Effects of smoking on arterial distensibility, central aortic pressures and left ventricular mass☆,☆☆
Introduction
Besides being a well-documented cardiovascular risk factor, smoking is also the most important avoidable source of cardiovascular morbidity and mortality in the world [1], [2]. It is already well-known that smoking is associated with vascular remodeling [3], but all the mechanisms that are involved in the deleterious effects of smoking on the arterial wall are still unclear. Possible pathophysiological mechanisms include impairment of endothelial function, activation and aggregation of platelets [3] and changes in hemostatic components and blood lipids [4] as well as changes in the arterial distensibility capacity [1], [5], [6]. Previous studies showed that a consumption of one cigarette was followed by a decrease in the distensibility of the aorta and medium-sized arteries [5], [6] and that chronic smoking, independent of the duration, is associated with a decrease in aortic distensibility [1]. The measurement of reflected arterial waves, which is an indirect parameter of arterial stiffness and related with a higher risk of cardiovascular death and disease [7], [8], permits the evaluation of functional properties of the arterial wall through the measurements of the augmentation index and aortic pressures.
Increasing evidence indicates that smoking also affects cardiac remodeling [9]. On the other hand, it is unclear to which extent and by which mechanisms smoking affects the functional and morphological changes of the heart. Two cross-sectional population-based studies [10], [11] had demonstrated an association between smoking and increased left ventricular mass (LVM) and more recently, Lieb and colleagues [9] showed a longitudinal association between smoking and LVM increases occurring after 4 and 16 years of follow-up.
There are few prospective population-based studies, which examined smoking as a factor that specifically modifies the age-related increase in LVM [9]. The purpose of our study is to analyze longitudinal effects of chronic smoking on LVM and cross-sectional effects on the aortic pressure waveform in two population-based studies.
Section snippets
The MONICA/KORA Augsburg Cohort Study
The MONICA/KORA Augsburg project was part of the international collaborative WHO MONICA (Monitoring Trends and Determinants on Cardiovascular Diseases) project [12]. The study design, sampling frame and data collection have been described in detail before [13]. Briefly, the third MONICA survey (KORA S3 study, from now on referred as KORA T0) took place between October 1994 and June 1995. All subjects were prospectively followed within the framework of the Cooperative Health Research in the
Characteristics of study groups
The anthropometric characteristics of the non-smokers and smokers at KORA T0 are listed in Table 1A. The smokers were younger and had lower levels of glycosylated hemoglobin. Moreover, smokers presented with lower levels of HDL cholesterol and higher alcohol consumption (Table 1A). There were no further differences between the groups regarding other features such as demographics, clinical characteristics, anthropometric measures, hemodynamics and medical history.
The anthropometric
Discussion
The association between smoking and reduced arterial distensibility [5], increased central pressures [4] and LVM [9] has already been demonstrated separately, but as far we know, this is the first study to show consistently, in the same population, the effects of smoking on arterial distensibility, pulse wave reflection, central pressures and left ventricular geometry. We hypothesize that the alterations of left ventricular geometry observed in smokers are substantially affected by the
Conclusions
Our findings are consistent with the hypothesis that smoking causes higher central systolic, end-systolic, mean systolic and pulse pressure based on earlier, enhanced and more prolonged wave reflection. As a result of this increase in afterload, the left ventricle increases its LV wall thickness with a resultant increase in LVM.
Acknowledgment
The authors wish to acknowledge Renate Domeier for her assistance with the preparation of the paper.
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Sources of funding: This work is supported by grants of the German Research Foundation (Deutsche Forschungsgemeinschaft [DFG], DFG Schu 672/12-1), the Federal Ministry of Education and Research (Bundesministerium für Bildung und Forschung [BMBF], NGFN2 [FKZ-01GS0418, H.S.]), the Competence Network of Heart Failure (BMBF-01GI0205, M.R.P.M., H.W.H., H.V., H.S.) and the University of Lübeck Medical School (J.S. A39-2005). The KORA research platform (KORA: Cooperative Research in the Region of Augsburg) and the MONICA Augsburg studies (Monitoring Trends and Determinants on Cardiovascular Diseases) were initiated and financed by the Helmholtz Zentrum München, German Research Center for Environmental Health, which is founded by the Federal Ministry of Education and Research and by the Bavarian Ministry of Finance.
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The Study of Health in Pomerania (SHIP) is part of the Community Medicine Research net (CMR) (http://medizin.uni-greifswald.de/icm) of the University of Greifswald funded by grants from the German Federal Ministry of Education and Research (BMBF, grant 01ZZ96030, 01ZZ0701), by the Competence Network Obesity and the network ‘Greifswald Approach to Individualized Medicine (GANI_MED)’. The GANI_MED consortium is funded by the German Federal Ministry of Education and Research and as well as by the Ministry of Cultural Affairs of the German Federal State of Mecklenburg—West Pomerania (grant 03IS2061A). This study was carried out in collaboration with the DZHK (German Centre for Cardiovascular Research), which is funded by the BMBF (German Ministry of Education and Research).
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This author takes responsibility for all aspects of the reliability and freedom from bias of the data presented and their discussed interpretation.
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For the MONICA/KORA investigators. The MONICA Augsburg Cohort Study was initiated and conducted by Ulrich Keil and co-workers. The KORA Group consists of H.E. Wichmann (speaker), A. Peters, C. Meisinger, T. Illig, R. Holle, J. John and their co-workers who are responsible for the design and conduct of the KORA studies.