Herpes Zoster and Transient Cardiovascular Vulnerability: Mechanisms and Implications for Vaccination

Herpes zoster (HZ), commonly known as shingles, results from reactivation of latent varicella-zoster virus (VZV). Beyond pain and postherpetic neuralgia, HZ is associated with a transient increase in vascular events. This narrative review examines HZ as a vascular trigger, the mechanisms of VZV-associated vascular injury, and the evidence for recombinant zoster vaccine (RZV). Self-controlled studies show that ischemic stroke and myocardial infarction rates peak during the first days to weeks after HZ and decline over subsequent months. Direct arterial infection provides the strongest mechanistic evidence; inflammatory, thrombotic, and autonomic pathways offer additional, less directly established explanations. Randomized trials demonstrate that RZV prevents HZ and postherpetic neuralgia, with sustained protection in long-term follow-up. Associations between vaccination and fewer cardiovascular events derive mainly from observational studies and vary by vaccine platform and endpoint. We use transient post-zoster cardiovascular vulnerability as a clinical framework, not a validated syndrome. Eligible adults should receive RZV for its established prevention benefits, while clinicians should remain alert to new vascular symptoms after HZ. Whether RZV causally reduces cardiovascular events requires dedicated prospective studies and randomized trials.