Collateral Damage: The Hidden Cardiovascular Consequences of Antibiotic Resistance

ABSTRACT Antibiotic resistance (AMR) is a critical global health challenge traditionally discussed within the domain of infectious diseases; however, emerging evidence suggests that its implications may extend to cardiovascular health. This review aims to synthesize current evidence on the potential links between resistant infections and cardiovascular injury, with emphasis on mechanisms that may distinguish resistant infections from infections in general. These factors may facilitate endothelial dysfunction, immune dysregulation, thrombo‐inflammatory activation, and the progression or destabilization of cardiovascular conditions such as atherosclerosis, heart failure, and stroke. This review examines the emerging interplay between antimicrobial resistance and cardiovascular pathology, with particular focus on the infection–inflammation–atherosclerosis axis as a plausible mechanistic framework. Key clinical contexts, including resistant infective endocarditis and cardiovascular device‐associated infections, are highlighted as important examples of this intersection, where multidrug‐resistant pathogens and biofilm formation may compromise clinical outcomes. Furthermore, the review addresses the broader clinical and public health implications of antimicrobial resistance as a potential amplifier of cardiovascular risk, underscoring the importance of integrated, multidisciplinary care and antibiotic stewardship. Clinically, this emerging connection suggests that selected patients recovering from severe or resistant infections may benefit from cardiovascular risk assessment and follow‐up. Public health strategies that reduce antibiotic resistance may also help mitigate downstream cardiovascular complications, although further longitudinal and mechanistic studies are needed. Major knowledge gaps remain, including the limited availability of longitudinal studies comparing cardiovascular outcomes following resistant versus susceptible infections, insufficient mechanistic evidence to establish causality, and the lack of validated biomarkers for identifying high‐risk patients.