脂蛋白(a)是过早出现冠状动脉疾病的原因;一名 34 岁男性患者因 ST 段抬高型心肌梗死而引发的病例报告。

Kateta Edward, Jane Chanda Kabwe, Agness Mtaja, L. Kabwe
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摘要

背景早发性冠状动脉疾病(PCAD)是指冠状动脉疾病(CAD)发生在年轻人群中,男性小于 45 岁。约 80% 的 PCAD 患者存在可改变的危险因素,如吸烟、糖尿病、高血压和肥胖。高血清脂蛋白(a)水平最近已成为 PCAD 的一个风险因素。然而,在急性冠状动脉综合征的年轻患者中,并没有对其进行常规检查。病例介绍 一名 34 岁的非洲男子因左侧胸痛加重 2 小时来我院就诊。他自述过去曾有过长期胸痛病史,当时被当作消化性溃疡病治疗。他还抱怨心率缓慢。他没有传统的心血管风险因素。唯一重要的病史是两个月前刚从 COVID-19 感染中恢复。他的体格检查仅发现心动过缓,心电图显示为高急性下STEMI,无右心室受累。回波显示左心室正常,但射血分数降低(EF:50%),室壁运动异常,与下壁心肌梗死一致。他立即接受了链激酶治疗,临床和心电图反应良好。冠状动脉造影显示,他的右冠状动脉中段出现严重病变和斑块破裂。经皮冠状动脉介入治疗(PCI)获得成功,植入了一个药物洗脱支架。他接受了指南指导的二级预防药物治疗。唯一可能的重要病因是脂蛋白(a)升高(137 毫克/分升)。尽管使用了大剂量烟酸治疗,但随后的血清脂蛋白(a)仍持续升高。医生建议他服用 PCSK9 受体阻断剂,但这种药物在国内无法买到,患者也无法承担费用。事件发生两年后,脂蛋白(a)水平仍然很高。结论:脂蛋白(a)似乎是过早发生冠心病的一个被忽视的重要心血管危险因素,尤其是在没有传统危险因素的情况下。在筛查早发冠心病时,应始终考虑到这一点。该患者的急性发病可能是由 SARS COV-2 感染引发的。
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Lipoprotein (a) as a cause of premature coronary artery disease; a case report of a 34-year-old male patient presenting with ST elevation myocardial infarction.
Background Premature coronary artery disease (PCAD) is considered when coronary artery disease (CAD) occurs in the younger population, less than 45 years old in males. Modifiable risk factors are present in about 80% of patients with PCAD such as smoking, diabetes, high blood pressure and obesity. High serum lipoprotein (a) level has recently emerged as a risk factor for PCAD. However, it is not routinely investigated in young patients presenting with acute coronary syndromes. Case Presentation A 34-year-old African man presented to our hospital with 2 hours of worsening left sided chest pain. He gave a history of long-standing chest pain in the past that was being managed as peptic ulcer disease. He also complained of a slow heart rate. He had no traditional cardiovascular risk factors. The only significant history was a recent recovery from COVID-19 infection two months prior. His physical examination was only significant for a bradycardia, ECG revealed a hyper acute inferior STEMI without right ventricular involvement. Echo showed a normal left ventricle with reduced ejection fraction (EF: 50%), wall motion abnormalities consistent of an inferior MI. He immediately received streptokinase with good clinical and ECG response. His coronary angiogram showed a severe lesion and plaque rupture in the mid-distal segment of a dominant right coronary artery. Percutaneous coronary intervention (PCI) was successfully done, and one drug eluting stent was implanted. He was placed on guideline directed medical therapy for secondary prevention. The only significant possible aetiology found was an elevated Lipoprotein (a) (137mg/dl). Subsequent serum Lipoprotein (a) remained persistently elevated despite therapy with high dose niacin. He was recommended for a PCSK9 receptor blocker, but this medication is not available in the country and the patient could not meet the costs. He remains stable to current medications with no recurrence of chest pain, two years after the index event, the Lipoprotein (a) levels are still high. Conclusions: Lipoprotein (a) appears to be an important overlooked cardiovascular risk factor for premature coronary artery disease especially in the absence of traditional risk factors. It should always be considered in the screening of premature coronary cardiovascular disease. The acute presentation in this patient was probably triggered by SARS COV-2 infection.
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