• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

先天性心脏病中用于评估肺血管疾病的开胸肺活检。关于矫正手术可操作性的预测价值。

Open lung biopsies in congenital heart disease for evaluation of pulmonary vascular disease. Predictive value with regard to corrective operability.

作者信息

Wagenvoort C A

出版信息

Histopathology. 1985 Apr;9(4):417-36. doi: 10.1111/j.1365-2559.1985.tb02825.x.

DOI:10.1111/j.1365-2559.1985.tb02825.x
PMID:4007787
Abstract

For evaluation of pulmonary vascular disease 140 open lung biopsies were performed in 137 patients with congenital heart disease in order to decide whether the state of the lung vessels would allow corrective surgery. As far as possible follow-up was obtained in patients who underwent a cardiac repair. From the study of these biopsy specimens it appeared that medial hypertrophy of pulmonary arteries and changes in pulmonary veins should not be considered an impediment for a corrective operation as long as more advanced changes are absent. The same is true for intimal thickening due to longitudinal smooth muscle, post-thrombotic changes or cellular proliferation. Concentric-laminar intimal fibrosis forms no contra-indication as long as it is mild but, if severe, it is likely that hypertensive pulmonary vascular disease will progress in spite of cardiac repair. In the presence of fibrinoid necrosis or plexiform lesions correction of a cardiac anomaly should not be attempted. The presence of dilatation lesions is more disputable but probably, as long as they are scarce and not accompanied by fibrinoid necrosis or plexiform lesions, corrective surgery may be attempted. This becomes very dubious when they are more numerous.

摘要

为评估肺血管疾病,对137例先天性心脏病患者进行了140次开胸肺活检,以确定肺血管状况是否允许进行矫正手术。对接受心脏修复手术的患者尽可能进行随访。通过对这些活检标本的研究发现,只要不存在更严重的变化,肺动脉中层肥厚和肺静脉改变不应被视为矫正手术的障碍。因纵向平滑肌、血栓形成后改变或细胞增殖导致的内膜增厚情况同样如此。同心层状内膜纤维化只要程度较轻就不构成禁忌,但如果严重,尽管进行了心脏修复,高血压性肺血管疾病仍可能进展。存在纤维蛋白样坏死或丛状病变时,不应尝试矫正心脏畸形。扩张性病变的情况更具争议性,但只要数量稀少且不伴有纤维蛋白样坏死或丛状病变,可能可以尝试进行矫正手术。当扩张性病变较多时,这就很值得怀疑了。

相似文献

1
Open lung biopsies in congenital heart disease for evaluation of pulmonary vascular disease. Predictive value with regard to corrective operability.先天性心脏病中用于评估肺血管疾病的开胸肺活检。关于矫正手术可操作性的预测价值。
Histopathology. 1985 Apr;9(4):417-36. doi: 10.1111/j.1365-2559.1985.tb02825.x.
2
Reversibility of plexogenic pulmonary arteriopathy following banding of the pulmonary artery.肺动脉束带术后丛状肺血管病的可逆性
J Thorac Cardiovasc Surg. 1984 Jun;87(6):876-86.
3
Lung biopsy specimens in the evaluation of pulmonary vascular disease.用于评估肺血管疾病的肺活检标本。
Chest. 1980 May;77(5):614-25. doi: 10.1378/chest.77.5.614.
4
Histopathologic findings of lung vessels in five children with primary pulmonary hypertension.
Tohoku J Exp Med. 1994 Jan;172(1):9-15. doi: 10.1620/tjem.172.9.
5
Significance of lung biopsy in determining surgical indication in cases of congenital cardiac anomalies with pulmonary hypertension.肺活检在先天性心脏畸形合并肺动脉高压病例手术指征判定中的意义
Tohoku J Exp Med. 1982 May;137(1):33-9. doi: 10.1620/tjem.137.33.
6
Different grades of medial hypertrophy and intimal changes in small pulmonary arteries among various types of congenital heart disease with pulmonary hypertension.不同类型先天性心脏病合并肺动脉高压时小肺动脉中膜肥厚及内膜改变的不同分级
Tohoku J Exp Med. 1997 May;182(1):83-91. doi: 10.1620/tjem.182.83.
7
Short-term survivors of pediatric heart transplantation: an autopsy study of their pulmonary vascular disease.小儿心脏移植短期存活者:其肺血管疾病的尸检研究
J Heart Lung Transplant. 1995 Nov-Dec;14(6 Pt 1):1116-25.
8
Secundum atrial septal defect with severe pulmonary hypertension. Open lung biopsy diagnosis of operative indication.继发孔型房间隔缺损伴重度肺动脉高压。开胸肺活检以明确手术指征。
Chest. 1987 Jan;91(1):33-8. doi: 10.1378/chest.91.1.33.
9
Vascular remodeling process in reversibility of pulmonary arterial hypertension secondary to congenital heart disease.先天性心脏病继发肺动脉高压可逆性中的血管重塑过程
Pathol Res Pract. 2003;199(8):521-32. doi: 10.1078/0344-0338-00457.
10
Longitudinal smooth muscle in pulmonary arteries. Occurrence in congenital heart disease.肺动脉中的纵行平滑肌。在先天性心脏病中的发生情况。
Virchows Arch A Pathol Anat Histopathol. 1984;404(3):265-74. doi: 10.1007/BF00694892.

引用本文的文献

1
Vital Roles of Gremlin-1 in Pulmonary Arterial Hypertension Induced by Systemic-to-Pulmonary Shunts.Gremlin-1 在体肺分流所致肺动脉高压中的重要作用。
J Am Heart Assoc. 2020 Aug 4;9(15):e016586. doi: 10.1161/JAHA.120.016586. Epub 2020 Jul 31.
2
Cellular senescence impairs the reversibility of pulmonary arterial hypertension.细胞衰老损害肺动脉高压的可逆性。
Sci Transl Med. 2020 Jul 29;12(554). doi: 10.1126/scitranslmed.aaw4974.
3
Remodeling Matrix Synthesis in a Rat Model of Aortocaval Fistula and the Cyclic Stretch: Impaction in Pulmonary Arterial Hypertension-Congenital Heart Disease.
大鼠腔静脉瘘和周期性拉伸模型中的重塑基质合成与肺动脉高压-先天性心脏病的撞击。
Int J Mol Sci. 2020 Jun 30;21(13):4676. doi: 10.3390/ijms21134676.
4
"Treat and repair" strategy for shunt lesions: a critical review.分流性病变的“治疗与修复”策略:批判性综述
Pulm Circ. 2020 Apr 9;10(2):2045894020917885. doi: 10.1177/2045894020917885. eCollection 2020 Apr-Jun.
5
Profound Increase of Lung Airway Resistance in Heart Failure: a Potential Important Contributor for Dyspnea.心力衰竭时肺气道阻力的显著增加:呼吸困难的一个潜在重要因素。
J Cardiovasc Transl Res. 2019 Aug;12(4):271-279. doi: 10.1007/s12265-019-9864-y. Epub 2019 Jan 24.
6
Pulmonary vascular disease related to hemodynamic stress in the pulmonary circulation.与肺循环中血流动力性应激相关的肺血管疾病。
Compr Physiol. 2011 Jan;1(1):123-39. doi: 10.1002/cphy.c090004.
7
Congenital pulmonary lymphangiectasis presenting as a unilateral hyperlucent lung.表现为单侧肺透亮度增加的先天性肺淋巴管扩张症。
Eur J Pediatr. 1994 Mar;153(3):202-5. doi: 10.1007/BF01958988.
8
Plexogenic arteriopathy.丛状动脉病
Thorax. 1994;49 Suppl(Suppl):S39-45. doi: 10.1136/thx.49.suppl.s39.
9
Exploration of the pulmonary circulation. Festschrift to Professor Donald Heath.肺循环的探索。献给唐纳德·希思教授的纪念文集。
Thorax. 1994;49 Suppl(Suppl):S1-62. doi: 10.1136/thx.49.suppl.s1.