Age and cigarette smoking modulate the relationship between pulmonary function and arterial stiffness in heart failure patients

Abstract

The aim of this study was to assess the relationship between arterial stiffness and pulmonary function in chronic heart failure (CHF).Outpatients previously diagnosed as CHF were enrolled between April 2008 and March 2010, and submitted to arterial stiffness measurement and lung function assessment. Spirometry was performed by measuring forced vital capacity (FVC), the fraction of predicted FVC, forced expiratory volume in 1 second (FEV1), the percentage of predicted FEV1 in 1 second, FEV1 to FVC ratio, and the percentage of predicted FEV1/FVC. Cardio-ankle vascular index (CAVI) was considered for the estimation of arterial stiffness.The 354 patients assessed included 315 nonsmokers, and were 68.2 ± 7.2 years’ old. Unadjusted correlation analyses demonstrated CAVI was positively related to age (r = 0.3664, P < 0.0001), and negatively related to body mass index (BMI, r = −0.2040, P = 0.0001), E/A ratio (r = −0.1759, P = 0.0010), and FEV1 (r = −0.2987, P < 0.0001). Stepwise multivariate regression analyses showed age (r2 = 0.2391, P < 0.0001), BMI (r2 = −0.2139, P < 0.0001), smoking (r2 = 0.1211, P = 0.0130), E/A ratio (r2 = −0.1082, P = 0.0386), and FEV1 (r2 = −0.2550, P < 0.0001) were independent determinants of CAVI. In addition, there is a significant interaction between CAVI and forced expiratory volume in 1 second (FEV1) in relation to age (Pint < 0.0001) and smoking (Pint = 0.0001). Meanwhile, pulmonary function was not associated with BMI or E/A ratio.These findings demonstrated that reduced pulmonary function is associated with the increased CAVI, and had an interactive effect with age and smoking on CAVI in patients with CHF.

Association between persistent smoking after a diagnosis of heart failure and adverse health outcomes: A systematic review and meta-analysis

“…Specifically, chemical constituents of smoke have high oxidant and inflammatory power that can directly induce endothelial damage and potentiate inflammatory response [28][29][30] . Namely, cigarette smoking can promote atherosclerosis by its effects on lipid profile 25,31 . Moreover, according to one study 32 , nicotine along with carbon monoxide and oxidative stress induce fibrosis at different cardiac sites; thus, generating a structural remodeling that may favor cardiac arrhythmia.…”

“…After performing a title and abstract review, 365 studies were excluded resulting in 153 studies that underwent full-text review. Finally, nine studies (five cohort [20][21][22][23][24] , two cross-sectional 14,25 , and two recent cohort 26,27 ) were included in the review (Figure 1). Table 1 summarizes the articles and their findings.…”

“…The incidence of VT was greater in current smokers than in non-smokers (OR=9.96; 95% CI: 1.93-51.48; n=87). One cross-sectional study conducted in China examined the incidence of arterial stiffness depending on the smoking status after HF diagnosis 25 . Current smoking was an independent determinant of arterial stiffness (β=0.121; p=0.013; n=354).…”

Arterial Stiffness Assessed by Cardio-Ankle Vascular Index

“…Chronic obstructive pulmonary disease (COPD) is known to often coexist in patients with heart failure and is considered to be a risk of adverse outcomes in patients with heart failure. CAVI is negatively associated with forced expiratory volume at 1.0 s in patients with heart failure [154,155]. Furthermore, CAVI increases with the grades of severity of COPD in symptomatic patients of heart failure [156].…”