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      Smoking intensity and duration is associated with cardiac structure and function: the ECHOcardiographic Study of Hispanics/Latinos

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          Abstract

          Objective

          Cardiovascular disease is the leading cause of death in smokers and this relationship is complicated by the multiplicity of cardiovascular effects of smoking. However, the relationship between intensity and duration of cigarette smoking and echocardiographic measures of right and left ventricular structure and function has been poorly studied.

          Methods

          We examined ECHO-SOL (Echocardiographic Study of Hispanics/Latinos) participants, a subset of the Hispanic Community Health Study/Study of Latinos. Participants were administered a detailed tobacco exposure questionnaire and a comprehensive echocardiography exam. Multivariable linear regression models (adjusted for age, sex, obesity, hypertension and diabetes statuses) were performed using sampling weights. Statistical significance was defined at p <0.01.

          Results

          There were 1818 ECHO-SOL participants (57.4% women, mean age 56.4 years). Among current smokers (n=304), increased duration of smoking, as measured by a younger age of smoking initiation, was significantly associated with higher mean left ventricular mass (LVM) and lower right ventricular (RV) function (lower right ventricular stroke volumes). More cigarettes smoked per day was significantly associated with higher mean LVM, worse diastolic function (higher E/e′ ratio), worse LV geometry (increased relative wall thickness) and worse RV function (decreasing right ventricular stroke volume). Among current smokers, higher mean lifetime pack-years (a combined measure of smoking intensity and duration) was associated with higher LVM, worse LV geometry, worse diastolic function, greater RV dilatation and worse RV function.

          Conclusions

          There is a dose–response relationship between intensity and duration of cigarette tobacco smoking with unfavourable changes of multiple measures of right-sided and left-sided cardiac structure and function.

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          Most cited references29

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          Design and implementation of the Hispanic Community Health Study/Study of Latinos.

          The Hispanic Community Health Study (HCHS)/Study of Latinos (SOL) is a comprehensive multicenter community based cohort study of Hispanics/Latinos in the United States. The Study rationale, objectives, design, and implementation are described in this report. The HCHS/SOL will recruit 16,000 men and women who self-identify as Hispanic or Latino, 18 to 74 years of age, from a random sample of households in defined communities in the Bronx, Chicago, Miami, and San Diego. The sites were selected so that the overall sample would consist of at least 2000 persons in each of the following origin designations: Mexican, Puerto Rican and Dominican, Cuban, and Central and South American. The study includes research in the prevalence of and risk factors for heart, lung, blood and sleep disorders, kidney and liver function, diabetes, cognitive function, dental conditions, and hearing disorders. The HCHS/SOL will (1) characterize the health status and disease burden in the largest minority population in the United States; (2) describe the positive and negative consequences of immigration and acculturation of Hispanics/Latinos to the mainstream United States life-styles, environment and health care opportunities; and (3) identify likely causal factors of many diseases in a population with diverse environmental exposures, genetic backgrounds, and early life experiences. Published by Elsevier Inc.
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            Developing COPD: a 25 year follow up study of the general population.

            Smokers are more prone to develop chronic obstructive pulmonary disease (COPD) than non-smokers, but this finding comes from studies spanning 10 years or less. The aim of this study was to determine the 25 year absolute risk of developing COPD in men and women from the general population. As part of the Copenhagen City Heart Study, 8045 men and women aged 30-60 years with normal lung function at baseline were followed for 25 years. Lung function measurements were collected and mortality from COPD during the 25 year observation period was analysed. The percentage of men with normal lung function ranged from 96% of never smokers to 59% of continuous smokers; for women the proportions were 91% and 69%, respectively. The 25 year incidence of moderate and severe COPD was 20.7% and 3.6%, respectively, with no apparent difference between men and women. Smoking cessation, especially early in the follow up period, decreased the risk of developing COPD substantially compared with continuous smoking. During the follow up period there were 2912 deaths, 109 of which were from COPD. 92% of the COPD deaths occurred in subjects who were current smokers at the beginning of the follow up period. The absolute risk of developing COPD among continuous smokers is at least 25%, which is larger than was previously estimated.
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              Norepinephrine and epinephrine release and adrenergic mediation of smoking-associated hemodynamic and metabolic events.

              We studied the effects of cigarette smoking, sham smoking and smoking during adrenergic blockade in 10 subjects to determine whether smoking released the sympathetic neurotransmitter norepinephrine, as well as the adrenomedullary hormone epinephrine, and whether smoking-associated hemodynamic and metabolic changes were mediated through adrenergic mechanisms. Smoking-associated increments in mean (+/- S.E.M.) plasma norepinephrine (227 +/- 23 to 324 +/- 39 pg per milliliter, P less than 0.01) and epinephrine (44 +/- to 113 +/- 27 pg per milliliter, P less than 0.05) were demonstrated. Smoking-associated increments in pulse rate, blood pressure, blood glycerol and blood lactate/pyruvate ratio were prevented by adrenergic blockade; increments in plasma growth hormone and cortisol were not. Since significant smoking-associated increments, in pulse rate, blood pressure and blood lactate/pyruvate ratio, preceded measurable increments in plasma catecholamine concentrations, but were adrenergically mediated, these changes should be attributed to norepinephrine released locally from adrenergic axon terminals within the tissues rather than to increments in circulating catecholamines.
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                Author and article information

                Journal
                Open Heart
                Open Heart
                openhrt
                openheart
                Open Heart
                BMJ Publishing Group (BMA House, Tavistock Square, London, WC1H 9JR )
                2053-3624
                2017
                14 June 2017
                : 4
                : 2
                : e000614
                Affiliations
                [1 ] Wake Forest School of Medicine , Winston-Salem, North Carolina, USA
                [2 ] Einstein College of Medicine , Bronx, North Carolina, USA
                [3 ] University of Virginia Health System , Charlottesville, Virginia, USA
                [4 ] University of Illinois at Chicago , Chicago, Illinois, USA
                [5 ] San Diego State University , San Diego, California, USA
                [6 ] University of North Carolina , Chapel Hill, North Carolina, USA
                [7 ] Johns Hopkins Health System , Baltimore, Maryland, USA
                [8 ] Boston University School of Medicine , Boston, Massachusetts, USA
                [9 ] American Heart Association , Louisville, Kentucky, USA
                [10 ] University of Louisville , Louisville, Kentucky, USA
                Author notes
                [Correspondence to ] Dr Carlos J Rodriguez; crodrigu@ 123456wakehealth.edu
                Article
                openhrt-2017-000614
                10.1136/openhrt-2017-000614
                5515129
                8f1821b4-9429-4c63-bbda-54b91c1da3e9
                © Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted.

                This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/

                History
                : 21 February 2017
                : 07 March 2017
                : 29 March 2017
                Funding
                Funded by: National Heart, Lung, and Blood Institute;
                Categories
                Heart Failure and Cardiomyopathies
                1506
                Original research article
                Custom metadata
                unlocked

                smoking,right ventricular function,left ventricular function,echocardiography,epidemiology

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