人类免疫缺陷病毒-1 型阳性患者导管消融术后的持续性心房颤动

IF 4.3 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS American journal of preventive cardiology Pub Date : 2024-09-01 DOI:10.1016/j.ajpc.2024.100805
Sophia Navajas MD
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引用次数: 0

摘要

治疗领域其他:电生理学病例介绍一名 35 岁的非裔美国男性,有 HIV-1 感染病史,服用 800 毫克达芦那韦、150 毫克科比司他、200 毫克恩曲他滨和 10 毫克替诺福韦-阿拉非那胺,主诉心悸和出汗。他的智能手表显示静息时心动过速,每分钟 120-140 次。到达医院后,12 导联心电图显示心房扑动,伴有可变的 A-V 传导阻滞。患者的肌钙蛋白 I 为 0.01 纳克/毫升。随后,他接受了经食道超声心动图检查,并通过一次 200 焦耳的同步心脏电复律成功转为窦性心律。经过多学科治疗后,患者出院时服用索他洛尔 80 毫克,一天两次,达比加群 150 毫克,一天两次。首次就诊 45 天后,患者在门诊成功接受了心房扑动消融术。消融术后 65 天,他再次因心房颤动伴室性早搏而入院。目前,患者仍在接受抗凝治疗和频繁的门诊监测,以控制心率。背景心房颤动(房颤)是最常见的心律失常类型。心房颤动是最常见的心律失常类型,是由于心脏心房内的异常电活动导致心房颤动。这种心律失常可能是阵发性的(少于七天),也可能是持续性的(超过七天)(1)。研究人员发现,人类免疫缺陷病毒(HIV)阳性患者的房颤诊断率为每千人年 18.2 例,而未感染 HIV 的患者为每千人年 8.9 例(2)。非肺静脉触发因素在艾滋病毒阳性房颤患者中非常普遍,而且据观察,中长期心律失常复发主要是由这些触发因素引起的(3)。我们介绍的患者是与心律失常复发相关的年轻 HIV-1 阳性男性研究人群中的一员。人们认为,HIV-1 感染会通过全身机制(如低度炎症和氧化应激增加)或直接的心脏毒性(可能导致房颤)增加中风风险(5)。在治疗接受联合抗逆转录病毒疗法(ART)的 HIV-1 患者的心房颤动时,一个重要的考虑因素是这些药物对 CYP2C9 和 CYP3A4 等肝酶的重大影响(6)。这些酶对包括各种口服抗凝剂在内的多种药物的代谢至关重要 (6)。鉴于此,维生素 K 拮抗剂与抗逆转录病毒疗法很可能发生相互作用,尤其是与蛋白酶抑制剂(PIs)或非核苷类逆转录酶抑制剂(NNRTIs)发生相互作用(7)。此外,含有 PIs 的抗逆转录病毒疗法,无论是否含有利托那韦或氯比司他等增强剂,都会显著增加抗心律失常药物的血清浓度(5)。值得注意的是,已证实利托那韦能显著提高血清中地高辛的浓度(5)。还有报道称,与蛋白酶抑制剂合用时,β受体阻滞剂和维拉帕米的浓度也会升高(5)。鉴于这些复杂的相互作用,可能需要为心房颤动的 HIV 患者量身定制调整药物剂量的指南,如 Eliquis 和抗心律失常药物。HIV-1 感染作为额外的卒中风险因素,其作用可能超出 CHA2DS2-VASc 评分,这一点必须进一步研究。
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PERSISTENT ATRIAL FIBRILLATION AFTER CATHETER ABLATION IN HUMAN IMMUNODEFICIENCY VIRUS TYPE‐1 POSITIVE PATIENTS

Therapeutic Area

Other: Electrophysiology

Case Presentation

A 35-year-old African-American male with medical history of HIV-1 infection on 800 mg Darunavir, 150 mg Cobicistat, 200 mg Emtricitabine, and 10 mg Tenofovir Alafenamide presented with the complain of palpitations and sweating. He reported resting tachycardia, 120-140 beats per minute, from his smartwatch. Upon arrival, 12-lead electrocardiogram showed atrial flutter with variable A-V block. Patient's troponin I was <0.01 ng/ml. Subsequently, he underwent transesophageal echocardiogram and was successfully cardioverted to sinus rhythm with one dose of 200 joules of synchronized cardioversion. After multidisciplinary management, patient was discharged on Sotalol 80 mg twice a day and Dabigatran 150 mg twice a day. 45 days after initial presentation, patient underwent successful outpatient atrial flutter ablation. 65 days status post ablation, he again presented and was admitted due to atrial fibrillation with premature ventricular complexes. Currently, patient remains on rate control with anticoagulation treatment and frequent outpatient surveillance. Since the last incidence, no inpatient hospitalizations have been reported.

Background

Atrial fibrillation (AF) is the most common type of cardiac arrhythmia. It is due to abnormal electrical activity within the atria of the heart, causing them to fibrillate. This arrhythmia may be paroxysmal (less than seven days) or persistent (more than seven days) (1). Researcher studies have found that Human Immunodeficiency Virus (HIV)-positive patients had an incidence of 18.2 AF diagnoses per thousand person-years, compared to 8.9 in patients without HIV (2). Non-pulmonary vein triggers are highly prevalent in HIV-positive AF patients and the mid- and long-term arrhythmia recurrence was observed to be mostly driven by those triggers (3). We present a patient who represents part of the growing study population of young HIV-1 positive male associated with arrhythmia recurrence.

Conclusions

The prothrombotic nature of HIV infection is well-documented (4). It is believed that HIV-1 infection elevates stroke risk via systemic mechanisms such as low-grade inflammation and heightened oxidative stress, or through direct cardiac toxicity potentially leading to AF (5). A key consideration in the treatment of atrial fibrillation in patients with HIV‐1 who are in combination antiretroviral therapy (ART), is the significant impact these drugs have on liver enzymes like CYP2C9 and CYP3A4 (6). These enzymes are crucial for metabolizing numerous medications, including various oral anticoagulants (6). Given this, there is a strong likelihood of interactions between vitamin K antagonists and ART, particularly with protease inhibitors (PIs) or non‐nucleoside reverse transcriptase inhibitors (NNRTIs) (7).
Additionally, ART regimens containing PIs with or without boosters like ritonavir or cobicistat, can notably increase the serum concentration of antiarrhythmic drugs (5). Notably, ritonavir has been shown to significantly raise serum digoxin concentration (5). There are also reports of increased beta blocker and verapamil levels when combined with protease inhibitors (5). Given these complex interactions, there may be a need for tailored guidelines for adjusting dosages of drugs, such as Eliquis and antiarrhythmic medications in HIV patients with atrial fibrillation. The role of HIV‐1 infection as an additional stroke risk factor, potentially extending beyond the CHA2DS2‐VASc score, must be further investigated.
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来源期刊
American journal of preventive cardiology
American journal of preventive cardiology Cardiology and Cardiovascular Medicine
CiteScore
6.60
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76 days
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