Recent studies have reported instances of bradyarrhythmia, including SSS, in patients with COVID-19.5–7 The mechanisms by which COVID-19 may induce SSS are multifactorial, encompassing direct invasion of myocardial cells and the conduction system via angiotensin-converting enzyme 2 (ACE2) receptors.8,9 Additionally, the systemic inflammatory response and cytokine storm can exacerbate myocardial injury and disrupt normal cardiac conduction.8–10 Hypoxia resulting from respiratory complications may further impair SA node function and contribute to arrhythmias.11 Here, ACE2 is linked to COVID-19.