Cardiovascular involvement in gram-negative bloodstream infection: Timing, phenotypes, and mechanisms

Gram-negative bloodstream infection (GN-BSI) is associated with a heterogeneous spectrum of cardiovascular manifestations extending beyond the hemodynamic consequences of sepsis. Epidemiological evidence identifies a transient period of heightened cardiovascular vulnerability, with myocardial infarction and ischemic stroke clustering close to BSI onset, alongside myocardial dysfunction, arrhythmias, thrombotic complications, and direct vascular or endovascular infection. These phenotypes likely reflect different interactions between systemic inflammation, endothelial dysfunction, immunothrombosis, underlying cardiovascular disease, and pathogen-specific factors. Persistent bacteremia, prosthetic cardiovascular material, vascular disease, and selected Gram-negative pathogens may identify settings warranting greater cardiovascular attention. However, current evidence remains limited by predominantly retrospective designs, heterogeneous outcome definitions, non-standardized cardiovascular assessment, and limited integration of microbiological and cardiovascular data. This review integrates clinical, epidemiological, and mechanistic evidence to define the timing, phenotypes, and mechanisms of cardiovascular involvement in GN-BSI and proposes a phenotype-driven framework for cardiovascular interpretation and future research.