As health systems mark World Heart Day, new clinical data highlights a critical intersection between common infections and acute cardiovascular emergencies: patients face a significantly elevated statistical probability of experiencing an acute myocardial infarction or a cerebrovascular accident following an episode of herpes zoster, commonly known as shingles.
Research indicates that the association is most marked close to the zoster episode and subsequently tends to diminish. Data shows that during the first three months following herpes zoster, the possibility of presenting a cerebrovascular event is 34% higher, according to a systematic review and meta-analysis published in PLOS One that gathered 12 studies and data from around 7.9 million people. In the case of a heart attack, another investigation published in Open Forum Infectious Diseases found a 35% higher probability during the first 30 days. Experts emphasize that this probability varies depending on the general health and age of the patient, while highlighting the role of vaccination as a prevention tool.
Inflammation and Vascular Risk
The condition appears due to the reactivation of the varicella-zoster virus, which remains latent in the nervous system after chickenpox. Luis Cicco, a cardiologist, explains that the body’s defense process against this reactivation generates systemic inflammation. Cuando se despierta, se reactiva y corre por los nervios, produciendo la conocida infección en la piel, que puede ser muy dolorosa. Todo esto genera un proceso de defensa, que es la inflamación, y se liberan sustancias que pueden afectar sistemicamente, es decir, a todo el cuerpo,
Cicco explains.
According to a 2024 review published in Vaccines, the infection triggers the release of proinflammatory substances that can affect the vascular system and favor coagulation. In individuals with atherosclerosis, this scenario can contribute to destabilizing a plaque and favoring the formation of a thrombus capable of obstructing a coronary artery.
Direct Impact on Cerebral Arteries
For cerebrovascular accidents, a second mechanism involves the direct infection of cerebral artery walls by the virus. Alejandro Andersson, director of the Instituto de Neurología de Buenos Aires, explains: El herpes zóster no produce solamente una inflamación sistémica transitoria. El virus varicela-zóster, cuando se reactiva en los ganglios sensitivos, puede desplazarse por las fibras nerviosas hasta las arterias cerebrales e infectar directamente su pared. Es lo que llamamos vasculopatía por virus varicela-zóster.
This is supported by post-mortem studies cited in the 2024 Vaccines review, which detected viral DNA and antigens in cerebral arteries, confirming the biological basis for this vascular complication.
