The pathophysiology of arrhythmias is complex, involving changes in cardiac contractile and conduction systems, electrical conduction heterogeneity, and structural alterations. Recent studies indicate that cardiac macrophages can induce arrhythmias by interacting with cardiomyocytes or altering tissue composition. Due to the heterogeneity and diversity, macrophages develop different cellular functions during pathological processes. This review identifies various macrophage subpopulations and focuses on their pathological mechanisms in arrhythmogenesis. Furthermore, we explore the interactions of macrophages with other immune cells and summarize the promising approaches for targeting macrophages in arrhythmias treatment. Macrophages directly or indirectly influence arrhythmogenesis through multiple systemic effects. Preclinical studies suggest that modifying macrophages' phenotype or regulating their activity may directly affect cardiac conduction. This review provides a theoretical basis for developing immunotherapies for patients with cardiac arrhythmias.