Desmarais Taylor, Yang Jenny, Narezkina Anna, Fernandes Timothy
Department of Medicine, University of California San Diego, San Diego, CA, USA.
Division of Pulmonary, Critical Care, and Sleep Medicine, University of California San Diego, San Diego, CA, USA.
Respir Med. 2023 Jan;206:107071. doi: 10.1016/j.rmed.2022.107071. Epub 2022 Dec 7.
Multiple myeloma is often complicated by pulmonary hypertension through a variety of mechanisms. These mechanisms include pulmonary hypertension (PH) due to concomitant cardiac amyloid, high output heart failure due to anemia or lytic bone lesions, chronic thromboembolic pulmonary hypertension (CTEPH), toxicity from medications to treat multiple myeloma, and congestive heart failure. This case series highlights the various mechanisms through which multiple myeloma patients develop pulmonary hypertension.
To identify the etiologies of pulmonary hypertension and their management among multiple myeloma patients treated at University of California San Diego.
A retrospective chart review was performed to identify patients with multiple myeloma and pulmonary hypertension who were evaluated at the University of California San Diego between July 2013 and July 2021. Patients also required a right heart catheterization to be included. Demographics, comorbidities, clinical course, and etiology of pulmonary hypertension were obtained from chart review.
There were 11 patients included. Of the 11 patients described, two had PH due to cardiac amyloid, one had PH due to high output heart failure, one had PH due to CTEPH, two had pulmonary arterial hypertension due to medications (carfilzomib), and five had PH due to congestive heart failure. The right heart catheterization and echocardiogram findings of the various mechanisms of PH in multiple myeloma are described.
Pulmonary hypertension in multiple myeloma is a common finding that necessitates further evaluation. The initial evaluation should include an echocardiogram and thorough medication review. Further diagnostic testing should be guided by the patient's history and can include right heart catheterization, cardiac biopsy, ventilation-perfusion scan, and bone scan.
多发性骨髓瘤常通过多种机制并发肺动脉高压。这些机制包括因合并心脏淀粉样变导致的肺动脉高压（PH）、因贫血或溶骨性骨病变导致的高输出量心力衰竭、慢性血栓栓塞性肺动脉高压（CTEPH）、治疗多发性骨髓瘤药物的毒性以及充血性心力衰竭。本病例系列强调了多发性骨髓瘤患者发生肺动脉高压的各种机制。
确定在加利福尼亚大学圣地亚哥分校接受治疗的多发性骨髓瘤患者中肺动脉高压的病因及其管理方法。
进行回顾性病历审查，以确定2013年7月至2021年7月期间在加利福尼亚大学圣地亚哥分校接受评估的患有多发性骨髓瘤和肺动脉高压的患者。患者还需要进行右心导管检查才能纳入研究。从病历审查中获取人口统计学、合并症、临床病程和肺动脉高压的病因。
共纳入11例患者。在所描述的11例患者中，2例因心脏淀粉样变导致PH，1例因高输出量心力衰竭导致PH，1例因CTEPH导致PH，2例因药物（卡非佐米）导致肺动脉高压，5例因充血性心力衰竭导致PH。描述了多发性骨髓瘤中PH各种机制的右心导管检查和超声心动图结果。
多发性骨髓瘤中的肺动脉高压是一个常见发现，需要进一步评估。初始评估应包括超声心动图和全面的药物审查。进一步的诊断测试应根据患者的病史进行指导，可包括右心导管检查、心脏活检、通气灌注扫描和骨扫描。
