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Sci Rep . Increased cardiomyopathy risk after viral infection evidence from a nationwide cohort in Taiwan

tetano

Editor, Senior Moderator
Sci Rep


. 2025 Nov 24;15(1):41561.
doi: 10.1038/s41598-025-25454-x. Increased cardiomyopathy risk after viral infection evidence from a nationwide cohort in Taiwan

Pi-Ching Yu[SUP] #[/SUP][SUP] 1 2 [/SUP], Ho-Tsung Hsin[SUP] #[/SUP][SUP] 2 3 [/SUP], Ren-Jei Chung[SUP] 4 [/SUP], Shi-Hao Huang[SUP] 4 [/SUP], Tsu-Hsuan Weng[SUP] 5 [/SUP], Bing-Long Wang[SUP] 6 7 [/SUP], Chi-Hsiang Chung[SUP] 5 6 8 [/SUP], Yao-Ching Huang[SUP] 9 10 11 [/SUP], Wu-Chien Chien[SUP] 12 13 14 15 16 [/SUP], Yi-Chang Lin[SUP] #[/SUP][SUP] 17 [/SUP], Chien-Sung Tsai[SUP] 18 19 [/SUP], Li-Yun Fann[SUP] 20 21 22 [/SUP]



Affiliations
Abstract

Viral infections have been linked to myocarditis and may contribute to the development of cardiomyopathy. However, large-scale population-based evidence remains limited. This study aimed to investigate the association between viral infections and the subsequent risk of cardiomyopathy using Taiwan's Longitudinal Generation Tracking Database (LGTD). We conducted a nationwide, retrospective cohort study using Taiwan's National Health Insurance Research Database/LGTD. Individuals with a first recorded viral infection were matched to unexposed controls using 1:4 propensity scores incorporating demographics, comorbidities, medications, healthcare utilization, and index year. Incident cardiomyopathy was ascertained from ICD-9-CM diagnosis codes in claims data, without clinical adjudication or imaging confirmation. Risks were estimated using Cox proportional hazards models to obtain adjusted hazard ratios (aHRs) and 95% confidence intervals (CIs). Robustness was assessed via Fine-Gray competing-risk models for death, proportional-hazards diagnostics, alternative exposure/lag definitions, and prespecified subgroup analyses by age, sex, comorbidity burden, and virus categories. Over a mean follow-up of approximately 10 years, the incidence rate of cardiomyopathy was higher in the viral infection group (98.42 per 100,000 person-years) than in the control group (45.69 per 100,000 person-years). Viral infection was significantly associated with increased risk of cardiomyopathy (aHR = 2.915, 95% CI 1.177-4.828, p < 0.001). Subgroup analyses showed consistent risk elevation across sex (male aHR = 2.775; female aHR = 3.097), age groups, income levels, seasons, and urbanization levels (all p < 0.05). Among viral subtypes, viral hepatitis (aHR = 3.435), influenza (aHR = 3.002), and viral pneumonia (aHR = 3.091) were most strongly associated with cardiomyopathy. In this population-based cohort, viral infection was associated with increased long-term risk of cardiomyopathy. Given that outcomes were identified from administrative codes without clinical or imaging validation, causal inference is not warranted; however, the findings support post-infection cardiovascular surveillance and prevention strategies. Further studies integrating adjudicated clinical data, imaging, and biomarkers are needed to clarify mechanisms and refine risk stratification.

Keywords: Cardiomyopathy; Cohort study; Competing risks; ICD-9-CM; Propensity score; Viral infection.

 
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