Arterial stiffness in symptomatic smokers with normal lung function

Abstract

Chronic obstructive pulmonary disease (COPD) is associated with cardiovascular morbidity and mortality. Arterial stiffness and endothelial dysfunction index are validated surrogate cardiovascular markers and are increased in subjects with COPD.We tested whether increased arterial stiffness and endothelial dysfunction occur in symptomatic smokers with no evidence of bronchial obstruction. Clinical and lung functional assessments were conducted in smoker subjects with chronic respiratory symptoms and in COPD patients. Pulse wave velocity (PWV), aortic augmentation index (AIx) and reactive hyperaemia index (RHI) were measured to estimate the cardiovascular risk.48 smokers (male n=37, female n=11; mean age 70±8.4 years) were studied. Smokers with respiratory symptoms without bronchial obstruction (n=13) did not differ from COPD patients (n=35) in terms of mean±sd PWV (12±3.2 m·s−1 versus 14±3.8 m·s−1; p=0.10), aortic AIx (25.2±11.8% versus 24.8±9.7%, p=0.89) and RHI (1.66±1.49 versus 1.62±1.43; p=0.79).The current investigation shows that the cardiovascular risk occurs in smokers with respiratory symptoms in the absence of bronchial obstruction. These findings need to be confirmed in larger populations in order to inform the design of intensive preventive programmes.

Inhalation therapy in the next decade: Determinants of adherence to treatment in asthma and COPD

“…Due to the prevalence of early onset of comorbidities in COPD, an early treatment of the disease could be suggested to prevent the burden of comorbid conditions, even if further studies are still required to confirm the efficacy of this approach. For example, an increased risk of cardiovascular disorders has been recently documented in smoker subjects who are symptomatic but have not developed airway obstruction [232]. It has been suggested that the long-lasting exposure to smoke is the driving factor that initiates the inflammatory process both in the lungs and in the arteries, which in turn promotes the excess cardiovascular risk in chronic respiratory patients.…”