C95. The electrocardiographic changes in a hypertensive COVID-19 patient who received beta-blocker and favipiravir: a case report

C95. 接受β受体阻滞剂和法匹拉韦治疗的高血压COVID-19患者的心电图变化:病例报告

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Abstract

BACKGROUND: Various electrocardiographic manifestations have been reported in COVID-19 which either result from myocarditis or insult-induced re-emerging of pre-existing condition. Some antiviruses used off-labelly for COVID-19, including favipiravir, are considered to be proarrhythmic. Meanwhile, anti-hypertensive drugs such as beta-blocker may induce bradyarrhythmia. CASE SUMMARY: A 69-year-old male with confirmed COVID-19 and a history of uncontrolled hypertension presented with blood pressure of 216/111mmHg at admission. No sign and symptom of acute target organ damage had been reported. His electrocardiography showed normal sinus rhythm (heart rate [HR] 60bpm). The echocardiographic finding revealed normal heart function. He received favipiravir for 5 days, intravenous nicardipine (0.5mcg/kgBW/hour), and peroral amlodipine (1x10mg), candesartan (1x16mg), and bisoprolol (1x2.5mg). During hospitalization, the HR fluctuated between 52-109. On the sixth day, a total atrioventricular (AV) block with junctional escape rhythm (HR 66bpm) was present. Both favipiravir and bisoprolol were ceased simultaneously. The AV block persisted for 4 days then transformed into a junctional rhythm for the next 3 days and sinus bradycardia (HR 48bpm) thereafter. No pacing was performed. DISCUSSION: The possible differential diagnoses in this case include sick sinus syndrome (SSS), COVID-19-induced myocarditis, and drug-induced. The SSS might explain the wide variability of the HR. There were some reports presenting the sinus node dysfunction as a manifestation of SARS-CoV-2 infection. Further evaluation using Holter and/or electrophysiological study is warranted. Drug-induced cause may be excluded because the bradyarrhythmia remained after the cessation of both beta-blocker and favipiravir.

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