Eun-Jeong Joo1, Yoosoo Chang2,3,4, Min-Jung Kwon5, Ara Cho2, Hae Suk Cheong1, Seungho Ryu2,3,4. 1. From the Division of Infectious Diseases, Department of Internal Medicine (E.-J.J., H.S.C.), Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea. 2. Center for Cohort Studies, Total Healthcare Center (Y.C., A.C., S.R.), Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea. 3. Department of Occupational and Environmental Medicine (Y.C., S.R.), Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea. 4. Department of Clinical Research Design & Evaluation, SAIHST, Sungkyunkwan University, Seoul, Republic of Korea (Y.C., S.R.). 5. Department of Laboratory Medicine (M.-J.K.), Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea.
Abstract
RATIONALE: Until now, no cohort studies have evaluated the relationship between high-risk human papillomavirus (HPV) infection and new-onset cardiovascular diseases (CVD). OBJECTIVE: We investigated an association between high-risk HPV infection and the development of CVD. METHODS AND RESULTS: We conducted a cohort study of 63 411 women aged 30 or older without CVD at baseline who underwent a high-risk HPV test and were followed annually or biennially from 2011 to 2016. CVD was ascertained through the linkage to the Health Insurance and Review Agency database. A Cox-proportional hazards regression model was used to estimate adjusted hazard ratios (HRs) with 95% CIs of incident CVD. The prevalence of high-risk HPV infection was 7.6%. During 261 598.9 person-years of follow-up, 1122 cases of new-onset CVD were identified (incidence rate of 4.3 per 103 person-years). High-risk HPV infection was significantly associated with incident CVD. After adjustment for possible confounders, and high sensitivity C-reactive protein, a significant association between high-risk HPV infection and incident CVD was still observed, with a corresponding HR (95% CI) of 1.25 (1.03-1.52). This association was stronger among individuals with obesity and those with metabolic syndrome. Multivariable-adjusted HR (95% CI) for incident CVD comparing high-risk HPV-positive- to high-risk HPV-negative participants was 1.10 (0.87-1.39) in the nonobese, whereas corresponding HR (95% CI) was 1.73 (1.19-2.51) in those with obesity ( P for interaction by obesity=0.02). Similarly, multivariable-adjusted HR (95% CI) for incident CVD comparing high-risk HPV-positive- to high-risk HPV-negative participants was 1.09 (0.87-1.36) in those without metabolic syndrome and 1.99 (1.28-3.08) in those with MetS ( P for interaction=0.05). CONCLUSION: In this large cohort, high-risk HPV infection was significantly associated with an increased risk of developing CVD, especially in obese individuals and those with MetS, indicating that high-risk HPV might affect CVD risk with possible effect modification by obesity and MetS.
RATIONALE: Until now, no cohort studies have evaluated the relationship between high-risk human papillomavirus (HPV) infection and new-onset cardiovascular diseases (CVD). OBJECTIVE: We investigated an association between high-risk HPV infection and the development of CVD. METHODS AND RESULTS: We conducted a cohort study of 63 411 women aged 30 or older without CVD at baseline who underwent a high-risk HPV test and were followed annually or biennially from 2011 to 2016. CVD was ascertained through the linkage to the Health Insurance and Review Agency database. A Cox-proportional hazards regression model was used to estimate adjusted hazard ratios (HRs) with 95% CIs of incident CVD. The prevalence of high-risk HPV infection was 7.6%. During 261 598.9 person-years of follow-up, 1122 cases of new-onset CVD were identified (incidence rate of 4.3 per 103 person-years). High-risk HPV infection was significantly associated with incident CVD. After adjustment for possible confounders, and high sensitivity C-reactive protein, a significant association between high-risk HPV infection and incident CVD was still observed, with a corresponding HR (95% CI) of 1.25 (1.03-1.52). This association was stronger among individuals with obesity and those with metabolic syndrome. Multivariable-adjusted HR (95% CI) for incident CVD comparing high-risk HPV-positive- to high-risk HPV-negative participants was 1.10 (0.87-1.39) in the nonobese, whereas corresponding HR (95% CI) was 1.73 (1.19-2.51) in those with obesity ( P for interaction by obesity=0.02). Similarly, multivariable-adjusted HR (95% CI) for incident CVD comparing high-risk HPV-positive- to high-risk HPV-negative participants was 1.09 (0.87-1.36) in those without metabolic syndrome and 1.99 (1.28-3.08) in those with MetS ( P for interaction=0.05). CONCLUSION: In this large cohort, high-risk HPV infection was significantly associated with an increased risk of developing CVD, especially in obese individuals and those with MetS, indicating that high-risk HPV might affect CVD risk with possible effect modification by obesity and MetS.
Authors: Daniel R Dickstein; Marc A Egerman; Anthony H Bui; John T Doucette; Sonam Sharma; Jerry Liu; Vishal Gupta; Brett A Miles; Eric Genden; William H Westra; Krzysztof Misiukiewicz; Marshall R Posner; Richard L Bakst Journal: Oral Oncol Date: 2020-08-31 Impact factor: 5.972
Authors: Daniel R Dickstein; Eric J Lehrer; Kristin Hsieh; Alexandra Hotca; Brianna M Jones; Ann Powers; Sonam Sharma; Jerry Liu; Vishal Gupta; Loren Mell; Zain Husain; Diana Kirke; Krzysztof Misiukiewicz; Marshall Posner; Eric Genden; Richard L Bakst Journal: Cancers (Basel) Date: 2022-06-05 Impact factor: 6.575