• Tomonori Sugiura, Yasuaki Dohi, Hiroyuki Takase, Satoshi Fujii, Yoshihiro Seo, and Nobuyuki Ohte.
• Department of Cardiology, Nagoya City University Graduate School of Medical Sciences.
• Medicine (Baltimore). 2020 Aug 28; 99 (35): e21945e21945.

AbstractAn association between pulmonary and cardiovascular impairment has been reported, but studies are lacking that focus on individuals without advanced impairment in the pulmonary or cardiovascular system. We aimed to investigate the relationship between myocardial microdamage and reduced pulmonary function in the Japanese population without a history of cardiopulmonary disease and to assess whether oxidative stress links the 2 features.We enrolled patients undergoing an annual health check-up and measured serum high-sensitivity cardiac troponin I (hs-cTnI) and derivatives of reactive oxygen metabolites (d-ROM) to evaluate myocardial microdamage and oxidative stress. To assess pulmonary function, we calculated forced vital capacity as a percentage of predicted value, forced expiratory volume in 1 second as a percentage of predicted value, and the ratio of forced expiratory volume in 1 second to forced vital capacity. Possible associations between each parameter of pulmonary function, hs-cTnI, and d-ROM were cross-sectionally investigated.The study included 1265 participants (57 ± 12 years). In multivariate regression analysis, the forced vital capacity as a percentage of predicted value was inversely associated with hs-cTnI levels after adjustment for possible confounders. In another multivariate model, all indices of pulmonary function were inversely correlated with d-ROM levels. We observed similar relationships in a multivariate regression model that included hs-cTnI and d-ROM simultaneously as independent variables. Levels of d-ROM and hs-cTnI also were significantly associated.These results highlight an inverse association of pulmonary function with hs-cTnI and d-ROM in the Japanese population without a history of cardiopulmonary disease. The findings suggest that in individuals without obvious cardiovascular and pulmonary diseases, reduced pulmonary function could reflect myocardial microdamage, at least in part through increased oxidative stress.

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