Notes: Sixteen balloon expandable Medtronic Wiktor tantalum stents were implanted in the major coronary arteries of six minipigs, which were maintained on a normal diet and given 500 mg aspirin per day. Angiographic and histologic examinations were performed 6 and 26 weeks after implantation. Angiographically reviewed, stenting increased the inner diameter of the coronary arteries from 2.61 ± 0.44 to 3.02 ± 0.34 mm (n = 16, P ≤ 0.001). Six weeks later, this value was reduced from 2.98 ± 0.35 to 2.33 ± 0.46 mm (n = 9, P ≤ 0.05), and between 6 and 26 weeks, an increase from 2.17 ± 0.44 to 2.93 ± 0.40 mm occurred (n = 6, P ≤ 0.05). Histologic evaluation at 26 weeks after stent implantation revealed an increase of the cross-sectional area of the total vessel from 4.30 ± 1.09 to 5.50 ± 1.67 mm2 (n = 9; P ≤ 0.01). This was due to widening of the total vessel and intimal proliferation, which amounted to 1.19 ± 0.46 mm2 within the stented segment, as compared to 0.03 ± 0.03 mm2 in control sections (P ≤ 0.01). The areas of free vessel lumen, media muscularis, and adventitia remained unchanged. In 15 of the 16 hislologically examined coronary arteries, the internal elastica was fractured at the site of stent implantation. Twelve stents had also penetrated through the external elastica without evidence of wall hemorrhage. Thirteen out of 16 stents were angiographically followed, of which 12 were patent at the final reangiography. In one animal, acute thrombosis of the stented vessel after guidewire induced coronary artery spasm caused chronic right heart failure due to right ventricular myocardial infarction. Sudden death occurred in another pig 2 hours after successful implantation of three grossly oversized stents (inner vessel diameter: 2.4 ± 0.2 mm, stent diameter 3.2 ± 0.5 mm). Autopsy revealed extensive dissections of the media with subsequent vessel occlusion. It is concluded that Medtronic Wiktor stents can be placed easily, even in more distal or curved coronary arteries. Despite antiaggregational medication, intimal proliferation is observed early after implantation, reaches a maximum at about 6 weeks, and is followed by a regression 26 weeks poststenting. At 26 weeks follow-up, the free vessel lumen at the stent site was not significantly reduced as compared to control segments. Proper adjustment of internal vessel diameter and stent diameter is necessary to prevent major dissections and thrombotic occlusions.

Notes: We report about the 6-month follow-up of 28 consecutive patients treated with a new tantalum stent (Wiktor™ stent, Medtronic, Inc.). Indication for stenting was the prevention of restenosis in eight patients (restenosis group), and threatening or acute closure after PTCA in 20 patients (acute closure group). Twenty-eight of 30 stents were successfully positioned in 27 of 28 patients (96%), whereas implantation failed twice in one patient. Immediate stent occlusion developed in two patients in the acute closure group (7.4%). Subacute stent occlusion was observed in three patients (11%), one in the restenosis group, two in the acute closure group, between 3 and 5 days after implantation. Coronary bypass surgery had to be performed in four patients (15%): one patient after failed stent placement, two after acute, and one after subacute stent thrombosis. Major bleeding complications related to the anticoagulative drug regimen occurred in nine patients (33%). Three patients (11%) died for reasons most probably not related to stent implantation. A 6-month angiographic follow-up revealed restenosis in two of 19 patients (11%), one patient in each group. Sixteen of the 27 stented patients (59%) reached 6-month follow-up without death, acute or subacute stent thrombosis, or restenosis. It is concluded that the Wiktor stent can be placed with a high rate of success. It may also reduce the risk of restenosis. The stent also offers the possibility to circumvent emergency bypass surgery in case of PTCA related vessel occlusion. Acute and subacute stent occlusion still remains an unsolved topic.