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保守治疗后自发性孤立性肠系膜上动脉夹层的形态重塑与血管造影类型之间的关系:影响系列放射学病程的决定因素

Relationship Between Morphological Remodeling and Angiographic Types of Spontaneous Isolated Superior Mesenteric Artery Dissection After Conservative Management: Determinant Affecting Serial Radiologic Courses.

作者信息

Yuan Zihui, Sheng Shi, You Yun, Li Defu, Wei Qi, Yan Kai, Wang Jian

机构信息

Department of Vascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Department of Hepatobiliary and Gastrointestinal Surgery, Hankou Hospital, Wuhan, China.

出版信息

Front Cardiovasc Med. 2022 Jul 7;9:945141. doi: 10.3389/fcvm.2022.945141. eCollection 2022.

Abstract

OBJECTIVE

To monitor the radiological courses of symptomatic spontaneous isolated superior mesenteric artery dissection (SISMAD) after conservation, clarify the relationship between its morphological change and initial imaging classification, and identify these factors that affect dissection remodeling.

METHODS

Eighty-nine conservative patients with SISMAD who underwent periodic follow-up of computed tomography angiography (CTA) were enrolled. Initial morphologic classification, imaging features and dissection remodeling were analyzed retrospectively. Logistic regression was used to identify predictors for remodeling. Receiver operating characteristics were performed for cutoff threshold.

RESULTS

Zerbib classification was adapted and initial CT appearance divided eighty-nine patients into: type I (15.7%), patent false lumen (FL) with both entry and re-entry; type II (37.1%), "cul-de-sac" shaped FL without re-entry; type III (27.0%), thrombosed FL with ulcer-like-projection (ULP); type IV (18%), intramural hematoma; type V (0%), dissecting aneurysm; and type VI (2.2%), total or partial occlusion of superior mesenteric artery (SMA). Follow-up CTA revealed complete remodeling (33.7%), partial remodeling (16.9%), no change (25.8%), type change (13.5%) and dissection progression (10.1%). There was no dissection-related mortality. Type I (92.9%) sustained patent FL and no angiographic change. Type II showed partial remodeling (42.4%), no change (27.3%) and dissection progression (27.3%), and the length of FL enhancement positively predicted dissection progression with the cutoff of 40.3 millimeters. Type III achieved complete remodeling (58.3%) or evolved into type II (41.7%), and the distance between SMA orifice and ULP negatively predicted type change with the cutoff of 23.5 millimeters. Type IV (87.5%) achieved complete remodeling due to hematoma absorption. One patient underwent stent placement for the evolution of ULP into an enlarged blind-ending FL 2 months after conservation.

CONCLUSION

After conservation, patent FL with a distal re-entry is no morphological change, FL thrombosis tends to be resolved, and the "cul-de-sac" shaped FL without re-entry is partially shortened, no change or progressively dilated. FL enhancement length ≥ 40.3 millimeters is a predictor for the blinding-end FL enlargement. Thrombosed FL with ULP evolves into a patent "cul-de-sac" shaped FL when the distance between SMA orifice to ULP is less than 23.5 millimeters. A careful follow-up is necessary for the lesions with demonstrated predictors.

摘要

目的

监测保守治疗后有症状的自发性孤立性肠系膜上动脉夹层(SISMAD)的影像学病程,阐明其形态学变化与初始影像学分型之间的关系,并确定影响夹层重塑的因素。

方法

纳入89例接受计算机断层血管造影(CTA)定期随访的保守治疗的SISMAD患者。回顾性分析初始形态学分型、影像特征和夹层重塑情况。采用逻辑回归分析确定重塑的预测因素。绘制受试者工作特征曲线以确定截断阈值。

结果

采用Zerbib分型,初始CT表现将89例患者分为:I型(15.7%),真假腔均通畅且有入口和再入口;II型(37.1%),“盲端”型假腔无再入口;III型(27.0%),血栓形成的假腔伴溃疡样突出(ULP);IV型(18%),壁内血肿;V型(0%),夹层动脉瘤;VI型(2.2%),肠系膜上动脉(SMA)完全或部分闭塞。随访CTA显示完全重塑(33.7%)、部分重塑(16.9%)、无变化(25.8%)、类型改变(13.5%)和夹层进展(10.1%)。无夹层相关死亡病例。I型(92.9%)假腔持续通畅且血管造影无变化。II型显示部分重塑(42.4%)、无变化(27.3%)和夹层进展(27.3%),假腔强化长度对夹层进展有正向预测作用,截断值为40.3毫米。III型实现完全重塑(58.3%)或演变为II型(41.7%),SMA开口与ULP之间的距离对类型改变有负向预测作用,截断值为23.5毫米。IV型(87.5%)因血肿吸收实现完全重塑。1例患者在保守治疗2个月后因ULP演变为扩大的盲端假腔而接受了支架置入术。

结论

保守治疗后,有远端再入口的通畅假腔无形态学变化,假腔血栓形成倾向于溶解,无再入口的“盲端”型假腔部分缩短、无变化或逐渐扩张。假腔强化长度≥40.3毫米是盲端假腔扩大的预测因素。当SMA开口与ULP之间的距离小于23.5毫米时,伴有ULP的血栓形成假腔演变为通畅的“盲端”型假腔。对于有明确预测因素的病变,需要密切随访。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36a9/9300881/415b8b78324b/fcvm-09-945141-g001.jpg

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