Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, No. 167, Beilishi Road, Beijing, 100037, China.
BMC Endocr Disord. 2020 Jul 31;20(1):115. doi: 10.1186/s12902-020-00601-9.
Primary aldosteronism (PA) increases the risk of cardiovascular morbidity, including stroke, coronary artery disease, atrial fibrillation, and heart failure. The relationship between primary aldosteronism and aortic dissection has rarely been reported. We report a case of aortic dissection caused by secondary hypertension from PA and review similar cases in the literature.
A 56-year-old woman with a history of surgery for aortic dissection presented for follow-up of hypertension and a left adrenal mass. She had been diagnosed with hypertension and hypokalemia in 2003. Blood pressure had been controlled by antihypertensive medications. In 2009, she presented with chest and back pain; she was diagnosed with aortic dissection by computed tomography (CT). She underwent placement of an endovascular aortic stent graft. CT at that time showed a left adrenal mass with a diameter of 1 cm. In 2017, CT reexamination revealed that the left adrenal mass had grown to 3 cm in diameter. Laboratory data showed blood potassium 2.4 mmol/L (reference range: 3.5-5.3 mmol/L). The plasma aldosterone/renin ratio was elevated because of suppressed plasma renin and elevated serum aldosterone levels. Plasma aldosterone levels were not suppressed after taking captopril. Positron emission tomography/CT showed that the left adrenal tumor radiographic uptake was slightly increased (maximum standardized uptake value of 2.2), and metastasis was not detected. Laparoscopic adrenalectomy was performed, and an adrenocortical adenoma was confirmed histopathologically. After surgery, blood pressure and laboratory findings were within their reference ranges without any pharmacological treatment.
Our patient and the literature suggest that PA is a potential cause of aortic dissection. Diagnosing PA in the early stages of the disease and early treatment are important because affected patients may be at increased risk of aortic dissection.
原发性醛固酮增多症(PA)增加了心血管疾病发病风险,包括中风、冠心病、心房颤动和心力衰竭。原发性醛固酮增多症与主动脉夹层之间的关系很少有报道。我们报告了一例由 PA 引起的继发性高血压导致的主动脉夹层病例,并回顾了文献中的类似病例。
一名 56 岁女性,曾因主动脉夹层接受过手术,因高血压和左肾上腺肿块就诊。她在 2003 年被诊断为高血压和低钾血症。血压通过降压药物得到控制。2009 年,她出现胸痛和背痛,经计算机断层扫描(CT)诊断为主动脉夹层。她接受了血管内主动脉支架移植术。当时的 CT 显示左肾上腺有一个直径 1 厘米的肿块。2017 年,CT 复查显示左肾上腺肿块直径已增至 3 厘米。实验室数据显示血钾 2.4mmol/L(参考范围:3.5-5.3mmol/L)。由于血浆肾素受抑制和血清醛固酮水平升高,血浆醛固酮/肾素比值升高。服用卡托普利后,血浆醛固酮水平未被抑制。正电子发射断层扫描/CT 显示左肾上腺肿瘤放射性摄取略有增加(最大标准化摄取值为 2.2),未发现转移。行腹腔镜肾上腺切除术,病理组织学证实为肾上腺皮质腺瘤。手术后,血压和实验室检查结果均在参考范围内,无需任何药物治疗。
我们的患者和文献表明,PA 是主动脉夹层的一个潜在病因。在疾病早期诊断并早期治疗 PA 非常重要,因为受影响的患者发生主动脉夹层的风险可能会增加。