured in conscious monkeys increased in old male monkeys (P<0.01). Histology showed an increase in medial thickness of the aorta and a maintained collagen density, but elastin density decreased significantly with aging (P<0.05) in male monkeys. Opposite to the rat, there was a significant decrease (P<0.05) in collagen type 1 and 3 in aging monkey aorta. In addition, collagen type 8 (which promotes the neo-intimal proliferation) also increased in the aging monkey aorta. Therefore, changes in collagen isoforms and a decrease in elastin may contribute to vascular stiffening in the aging monkey, mechanisms which appear to be dramatically different from the data in aging rodents. [ABSTRACT FROM AUTHOR]