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Pulmonary dysfunction and development of different cardiovascular outcomes in the general population.
Archives of Cardiovascular Diseases 2018 April
BACKGROUND: Pulmonary dysfunction and cardiovascular disease are major causes of impaired health status in later life, and co-development of these diseases has been reported.
AIM: To better understand the pathobiology involved in the co-development of these diseases.
METHODS: We investigated the impact of pulmonary dysfunction on the development of cardiovascular disease among people aged≥50 years in the English longitudinal study of ageing (ELSA). Hazard ratios were estimated by Cox proportional hazards regression models, with and without a time-dependent update of exposure and confounders. Pulmonary function was divided into three categories, with the least affected category as the reference.
RESULTS: People with pulmonary dysfunction were at higher risk of developing cardiovascular disease than those with normal pulmonary function: the hazard ratio for pulmonary dysfunction versus healthy in the time-dependent crude analysis of model 1, adjusted for age, body mass index, sex, angina pectoris and heart arrhythmia, was 1.49 (95% confidence interval 1.2-1.9). The effect varied with the precise definition of pulmonary dysfunction and the subtype of the cardiovascular disease, and decreased after correction for some additional confounders but not after correction for inflammatory biomarkers.
CONCLUSIONS: A history of pulmonary disease increased the risk of developing cardiovascular disease, but inflammation did not seem to alter the effect of pulmonary dysfunction on cardiovascular disease development. This insight may lead to better understanding and treatment of cardiovascular comorbidities in pulmonary disease; it also indicates that the potentially beneficial effect of targeted anti-inflammatory drugs for pulmonary disease, in terms of reducing cardiovascular risk in these patients, may be limited.
AIM: To better understand the pathobiology involved in the co-development of these diseases.
METHODS: We investigated the impact of pulmonary dysfunction on the development of cardiovascular disease among people aged≥50 years in the English longitudinal study of ageing (ELSA). Hazard ratios were estimated by Cox proportional hazards regression models, with and without a time-dependent update of exposure and confounders. Pulmonary function was divided into three categories, with the least affected category as the reference.
RESULTS: People with pulmonary dysfunction were at higher risk of developing cardiovascular disease than those with normal pulmonary function: the hazard ratio for pulmonary dysfunction versus healthy in the time-dependent crude analysis of model 1, adjusted for age, body mass index, sex, angina pectoris and heart arrhythmia, was 1.49 (95% confidence interval 1.2-1.9). The effect varied with the precise definition of pulmonary dysfunction and the subtype of the cardiovascular disease, and decreased after correction for some additional confounders but not after correction for inflammatory biomarkers.
CONCLUSIONS: A history of pulmonary disease increased the risk of developing cardiovascular disease, but inflammation did not seem to alter the effect of pulmonary dysfunction on cardiovascular disease development. This insight may lead to better understanding and treatment of cardiovascular comorbidities in pulmonary disease; it also indicates that the potentially beneficial effect of targeted anti-inflammatory drugs for pulmonary disease, in terms of reducing cardiovascular risk in these patients, may be limited.
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