Altered Arterial Stiffness and Subendocardial Viability Ratio in Young Healthy Light Smokers after Acute Exercise

Robert J Doonan,Franco Carli,Andrew Mutter,Patrick Scheffler,Stella S Daskalopoulou,Simon Bacon,Giordano Egiziano,Alice Yu,Marios E Daskalopoulos,Antonio Abbate

doi:10.1371/journal.pone.0026151

Abstract

BackgroundStudies showed that long-standing smokers have stiffer arteries at rest. However, the effect of smoking on the ability of the vascular system to respond to increased demands (physical stress) has not been studied. The purpose of this study was to estimate the effect of smoking on arterial stiffness and subendocardial viability ratio, at rest and after acute exercise in young healthy individuals.Methods/ResultsHealthy light smokers (n = 24, pack-years = 2.9) and non-smokers (n = 53) underwent pulse wave analysis and carotid-femoral pulse wave velocity measurements at rest, and 2, 5, 10, and 15 minutes following an exercise test to exhaustion. Smokers were tested, 1) after 12h abstinence from smoking (chronic condition) and 2) immediately after smoking one cigarette (acute condition). At rest, chronic smokers had higher augmentation index and lower aortic pulse pressure than non-smokers, while subendocardial viability ratio was not significantly different. Acute smoking increased resting augmentation index and decreased subendocardial viability ratio compared with non-smokers, and decreased subendocardial viability ratio compared with the chronic condition. After exercise, subendocardial viability ratio was lower, and augmentation index and aortic pulse pressure were higher in non-smokers than smokers in the chronic and acute conditions. cfPWV rate of recovery of was greater in non-smokers than chronic smokers after exercise. Non-smokers were also able to achieve higher workloads than smokers in both conditions.ConclusionChronic and acute smoking appears to diminish the vascular response to physical stress. This can be seen as an impaired ‘vascular reserve’ or a blunted ability of the blood vessels to accommodate the changes required to achieve higher workloads. These changes were noted before changes in arterial stiffness or subendocardial viability ratio occurred at rest. Even light smoking in young healthy individuals appears to have harmful effects on vascular function, affecting the ability of the vascular bed to respond to increased demands.

Highlights

Arterial stiffness is considered a composite measure of vascular health and a predictor of cardiovascular events independent of traditional risk factors; it is caused by structural changes in the vascular wall, including fibrosis, medial smooth muscle cell necrosis, breaks in elastin fibers, calcifications, and diffusion of macromolecules into the arterial wall[1,2,3]
Our findings suggest that while higher arterial stiffness, aortic pulse pressure (PP) and lower subendocardial viability ratio (SEVR) at rest is considered ‘detrimental’, this may not be the case for postexercise
SEVR was significantly decreased after the acute smoking condition compared with nonsmokers and the chronic condition

Summary

Introduction

Arterial stiffness is considered a composite measure of vascular health and a predictor of cardiovascular events independent of traditional risk factors; it is caused by structural changes in the vascular wall, including fibrosis, medial smooth muscle cell necrosis, breaks in elastin fibers, calcifications, and diffusion of macromolecules into the arterial wall[1,2,3]. In the Framingham Heart Study, a one standard deviation (SD) increment in arterial stiffness, as measured by carotid-femoral pulse wave velocity (cfPWV), the ‘gold standard’, was associated with a 48% increase in arterial disease risk, independently of individual vascular risk factors[3]. PWA can provide important information about several arterial stiffness and hemodynamic parameters including augmentation index (AIx) and subendocardial viability ratio (SEVR), an indicator of myocardial workload and perfusion (O2 supply vs demand)[4,5]. The purpose of this study was to estimate the effect of smoking on arterial stiffness and subendocardial viability ratio, at rest and after acute exercise in young healthy individuals

Objectives

Results

Discussion

Conclusion