Abstract Background Cardiovascular diseases (CVDs) remain the leading cause of mortality globally. Despite improved management of conventional CVD risk factors, some CVD cases occur without them, suggesting the potential role of non-conventional factors. Human papillomavirus (HPV), a prevalent sexually transmitted infection, is a well-known causative agent of anogenital cancers. Recent studies have proposed positive associations between HPV and CVD. However, evidence in European populations remains limited. Aim To explore the associations of HPV infection with CVD incidence and mortality. Methods In this population-matched cohort study, we identified exposed women with a new HPV infection before new outcomes during 2006-2022 from Swedish nationwide registers (459,217 for CVD incidence and 479,795 for CVD mortality). Each exposed woman was age-matched with five unexposed women without HPV infection and outcomes at the exposed woman’s index date (HPV infection date), yielding 2,296,085 unexposed women for CVD incidence and 2,398,975 for CVD mortality. Unexposed women were assigned a pseudo-index date corresponding to the index date of their matched exposed woman. Follow-up began at the index/pseudo-index date and continued until the occurrence of the outcome, death, emigration, loss to follow-up, or 31 December 2022, whichever occurred first. Moreover, unexposed women were censored upon developing HPV infection. HPV infection was defined as an abnormal cytological result or a positive high-risk HPV test. CVD diagnoses and deaths were identified using the International Classification of Diseases codes. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using multivariable Cox models stratified by the matching variable, with follow-up time as the underlying time scale. We adjusted for confounders like demographic, socioeconomic factors and medical histories. Results For CVD incidence, the mean age at HPV infection was 36.3 years (standard deviation SD 11.9). Over a follow-up period of up to 17 years (mean 5.62, SD 4.36), the CVD incidence was 8.47 and 7.84 per 1,000 person-years in women with HPV infection and their matched populations, respectively. Women with HPV infection had an elevated risk of developing CVD than the matched population, with an HR (95% CI) of 1.07 (1.06-1.09) after adjustments. For CVD mortality, the mean age at HPV infection was 37.2 years (SD, 12.6). During a mean follow-up time of 5.76 years (SD 4.43), the CVD mortality was 56.62 and 36.57 per 100,000 person-years in women with and without HPV infection, respectively. Women with HPV infection had a higher risk of CVD death than the matched population, with a full-adjusted HR of 1.57 (95% CI 1.47-1.66). Conclusion HPV infection was positively related to CVD incidence and mortality in the study population. Beyond conventional CVD risk factors, HPV infection may warrant consideration in the prevention of CVDs.
Deng et al. (Sat,) studied this question.