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首页> 外文期刊>European Heart Journal - Case Reports >Spontaneous coronary artery dissection in a patient with hereditary polycystic kidney disease and a recent liver transplant: a case report
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Spontaneous coronary artery dissection in a patient with hereditary polycystic kidney disease and a recent liver transplant: a case report

机译:遗传性多囊肾病患者和近期肝移植患者的自发性冠状动脉解剖:一例报告

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Background Spontaneous coronary artery dissection (SCAD) is an underestimated cause of acute coronary syndromes. A predisposing arteriopathy is often present and a stressor can sometimes be identified. Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary kidney disorder; its associated arteriopathy has been described as a predisposing condition for SCAD.Case summaryA 44-year-old woman with ADPKD presented in the emergency room with recent onset thoracic pain radiating to the left arm at rest. She had undergone a recent liver transplant, for which she had received high-dose corticosteroids during 1 month. She was still taking tacrolimus and mycophenolate mofetil. She had no traditional risk factors but had experienced stress postoperatively. She was known with moderate chronic kidney disease. The initial electrocardiogram (ECG) was normal but high-sensitive troponin T was significantly elevated. Coronary angiography demonstrated diffuse narrowing of the distal left anterior descending artery with preserved flow, compatible with a SCAD Type 2 that was treated conservatively. However, under dual antiplatelet therapy (DAPT) with clopidogrel, the coronary dissection was progressive with new ischaemic ECG changes, further rise of troponins and development of apicoseptal hypokinesia. Because of the small vessel diameter and the preserved distal flow, conservative treatment was maintained. Clopidogrel was interrupted and the patient remained stable.DiscussionAs SCAD remains an underestimated cause of myocardial infarction, clinicians should be aware of the possibility of SCAD in ADPKD patients with chest pain. This case report illustrates that the decision DAPT vs. aspirin should be individualized in these patients.
机译:背景自发性冠状动脉夹层术(SCAD)是急性冠状动脉综合征低估的原因。容易出现易感性动脉病,有时可以确定应激源。常染色体显性遗传性多囊肾病(ADPKD)是最常见的遗传性肾脏疾病;其相关的动脉病变已被描述为SCAD的诱因。案例总结一名44岁患有ADPKD的妇女出现在急诊室,最近发作的胸痛放射到休息的左臂。她最近接受了一次肝移植,并在1个月内接受了大剂量的糖皮质激素治疗。她仍在服用他克莫司和霉酚酸酯。她没有传统的危险因素,但术后经历过压力。她以中度慢性肾脏病而闻名。初始心电图(ECG)正常,但高敏感性肌钙蛋白T明显升高。冠状动脉造影显示左前降支远端远侧弥漫性狭窄,血流得以保留,与经保守治疗的2型SCAD兼容。然而,在使用氯吡格雷双重抗血小板治疗(DAPT)的情况下,冠状动脉夹层进展,伴有新的缺血性ECG改变,肌钙蛋白的进一步升高和阿片中隔运动障碍的发展。由于小血管直径和保留的远端血流,维持了保守治疗。氯吡格雷被打断,患者保持稳定。讨论由于SCAD仍被低估为心肌梗死的原因,因此临床医生应意识到患有胸痛的ADPKD患者的SCAD可能性。该病例报告说明,在这些患者中,DAPT与阿司匹林的决定应个性化。

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