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Herpes zoster infection increases risk for stroke, TIA
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Patients with herpes zoster infection appear to be at increased risk for experiencing a stroke or transient ischemic attack, according to data from a South Korean study.
This risk persisted for years after infection, but was less pronounced among older patients, Sung-Han U. Kim, MD, epidemiologist and researcher at Asan Medical Center’s department of infectious diseases, University of Ulsan College of Medicine, South Korea, and colleagues wrote.
“Herpes zoster infection in young people occurs against a background of few other traditional risk factors for stroke, so this is not really a surprise,” Kim said in a press release. “However, it is interesting and more unexpected that the increased stroke risk that followed herpes zoster infection lasted for several years.”
To investigate previous epidemiological studies reporting associations between herpes zoster (HZ) and stroke incidence, Kim and colleagues conducted a population-based cohort study using data from a national South Korean health insurance database. They identified adult patients with ICD-10 codes that indicated a first-ever diagnosis of HZ infection, stroke or transient ischemic attack (TIA) between 2003 and 2013, and compared the risk for stroke/TIA among those with HZ infection to those without HZ infection.
Of the 766,179 patients followed from 2003 for 11 years, first-time incidence of HZ infection was 9.4 cases per 1,000 person-years (95% CI, 9.33-9.47), and there were 9.77 cases per 1,000 person-years (95% CI, 9.7-9.84) for first-time stroke/TIA. Incidence of both outcomes increased with age (P < .001), while HZ was more prevalent among women (P < .001).
The risk for stroke or TIA was greater in patients with previous HZ than in those without (incidence RR = 1.9; 95% CI, 1.85-1.95). This increased risk, however, decreased with age and was greatest among HZ patients aged 18 to 30 years (adjusted HR = 1.52; 95% CI, 1.26-1.83). Further, the researchers noted that the increased risk for stroke and TIA persisted regardless of the number of years since HZ infection.
“We found people to be more at risk of stroke for a long period after infection, even when we adjusted for other known stroke risk factors,” Kim said. “This suggests that infection with this virus is an independent risk factor in stroke pathogenesis that changes the lifetime set point of stroke/TIA risk.”
Although these data demonstrated HZ’s association with increased stroke and TIA risk, the researchers wrote that the biological mechanisms related to these outcomes require more investigation.
“It is possible that the reactivated VZV spreads transaxonally in a centripetal direction like rabies, and reaches the cerebral arteries, and this is followed by transmural spread of the virus,” they wrote. “Another possible mechanism is that zoster itself or post-herpetic neuralgia increases sympathetic status and adverse emotional reactions, theoretically increasing cerebrovascular risk. Alternatively, the reactivation of HZ could alter overall immunological status and increase vulnerability to cerebrovascular events.
“Further studies are needed to elucidate the mechanisms underlying HZ-related stroke.” – by Dave Muoio
Disclosure: The researchers report no relevant financial disclosures.
Perspective
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Brian Silver, MD, FAHA
Consistent with previous studies, the authors found an increased risk for stroke and TIA associated with zoster infection. The additional finding of this study is that the association between zoster infection and stroke/TIA decreased with increasing age. The main limitation of this study, as with all administrative database studies, is the use of codes for identification of disease, which may lead to a bias in detection of true disease.
Despite that limitation, this result, in addition to prior studies, suggests that shingles vaccinations may lead to a reduction in stroke and TIA incidence, assuming zoster infection is truly causal of cerebrovascular disease.
Perspective
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Jean-Paul Stahl, MD, PhD
Kwon and colleagues report a strong association between herpes zoster and stroke, even years after zoster symptoms. Moreover, they demonstrate that young age is clearly associated with stroke. VZ virus with neurological presentations (including ophthalmic and trigeminal zoster), not surprisingly, was correlated with stroke. It is well-known that vasculitis in the brain is common in these presentations, and most frequently responsible for symptoms. Much more surprising is the finding that other zoster presentations are also associated with stroke, as it clearly means that a pathological neurological process is developing, even with no neurological symptoms at the onset. This has to be correlated with recent reports about the frequency of sequels, years after acute encephalitis presentation.
Following this paper, not only encephalitis should be considered. Questions of major importance should be addressed for the future: What about the antiviral efficacy for preventing stroke or for treating it? What about vaccination? Against varicella? Against zoster? What could be the targeted population for this vaccination, as young people seem at higher risk? Should diagnosis procedures, in case of stroke without standard risk factors, include tests for zoster, and what test if any?
An important new concept could be opened after this publication: Physicians should be aware that a lot of infections are not cured at the end of the acute phase. We have to learn to deal with late disorders that are possibly consequences of the infection. We knew that with HIV infections, other pathogens are in the same case, VZ virus being one of them.
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