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      Longitudinal Effects of Cigarette Smoking and Smoking Cessation on Aortic Wave Reflections, Pulse Wave Velocity, and Carotid Artery Distensibility

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          Abstract

          Background

          We evaluated the effects of smoking and smoking cessation on aortic wave reflections (augmentation index), aortic pulse wave velocity, and carotid artery distensibility and stiffness (distensibility coefficient, Young's elastic modulus).

          Methods and Results

          Current smokers underwent carotid, radial, and femoral artery tonometry and carotid ultrasound at baseline and 3 years after a quit attempt. Baseline associations of smoking heaviness markers (exhaled carbon monoxide and cigarettes smoked/d) and effects of smoking cessation at year 3 on changes in arterial measures were assessed using multivariable linear regression models. The 1417 smokers (54% female) were mean (SD) 49.3 (11.6) years old and smoked 17.2 (8.3) cigarettes/d (exhaled carbon monoxide 14.7 [8.2] parts per million). Arterial measures were associated more strongly with age, blood pressure (BP), and waist circumference than with smoking heaviness markers. Augmentation index was associated independently with carbon monoxide ( P=0.004). Pulse wave velocity, distensibility coefficient, and Young's elastic modulus had small, inconsistent associations with smoking heaviness markers. At year 3, augmentation index improved with smoking cessation ( P=0.006) despite more weight gain (2.54 vs 0.36 kg, P<0.001) and insulin resistance ( P=0.001) among abstainers, but distensibility coefficient decreased ( P=0.004). Changes in arterial measures were related more strongly to changes in BP than smoking cessation.

          Conclusions

          Arterial wave reflection and stiffness measures were associated more strongly with age, BP, and waist circumference than smoking heaviness. Smoking cessation was associated with weight gain and increased insulin resistance. Changes in arterial measures were predicted by changes in BP, highlighting the need to address weight gain and BP changes during a quit attempt.

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          Most cited references50

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          Cardiovascular effects of secondhand smoke: nearly as large as smoking.

          Secondhand smoke increases the risk of coronary heart disease by approximately 30%. This effect is larger than one would expect on the basis of the risks associated with active smoking and the relative doses of tobacco smoke delivered to smokers and nonsmokers. We conducted a literature review of the research describing the mechanistic effects of secondhand smoke on the cardiovascular system, emphasizing research published since 1995, and compared the effects of secondhand smoke with the effects of active smoking. Evidence is rapidly accumulating that the cardiovascular system--platelet and endothelial function, arterial stiffness, atherosclerosis, oxidative stress, inflammation, heart rate variability, energy metabolism, and increased infarct size--is exquisitely sensitive to the toxins in secondhand smoke. The effects of even brief (minutes to hours) passive smoking are often nearly as large (averaging 80% to 90%) as chronic active smoking. The effects of secondhand smoke are substantial and rapid, explaining the relatively large risks that have been reported in epidemiological studies.
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            Role of smoking in global and regional cardiovascular mortality.

            Smoking is a major cause of cardiovascular disease mortality. There is little information on how it contributes to global and regional cause-specific mortality from cardiovascular diseases for which background risk varies because of other risks. We used data from the American Cancer Society's Cancer Prevention Study II (CPS II) and the World Health Organization Global Burden of Disease mortality database to estimate smoking-attributable deaths from ischemic heart disease, cerebrovascular disease, and a cluster of other cardiovascular diseases for 14 epidemiological subregions of the world by age and sex. We used lung cancer mortality as an indirect marker for accumulated smoking hazard. CPS-II hazards were adjusted for important covariates. In the year 2000, an estimated 1.62 (95% CI, 1.27 to 2.04) million cardiovascular deaths in the world, 11% of total global cardiovascular deaths, were due to smoking. Of these, 1.17 million deaths were among men and 450,000 among women. There were 670,000 (95% CI, 440,000 to 920,000) smoking-attributable cardiovascular deaths in the developing world and 960,000 (95% CI, 770,000 to 1,200,000) in industrialized regions. Ischemic heart disease accounted for 54% of smoking-attributable cardiovascular mortality, followed by cerebrovascular disease (25%). There was variability across regions in the role of smoking as a cause of various cardiovascular diseases. More than 1 in every 10 cardiovascular deaths in the world in the year 2000 were attributable to smoking, demonstrating that it is an important preventable cause of cardiovascular mortality.
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              Arterial stiffness, systolic blood pressure, and logical treatment of arterial hypertension.

              Arterial stiffening is the principal cause of increasing systolic pressure with advancing years and in patients with arterial hypertension. It is associated with progressive arterial dilation and is due to degeneration of the arterial wall, probably as a consequence of repetitive cyclic stress; it increases systolic pressure directly by increasing amplitude of the pressure wave generated by a given flow impulse from the heart and indirectly by increasing wave velocity so that wave reflection from the periphery occurs earlier, augmenting pressure in late systole. The first mechanism affects pressure in both the central and peripheral arteries, the second predominantly in the central arteries. Change in brachial systolic pressure with age underestimates the rise in systolic pressure in the aorta and left ventricle. Arterial stiffness is reduced passively with reduction in arterial pressure. Drugs have little or no direct effect on arterial stiffness but can markedly reduce wave reflection. In patients with stiffened arteries, reduction in wave reflection decreases aortic systolic pressure augmentation. The decreased systolic pressure in central arteries brought about by this mechanism is not detected when systolic pressure is measured in a peripheral (brachial or radial) artery but can be inferred from change in contour of the pressure wave recorded in peripheral arteries.
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                Author and article information

                Contributors
                jhs@medicine.wisc.edu
                Journal
                J Am Heart Assoc
                J Am Heart Assoc
                10.1002/(ISSN)2047-9980
                JAH3
                ahaoa
                Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
                John Wiley and Sons Inc. (Hoboken )
                2047-9980
                04 December 2019
                17 December 2019
                : 8
                : 24 ( doiID: 10.1002/jah3.v8.24 )
                : e013939
                Affiliations
                [ 1 ] School of Medicine and Public Health University of Wisconsin Madison WI
                Author notes
                [*] [* ] Correspondence to: James H. Stein, MD, University of Wisconsin School of Medicine and Public Health, 600 Highland Ave, H4/520 CSC (MC 3248), Madison, WI 53792. E‐mail: jhs@ 123456medicine.wisc.edu
                Article
                JAH34647
                10.1161/JAHA.119.013939
                6951052
                31795823
                cc471e46-b155-4aac-a787-f4ef19bf17d7
                © 2019 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                History
                : 12 July 2019
                : 30 October 2019
                Page count
                Figures: 0, Tables: 7, Pages: 9, Words: 7769
                Funding
                Funded by: NHLBI
                Award ID: 5R01 HL109031
                Award ID: T32 HL007936
                Funded by: NCI
                Award ID: K05 CA139871
                Funded by: VA Advanced Fellowship in Women's Health
                Categories
                Original Research
                Original Research
                Vascular Medicine
                Custom metadata
                2.0
                jah34647
                17 December 2019
                Converter:WILEY_ML3GV2_TO_NLMPMC version:5.7.2 mode:remove_FC converted:16.12.2019

                Cardiovascular Medicine
                arterial stiffness,blood pressure,smoking,vascular disease,lifestyle,primary prevention,risk factors

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