van den Brand M, Essed C E, Di Mario C, Plante S, Mochtar B, de Feyter P J, Suryapranata H, Serruys P W
Department of Cardiology, University Hospital, Rotterdam, Dijkzigt.
Br Heart J. 1992 Jun;67(6):445-9. doi: 10.1136/hrt.67.6.445.
To investigate whether balloon dilatation of the aortic valve induces long-term macroscopic or histological changes or both to explain the restenosis process.
Prospective study of 39 consecutive patients. Sixteen later (mean (SD) 12 (10) months) required operation. This non-randomised subgroup was compared with 10 patients who had aortic valve replacement without prior dilatation.
University cardiology and cardiac surgery centre and pathology department.
16 patients who had aortic valve replacement because of failure of or restenosis after balloon dilatation of the aortic valve. Twelve resected valves were examined.
Percutaneous balloon dilatation of the aortic valve (maximal balloon size: trefoil 3 x 12 mm balloon or bifoil 2 x 19 mm balloon) and surgical inspection before excision of the aortic valve leaflets during open-chest aortic valve replacement. Fixation, decalcification, and staining for histology.
Presence of long-term pathological changes in the resected valve and their relation to restenosis after balloon dilatation.
Macroscopically the previously dilated valves were indistinguishable from valves from the patients who had valve replacement only. Microscopically, the dilated aortic valves showed areas of young scar tissue that were not seen in a control group of surgically excised stenotic aortic valves. This persistent scarring reaction was seen around small tears or lacerations of the collagenous valve stroma, fractures in calcified areas, and splits in commissures. Young scar tissue without collagenisation was still present 24 months after dilatation.
Organisation and collagenisation of scar tissue develops slowly after balloon dilatation of the aortic valve. This prolonged scarring reaction may explain the late development of restenosis in some patients.
研究主动脉瓣球囊扩张术是否会引起长期的宏观或组织学改变，或两者兼而有之，以解释再狭窄过程。
对39例连续患者进行前瞻性研究。其中16例患者在（平均（标准差）12（10）个月）后需要进行手术。将这个非随机分组的亚组与10例未预先扩张而进行主动脉瓣置换术的患者进行比较。
大学心脏病学和心脏外科中心及病理科。
16例因主动脉瓣球囊扩张术失败或再狭窄而进行主动脉瓣置换术的患者。检查了12个切除的瓣膜。
经皮主动脉瓣球囊扩张术（最大球囊尺寸：三叶瓣用3×12mm球囊或双叶瓣用2×19mm球囊），并在开胸主动脉瓣置换术切除主动脉瓣叶之前进行手术检查。进行组织学固定、脱钙和染色。
切除瓣膜中是否存在长期病理改变及其与球囊扩张术后再狭窄的关系。
宏观上，先前扩张的瓣膜与仅接受瓣膜置换术患者的瓣膜无法区分。微观上，扩张的主动脉瓣显示出年轻瘢痕组织区域，而在手术切除的狭窄主动脉瓣对照组中未见此现象。这种持续的瘢痕反应出现在胶原瓣膜基质的小撕裂或裂伤周围、钙化区域的骨折处以及瓣叶交界处的裂开处。扩张后24个月仍存在无胶原化的年轻瘢痕组织。
主动脉瓣球囊扩张术后瘢痕组织的机化和胶原化发展缓慢。这种延长的瘢痕反应可能解释了一些患者再狭窄的晚期发生。
