SMOKE EXPOSURE PRECOCIOUSLY AFFECT CARDIAC PERFORMANCE IN YOUNG HEALTHY SMOKERS

Little is known on the early impact of smoking on cardiac function in young smokers. The new complementary echocardiography speckle-tracking (STE) software adds specific information on left ventricular (LV) global strain (GS) and torsion providing a non invasive estimate on LV systolic deformation. We investigated the subclinical LV dysfunction by STE in active cigarette smokers with no additional risk factors. Fifty smokers (mean age 24±5 years) and 60 matched controls were enrolled for this study. Plasma concentration of lipids, glucose, fibrinogen, C-reactive protein (CRP), interleukin-6 (IL-6), and blood pressure values were evaluated. Arterial stiffness indices (AIx and PWV), carotid intima-media thickness (cIMT) values and echocardiographic parameters were also evaluated. Left ventricular GS (longitudinal, radial and circumferential strain) and torsion were measured at rest and during exercise (STE software: GE, EchoPac-v.7.0.0). To evaluate the inuence of smoking on study variables a score of smoke exposure was estimated (SEIx). With respect to controls fibrinogen (p<0.05), CRP (p<0.01), IL-6 (p<0.01) and arterial stiffness (AIx: p<0.05; PW p<0.01) were higher in smokers while HDL-C (p<0.01) was lower. No difference was found in cIMT values between smokers and controls. At rest, GS and torsion were not different with respect to controls. During exercise, we found worse values of GS and torsion at 50w (p<0.001 and p<0.05, respectively), at 100w (p<0.05 and p<0.001, respectively), and of torsion at recovery (p<0.001) with respect to controls. Regression analysis indicated a significant association between SEIx and HDL, between HDL and inflammatory markers and between inflammatory markers and AIx, PWV, GLS at 50w and torsion at recovery. These findings provide a model according to which in young smokers occurs a slower adaptation to physical effort and confirm that smoking affects HDL concentration inducing a proinflammatory status. Furthermore we suggest that inflammation in smokers may precociously influence cardiac function.