Acute High-Output Heart Failure with Pulmonary Hypertension and Severe Liver Injury Caused by Amlodipine Poisoning: A Case Report.

IF 3.4 3区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Cardiovascular Toxicology Pub Date : 2024-05-01 Epub Date: 2024-03-26 DOI:10.1007/s12012-024-09849-2
Chenlong Wang, Qingcheng Zhu, Dingyu Tan, Joseph Walline, Yachao Wang
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Abstract

Acute high-output heart failure (HOHF) with pulmonary hypertension and liver injury caused by amlodipine poisoning is very rare. We report a 52-year-old woman who suffered from severe shock after an overdose of amlodipine. Hemodynamic monitoring showed that while her left ventricular systolic function and cardiac output were elevated, her systemic vascular resistance decreased significantly. At the same time, the size of her right heart, her central venous pressure, and the oxygen saturation of her central venous circulation all increased abnormally. The patient's circulatory function and right ventricular dysfunction gradually improved after large doses of vasopressors and detoxification measures. However, her bilirubin and transaminase levels increased significantly on hospital day 6, with a CT scan showing patchy, low-density areas in her liver along with ascites. After liver protective treatment and plasma exchange, the patient's liver function gradually recovered. A CT scan 4 months later showed all her liver abnormalities, including ascites, had resolved. The common etiologies of HOHF were excluded in this case, and significantly reduced systemic vascular resistance caused by amlodipine overdose was thought to be the primary pathophysiological basis of HOHF. The significant increase in venous return and pulmonary blood flow is considered to be the main mechanism of right ventricular dysfunction and pulmonary hypertension. Hypoxic hepatitis caused by a combination of hepatic congestion and distributive shock may be the most important factors causing liver injury in this patient. Whether amlodipine has other mechanisms leading to HOHF and pulmonary hypertension needs to be further studied. Considering the significant increase of right heart preload, aggressive fluid resuscitation should be done very cautiously in patients with HOHF and shock secondary to amlodipine overdose.

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氨氯地平中毒导致急性高输出量心力衰竭伴肺动脉高压和严重肝损伤:病例报告。
由氨氯地平中毒引起的急性高输出量心力衰竭(HOHF)伴肺动脉高压和肝损伤非常罕见。我们报告了一名因过量服用氨氯地平而导致严重休克的 52 岁女性。血流动力学监测显示,虽然她的左心室收缩功能和心输出量升高,但全身血管阻力明显下降。同时,她的右心大小、中心静脉压和中心静脉循环的氧饱和度都异常升高。经过大剂量的血管加压和解毒措施后,患者的循环功能和右心室功能障碍逐渐好转。然而,住院第 6 天,她的胆红素和转氨酶水平明显升高,CT 扫描显示她的肝脏有斑块状低密度区,并伴有腹水。经过保肝治疗和血浆置换后,患者的肝功能逐渐恢复。4 个月后的 CT 扫描显示,包括腹水在内的所有肝脏异常均已消失。该病例排除了 HOHF 的常见病因,认为氨氯地平过量导致的全身血管阻力显著降低是 HOHF 的主要病理生理基础。静脉回流和肺血流量明显增加被认为是右心室功能障碍和肺动脉高压的主要机制。肝充血和分布性休克共同导致的缺氧性肝炎可能是造成该患者肝损伤的最重要因素。氨氯地平导致 HOHF 和肺动脉高压的其他机制还有待进一步研究。考虑到右心前负荷的显著增加,对于氨氯地平过量继发 HOHF 和休克的患者,应非常谨慎地进行积极的液体复苏。
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来源期刊
Cardiovascular Toxicology
Cardiovascular Toxicology 医学-毒理学
CiteScore
6.60
自引率
3.10%
发文量
61
审稿时长
>12 weeks
期刊介绍: Cardiovascular Toxicology is the only journal dedicated to publishing contemporary issues, timely reviews, and experimental and clinical data on toxicological aspects of cardiovascular disease. CT publishes papers that will elucidate the effects, molecular mechanisms, and signaling pathways of environmental toxicants on the cardiovascular system. Also covered are the detrimental effects of new cardiovascular drugs, and cardiovascular effects of non-cardiovascular drugs, anti-cancer chemotherapy, and gene therapy. In addition, Cardiovascular Toxicology reports safety and toxicological data on new cardiovascular and non-cardiovascular drugs.
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