表面之下:探究一例左侧环状动脉夹层

IF 4.3 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
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引用次数: 0

摘要

治疗领域其他:非动脉粥样硬化性急性冠状动脉综合征(自发性冠状动脉疾病)病例介绍一名 53 岁的女性患者,有高血压病史,曾患 NSTEMI,左侧心脏造影显示左侧环状动脉有自发性冠状动脉夹层 (SCAD),最初已出院。三天后,她因胸痛返回急诊室。尽管最初计划使用硝基滴注进行积极的血压管理后出院,但由于肌钙蛋白水平不断升高,她不得不接受彻夜观察。进一步的心导管检查显示她患有广泛的 SCAD(起源于左主干远端,延伸至环状动脉,终止于左 PDA 和钝缘支),与一周前做的最后一次血管造影相比,情况有所恶化,可能是由于高血压未得到控制。她被送入重症监护室48小时,接受肝素治疗并严格控制血压,随后出院,医生嘱咐她在心内科门诊进行密切随访。背景SCAD作为非动脉粥样硬化性急性冠状动脉综合征的病因日益得到认可。在所有急性冠状动脉综合征(ACS)病例中,SCAD 占 0.1% 至 0.4%,在 50 岁以下女性急性冠状动脉综合征病例中,SCAD 约占 25%,而在男性急性冠状动脉综合征病例中,SCAD 的发病率较低(男性发病率不足 15%)。风险因素包括女性性别、怀孕、纤维肌发育不良以及与遗传性结缔组织疾病(如马凡综合征和埃勒斯-丹洛斯综合征)有关。它最常发生在左心室动脉。在 46% 到 61% 的病例中,对角支和室间隔支也会受累;15% 到 45% 的病例会累及圆周支、横突支和边缘支。影响多个冠状动脉分支的情况并不常见,但可能发生在 9% 到 23% 的患者身上。诊断主要依靠冠状动脉造影,通过造影可以发现假腔以及内膜破坏和血管出血导致的壁内血肿。对于无进展、血流动力学不稳定或心肌严重受累的病例,主要采用药物治疗,使用阿司匹林、普拉韦克、血管紧张素转换酶抑制剂、β受体阻滞剂和肝素。难治性病例可能需要进行介入治疗,如支架植入术、血管成形术、冠状动脉旁路移植术(CABG)或经皮腔内冠状动脉血管成形术。)10%至30%的患者会因高血压再发心肌梗死。结论SCAD正逐渐被认为是急性心肌梗死的病因,尤其是在心血管风险较低的年轻女性患者中。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
BENEATH THE SURFACE: EXPLORING A CASE OF LEFT CIRCUMFLEX ARTERY DISSECTION

Therapeutic Area

Other: Non Atherosclerotic Acute Coronary Syndromes ( Spontaneous Coronary Artery Disease)

Case Presentation

A 53-year-old woman with a history of hypertension was initially discharged after an NSTEMI and left heart cath showing spontaneous coronary artery dissection (SCAD) in the left circumflex artery. She returned to the ER three days later with chest pain. Despite initial plans for discharge with aggressive BP management using a nitro drip, her rising troponin levels necessitated overnight observation. Further cardiac cath revealed extensive SCAD (originating in the distal left main, extending into the circumflex, and terminating in the left PDA, as well as the obtuse marginal branch), worsening from the last angiogram done a week ago, likely due to uncontrolled hypertension. She was admitted to the ICU for 48 hours for heparin therapy and strict BP control, and was later discharged with instructions for close outpatient cardiology follow-up.

Background

SCAD emerges as an increasingly acknowledged etiology behind non-atherosclerotic acute coronary syndromes. SCAD is implicated in 0.1% to 0.4% of all acute coronary syndrome (ACS) occurrences and is re-sponsible for about 25% of ACS instances in women under 50 and less commonly in men ( less than 15% of instances affect men). Risk factors include female sex, pregnancy, fibromuscular dysplasia, and associations with genetic connective tissue disorders such as Marfan and Ehlers-Danlos syndromes. It most commonly occurs in the LAD artery. In 46 to 61% of instances, the diagonal and septal branches are also in-volved; 15 to 45% of cases involve the circumflex, ramus, and marginal branches. Affecting several coronary branches is uncommon, but may occur in 9 to 23% of patients. Diagnosis predominantly relies on coronary angiography, which identifies the false lumen and intramural hematoma resulting from intimal disruption and vasa vasorum bleeding. Treatment is primarily medical for cases without progression, hemodynamic instability, or significant myocardial involvement, utilizing aspirin, plavix, ACE inhibitors, beta blockers, and heparin. Refractory cases may necessitate interventional strategies like stenting, angioplasty, coronary artery bypass grafting (CABG), or percutaneous transluminal coronary angioplasty). Reoccurrence from HTN occurs in 10 to 30% of patients.

Conclusions

SCAD is becoming recognized as the cause of acute myocardial infarction, particularly in young female patients with low cardiovascular risks.
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来源期刊
American journal of preventive cardiology
American journal of preventive cardiology Cardiology and Cardiovascular Medicine
CiteScore
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76 days
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