No abstract available.
Hyperplasia* ; Neointima* ; Thalidomide*

No abstract available.
Hyperplasia* ; Neointima* ; Thalidomide*

The purpose of this study was to investigate the patency rates and the histologic findings of neoendothelialization according to the length of implanted polytetrafluoroethylene (PTFE) with an internal diameter of 3mm. Under the operating microscope, grafts of 8 and 24mm in length were implanted in the right carotid arteries of thirty rabbits by interrupted end-to-end microanastomosis. They were divided into two groups according to the length of implanted PTFE. Each group had fifteen rabbits. All implanted grafts were 25micro meter in fibril length and 0.39mm in wall thickness. Three grafts per group were harvested at 1, 2, 4, 8, and 12 weeks after implantation and all grafts were observed for patency rates and the histologic findings with a light microscope and scanning electron microscope. In conclusion, there was no difference in patency rates according to the length of implanted PTFE. However, the formation of neointima and subintimal tissue was delayed and incomplete in the longer implanted PTFE group.
Carotid Arteries ; Neointima ; Polytetrafluoroethylene* ; Rabbits ; Transplants

The purpose of this study was to investigate the patency rates and the histologic findings of neoen- dothelialization according to the length of implanted polytetrafluoroethylene (PTFE) with an internal diameter of 3 mm. Under the operating microscope, grafts of 8 and 24 mm in length were implanted in the right carotid arteries of thirty rabbits by interrupted end-to-end microanastomosis. They were divided into two groups according to the length of implanted PTFE. Each group compised fifteen rabbits. All implanted grafts were 25 pm in fibril length and 0.39 mm in wall thickness. Three grafts per group were harvested at 1, 2, 4, 8, and 12 weeks after implantation respectively and all grafts were observed for patency rates and the histologic findings with light microscope and scanning electron microscope. In conclusion, there was no difference in patency rates according to the length of implanted PTFE and histologically the formation of neointima and subintimal tissue was delayed and incomplete in longer implanted PTFE.
Carotid Arteries ; Neointima ; Polytetrafluoroethylene* ; Rabbits ; Transplants

Neointimal hyperplasia is the main mechanism of stent restenosis. Therefore, drug-eluting stents have replaced bare metal stents because there is less neointima and scar formation. Recently, some cases of stent restenosis after using a bare metal stent were found to involve calcification, not neointimal hyperplasia, and regarded as de novo atherosclerosis. We report unusual circular calcification inside a drug-eluting stent, which we called neointimal calcification.
Atherosclerosis ; Cicatrix ; Drug-Eluting Stents ; Hyperplasia ; Neointima ; Stents

Neointimal hyperplasia is the main mechanism of stent restenosis. Therefore, drug-eluting stents have replaced bare metal stents because there is less neointima and scar formation. Recently, some cases of stent restenosis after using a bare metal stent were found to involve calcification, not neointimal hyperplasia, and regarded as de novo atherosclerosis. We report unusual circular calcification inside a drug-eluting stent, which we called neointimal calcification.
Atherosclerosis ; Cicatrix ; Drug-Eluting Stents ; Hyperplasia ; Neointima ; Stents

BACKGROUND AND OBJECTIVES: Artemisinin and dihydroartemisinin are drugs used to treat malaria. These drugs suppress inflammatory reactions. The aim of this study was to examine the anti-intima hyperplasia effect of a novel drug-eluting stent with artemisinin or dihydroartemisinin in a porcine coronary restenosis model. MATERIALS AND METHODS: Pigs were randomized into four groups; in the first, the coronary arteries (20 pigs, a total of 40 coronary arteries, with 10 coronary arteries in each group) was implanted with bare metal stents (BMS, n=10); the second group was given polymer-coated stents (PCS, n=10); the third group was treated with artemisinin-eluting stents (AES, n=10); and the fourth group was given dihydroartemisinin-eluting stents (DAES, n=10). Histopathologic analysis was performed 28 days after stenting. RESULTS: The injury and fibrin scores among the four groups were not significantly different. However, the internal elastic lamina, lumen area, and neointima area were significantly different. Moreover, the percent area of stenosis (46.2±18.66% in BMS vs. 89.4±10.92% in PCS vs. 83.3±17.07% in AES vs. 36.7±11.20% in DAES, p<0.0001) and inflammation score (1.0 [range: 1.0-1.0] vs. 3.0 [range: 2.25-3.0] vs. 3.0 [range: 1.0-3.0] vs. 2.0 [range: 1.75-3.0] in BMS, PCS, AES, and DAES, respectively; p<0.001) were markedly decreased in the DAES group compared to the PCS group. CONCLUSION: DES, which uses a natural substance, dihydroartemisinin, showed a neointima and inflammatory suppressive effect in a porcine coronary restenosis model.
Constriction, Pathologic ; Coronary Restenosis* ; Coronary Vessels ; Drug-Eluting Stents ; Fibrin ; Hyperplasia ; Inflammation ; Malaria ; Neointima ; Stents* ; Swine

BACKGROUND AND OBJECTIVES: Radiation therapy is one of the promising new treatment for restenosis, which is a major problem for the long-term success after angioplasty. We compared radiation therapy only and combined therapy of paclitaxel and radiation on neointimal hyperplasia after injury of rat carotid artery to see whether we can reduce the effective dosage of radiation and thus diminish untoward consequence of radiation if paclitaxel could function as a cell-cycle selective radiosensitizer. MATERIAL AND METHODS: A standardized carotid balloon catheter arterial injury was produced in 65 rats. First group was composed of a single dose of paclitaxel 1 mg/kg body weight, 2 mg/kg or 4 mg/kg, which was administrated intraperitoneally at 2 hours after injury. Second group received external radiation at doses of 2.5 or 5 Gy at 24 hours after injury. Third group was treated with combined paclitaxel-radiation: paclitaxel was injected at 2 hours after injury and then external radiation was delivered 24 hours later. At 21 days after injury, the cross-sectional area of neointima and the ratio of intima/medial area were determined from axial sections using image analysis. RESULTS: Single dose of paclitaxel had no effect in reducing smooth muscle cell proliferation. Minimum effective single dose to inhibit neointimal hyperplasia was 5 Gy. Combined paclitaxel-radiation group except subgroup with paclitaxel 1 mg/kg and 2.5 Gy radiation showed significant reduction of neointimal area compared to group with 2.5 Gy radiation. CONCLUSION: Low-dose external radiation combined with paclitaxel can more effectively inhibit smooth muscle cell pro-liferation and neointimal hyperplasia than radiation only in the rat carotid injury model.
Angioplasty ; Animals ; Body Weight ; Carotid Arteries ; Catheters ; Hyperplasia* ; Myocytes, Smooth Muscle ; Neointima ; Paclitaxel* ; Radiation Dosage ; Rats*

Neointimal hyperplasia mainly develops within several months of coronary stent deployment, after which it stabilizes. Although it was widely accepted, particularly during the bare-metal stent (BMS) era, that in-stent restenosis (ISR) generally does not present as an acute coronary syndrome (ACS), but rather as a gradual recurrence of angina symptoms, recent data have shown that a substantial number of patients with ISR present as ACS. There has also been consistent postmortem evidence of plaque rupture secondary to atherosclerotic change within the neointima of a BMS. We report here a case of ACS in which intravascular ultrasound and optical coherent tomographic assessments revealed neointimal atherosclerotic change and ruptured plaque 10 years after BMS deployment.
Acute Coronary Syndrome ; Coronary Restenosis ; Humans ; Hyperplasia ; Neointima ; Recurrence ; Rupture ; Stents

Intimal accumulation of smooth muscle cells contributes to the development and progression of atherosclerotic lesions and restenosis following endovascular procedures. Arterial smooth muscle cells display heterogeneous phenotypes in both physiological and pathological conditions. In response to injury, dedifferentiated or synthetic smooth muscle cells proliferate and migrate from the tunica media into the intima. As a consequence, smooth muscle cells in vascular lesions show a prevalent dedifferentiated phenotype compared to the contractile appearance of normal media smooth muscle cells. The discovery of abundant stem antigen-expressing cells in vascular lesions also rarely detected in the tunica media of normal adult vessels stimulated a great scientific debate concerning the possibility that proliferating vascular wall-resident stem cells accumulate into the neointima and contribute to the progression of lesions. Although several experimental studies support this hypothesis, others researchers suggest a positive effect of stem cells on plaque stabilization. So, the real contribute of vascular wall-resident stem cells to pathological vascular remodelling needs further investigation. This review will examine the evidence and the contribution of vascular wall-resident stem cells to arterial pathobiology, in order to address future investigations as potential therapeutic target to prevent the progression of vascular diseases.
Adult ; Endovascular Procedures ; Humans ; Myocytes, Smooth Muscle ; Neointima ; Pathology* ; Phenotype ; Stem Cells* ; Tunica Media ; Vascular Diseases