Table 2: Summary of Mechanisms Underlying Drug-induced AF Discussed in this Review.

Classifications	Drugs	Mechanisms by Which Drugs Might Induce AF										Incidence
		EADs	DADs	Abnormal Automaticity	Reentry	Sympathomimetic Actions	Parasympathomimetic Actions	Cardiotoxicity and Injury	Electrolyte Disturbance	SAN Dysfunction	Hyperthyroidism		Data Source
Sympathetic activating agents	Dobutamine		√	√		√						0–18%	Randomised, open-label, multicentre study
Cholinergic activators	ACh				√		√					0.1–17.1%	Single-centre study
Diuretics	Loop diuretics, thiazides								√			NA	Case reports
Cardiac calcitropes	Milrinone		√									4.6–5%	Randomised, open-label, multicentre study
Vasodilator	Nicorandil				√							NA	Nested case-control study
Antiarrhythmic agents	Adenosine				√							1–12%	Prospective analysis
	Amiodarone										√	NA	Case reports
	Ivabradine									√		1.30%	Meta-analysis
Traditional cytotoxic drugs	Anthracyclines		√					√				6–10.3%	Single-centre study
Novel molecular anti-tumour therapy	Ibrutinib		√					√				3–16%	Meta-analysis
	Trastuzumab		√					√				1.20%	Meta-analysis
Immunotherapies	ICIs		√					√				1.1–30%	Meta-analysis
	CAR-T therapy		√					√				2.07%	Meta-analysis
Drugs of abuse	Alcohol				√	√		√				Acute: 0.8%; chronic 25–47%	Meta-analysis
	Tobacco					√		√				1.17% for substance use disorder	Prospective studies
	Marijuana					√		√

ACh = acetylcholine; CAR-T therapy = chimeric antigen receptor T-cell therapy; DAD = delayed afterdepolarisation; EAD = early afterdepolarisation; ICI = immune checkpoint inhibitor; NA = not applicable; SAN = sinoatrial node.