Spontaneous atraumatic epipericardial fat necrosis in the context of recent oocyte retrieval and ovarian hyperstimulation syndrome

IF 2.2 4区 医学 Q2 RADIOLOGY, NUCLEAR MEDICINE & MEDICAL IMAGING
Lea Tiffany, Ranjit Singh, Lincoln J Lim
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引用次数: 0

Abstract

Epipericardial fat necrosis (EFN) is a rare benign, self-limiting cause of acute chest pain that mimics serious clinical conditions such as acute coronary syndrome and pulmonary embolism.1

The exact prevalence is unknown due to its rare occurrence.1 Seventy to ninety per cent of EFN cases are misdiagnosed and often result in over-investigation and unnecessary invasive biopsies.2 Clinically, EFN manifests as acute chest pain, tachycardia and diaphoresis.1, 3 Blood results may include elevated D-dimer, CRP and white blood cell counts.1, 3 Serum troponin levels are usually within normal limits.1

Given the low specificity of clinical findings and blood tests, computed tomography (CT) is paramount for its opportunistic diagnosis. The main CT findings include an encapsulated or well-circumscribed ovoid fatty lesion with surrounding inflammatory changes within epicardial fat.1, 3

A 39-year-old woman (Gravida-2, Para-1) presented with acute retrosternal chest pain, pleurisy and palpitations 4 days after an egg retrieval procedure. Her past medical history includes stage four endometriosis and mild–moderate ovarian hyperstimulation syndrome (conservatively managed).

Her medications include Orgalutran (gonadotrophin-releasing hormone antagonist), and Ovidrel trigger shot (beta-human chorionic gonadotrophin) administered 48 h before oocyte retrieval. There was no history of sepsis or preceding trauma.

The patient was mildly hypertensive (143/92 mmHg) and tachycardic (107 bpm) with good oxygen saturation (98%) and normal respiratory rate (12/min). She had vague focal tenderness on palpation over the left parasternal region. She had an elevated white blood cell count 16.5 (×109/L) (4–11 × 109/L) with neutrophilia 15.5 (×109/L) (2–8 × 109/L), C-reactive protein 56 mg/L (<10 mg/L), D-dimer 14.96 μg/mL (<0.5 μg/mL) and troponin 4 ng/L (<11 ng/L). ECG showed sinus tachycardia. The remaining clinical and biochemical profiles were unremarkable.

Computed tomography pulmonary angiogram was negative for pulmonary embolism. Within the epicardial fat, there was a 15 × 18 × 10 mm soft tissue density structure with surrounding extensive fat stranding (Figs 1-3). There was no pericardial effusion or overlying chondroosseous fracture.

The patient was discharged with a working diagnosis of EFN and had a 3-month follow-up CT which demonstrated complete resolution of the ovoid soft tissue structure with mild residual fat stranding (Figs 4,5).

The exact pathophysiology of EFN is not well understood. Major theories include inflammatory changes within the epipericardial fat and necrosis triggered by torsion of a vascularised fat appendage, Valsalva manoeuvre and trauma.1, 3

Although in vitro fertilisation (IVF)-induced EFN has not been reported in the literature, perhaps inflammation and cardiometabolic changes associated with IVF may have contributed to EFN in our patient. Firstly, inflammatory cascades tend to target highly lipogenic epipericadial fat.4 Moreover, high oestrogen concentrations are associated with a transient increase in left ventricular end-diastolic volume and a decrease in left ventricular ejection fraction up to 7 days post-oocyte retrieval, contributing to ventricular hypertrophy/dilation.5 Elevated steroid levels in ovarian stimulation also increase susceptibility to arrhythmia.5 The exact pathophysiology and association of IVF with EFN remains unclear and should be further explored with future research.

This case aims to increase the awareness of this rare phenomenon which could be opportunistically diagnosed on CT imaging. This would help with the detection, diagnosis and prevent unnecessary invasive investigations. We also hope that this will widen the differential diagnosis of acute chest pain.

Magnetic resonance imaging, a superior imaging modality, could be an alternative imaging alternative to distinguish EFN from fat-containing tumours/lipomatous lesions.1 Despite its unique fat suppression techniques and potential for further characterisation with post-contrast imaging, the downside would be cost, availability of scan slots and lack of cardiac MRI-trained imaging specialists.

Abstract Image

近期取卵和卵巢过度刺激综合征背景下的自发性外伤性心外膜脂肪坏死。
心外膜脂肪坏死(EFN)是一种罕见的良性、自限性急性胸痛病因,可模拟急性冠状动脉综合征和肺栓塞等严重的临床症状。临床上,EFN 表现为急性胸痛、心动过速和心悸。1, 3 血液检查结果可能包括 D-二聚体、CRP 和白细胞计数升高。1, 3 血清肌钙蛋白水平通常在正常范围内。1, 3 一位 39 岁的女性(Gravida-2,Para-1)在取卵术后 4 天出现急性胸骨后胸痛、胸膜炎和心悸。她的药物包括 Orgalutran(促性腺激素释放激素拮抗剂)和取卵前 48 小时注射的 Ovidrel 触发针(β-人绒毛膜促性腺激素)。患者轻度高血压(143/92 mmHg),心动过速(107 bpm),血氧饱和度良好(98%),呼吸频率正常(12/分钟)。触诊时,她的左胸骨旁区域有模糊的局灶性压痛。她的白细胞计数升高,为16.5(×109/L)(4-11×109/L),中性粒细胞增多,为15.5(×109/L)(2-8×109/L),C反应蛋白为56毫克/升(10毫克/升),D-二聚体为14.96微克/毫升(0.5微克/毫升),肌钙蛋白为4纳克/升(11纳克/升)。心电图显示为窦性心动过速。计算机断层扫描肺血管造影显示肺栓塞阴性。心外膜脂肪内有一个 15 × 18 × 10 毫米的软组织密度结构,周围有广泛的脂肪束(图 1-3)。患者出院时被诊断为 EFN,3 个月后进行 CT 随访,结果显示卵圆形软组织结构完全消失,但有轻度残留脂肪滞留(图 4、5)。主要理论包括心外膜脂肪内的炎症变化以及血管化脂肪阑尾扭转、瓦尔萨尔瓦动作和外伤引发的坏死。1, 3 虽然体外受精(IVF)诱发 EFN 的文献未见报道,但与体外受精相关的炎症和心脏代谢变化可能是导致本例患者 EFN 的原因。4 此外,高浓度雌激素与取卵后 7 天内左心室舒张末期容积一过性增加和左心室射血分数下降有关,从而导致心室肥大/扩张。5 试管婴儿与 EFN 的确切病理生理学和关联性仍不清楚,应在今后的研究中进一步探讨。本病例旨在提高人们对这一罕见现象的认识,这种现象可通过 CT 成像择机诊断。本病例旨在提高人们对这一罕见现象的认识,这种现象可通过 CT 成像诊断出来,这将有助于检测和诊断,避免不必要的侵入性检查。1 尽管磁共振成像具有独特的脂肪抑制技术,并具有通过对比后成像进一步确定特征的潜力,但其缺点是成本、扫描时段的可用性以及缺乏经过心脏磁共振成像培训的成像专家。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
3.30
自引率
6.20%
发文量
133
审稿时长
6-12 weeks
期刊介绍: Journal of Medical Imaging and Radiation Oncology (formerly Australasian Radiology) is the official journal of The Royal Australian and New Zealand College of Radiologists, publishing articles of scientific excellence in radiology and radiation oncology. Manuscripts are judged on the basis of their contribution of original data and ideas or interpretation. All articles are peer reviewed.
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