ArticleJournal of cardiology cases2019
Coronary vasospasm caused by intravenous infusion of dexmedetomidine: Unrecognized pitfall of catheter ablation procedures of atrial fibrillation.
Article in Journal of cardiology cases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 6 citations in OpenAlex.
- Multivessel Coronary Vasospasm Causing Cardiogenic Shock After Anatomically Remote Pulsed Field Ablation for Atrial Fibrillation.JACC. Case reports · 2026Article
- Sedation Strategies, Drugs, and Protocols Used in Catheter Ablation of Atrial Fibrillation: A Focused Review.Reviews in cardiovascular medicine · 2026Review
- Safety of Anesthesia With Dexmedetomidine for Muscle and Nerve Biopsy - A Review of 100 Cases.Cureus · 2025Article
- Coronary vasospasms induced by a dexmedetomidine infusion for deep sedation during catheter ablation in a patient with negative findings of an acetylcholine provocation test.Journal of arrhythmia · 2023Article
- Cardiac arrest due to late-onset coronary artery spasm after radiofrequency catheter ablation in a patient with an implantable cardioverter-defibrillator.Journal of cardiology cases · 2023Article
- Coronary Spasm During Postoperative Sedation With Dexmedetomidine.Anesthesia progress · 2022Article
- Coronary Artery Spasm During Catheter Ablation Caused by the Intravenous Infusion of Isoproterenol.Internal medicine (Tokyo, Japan) · 2021Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Coronary vasospasm is an emerging potentially lethal complication of catheter ablation for atrial fibrillation (AF), however, its mechanism in this setting has not been well elucidated. A 55-year-old man with symptomatic paroxysmal AF underwent pulmonary vein isolation under sedation with propofol. The procedure was completed without any complications. Fifteen months later, a repeated session was performed because of AF recurrence. Initially, a high-dose infusion of dexmedetomidine instead of propofol was administered to introduce sedation. Then, an ST-segment elevation developed in the inferior leads and the diagnosis of coronary vasospasm was made by urgent coronary angiography. A comparison of the procedural details between the first and second sessions identified dexmedetomidine, an α-2 adrenergic agonist with a short distribution half-life, as a potential cause of coronary vasospasm seen only in the second session in the same individual. Since it has been shown that α-2 adrenoreceptor-mediated vasoconstriction can involve the coronary circulation, it is thus possible that a stimulation of α-2 adrenergic receptors induced by dexmedetomidine caused a coronary vasospasm. The present case provides new insights into dexmedetomidine-induced vasospasm. Physicians should be aware of this potentially lethal side effect of dexmedetomidine which is increasingly used in the current AF ablation practice. <
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