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      Lung Function in Young Adults and Risk of Cardiovascular Events Over 29 Years: The CARDIA Study

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          Abstract

          Background

          Diminished peak lung function in young adulthood is a risk factor for future chronic obstructive pulmonary disease. The association between lung disease and cardiovascular disease later in life is well documented. Whether peak lung function measured in young adulthood is associated with risk of future cardiovascular events is unknown.

          Methods and Results

          CARDIA (The Coronary Artery Risk Development in Young Adults) study is a prospective, multicenter, community‐based, longitudinal cohort study including 4761 participants aged 18 to 30 years with lung function testing we investigated the association between lung health in young adulthood and risk of subsequent cardiovascular events. We performed Cox proportional hazards regression to test the association between baseline and years 10 and 20 pulmonary function with incident cardiovascular events. Linear and logistic regression was performed to explore the associations of lung function with development of risk factors for cardiovascular disease as well as carotid intima‐media thickness and coronary artery calcified plaque. At baseline, mean age (± SD) was 24.9±3.6 years. Baseline forced expiratory volume in 1 second (hazard ratio) per −10‐unit decrement in percent predicted forced expiratory volume in 1 second (hazard ratio, 1.18; 95% CI, 1.06–1.31 [ P=0.002]) and FVC per −10‐unit decrement in percent predicted FVC (hazard ratio, 1.19; 95% CI, 1.06–1.33 [ P=0.003]) were associated with future cardiovascular events independent of traditional cardiovascular risk factors. Baseline lung function was associated with heart failure and cerebrovascular events but not coronary artery disease events.

          Conclusions

          Lung function in young adulthood is independently associated with cardiovascular events into middle age. This association appears to be driven by heart failure and cerebrovascular events rather than coronary heart disease.

          Clinical Trial Registration

          URL: https://www.clinicaltrials.gov. Unique identifier: NCT00005130.

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          Most cited references36

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          Phenotype-Specific Treatment of Heart Failure With Preserved Ejection Fraction: A Multiorgan Roadmap.

          Heart failure (HF) with preserved ejection fraction (EF; HFpEF) accounts for 50% of HF cases, and its prevalence relative to HF with reduced EF continues to rise. In contrast to HF with reduced EF, large trials testing neurohumoral inhibition in HFpEF failed to reach a positive outcome. This failure was recently attributed to distinct systemic and myocardial signaling in HFpEF and to diversity of HFpEF phenotypes. In this review, an HFpEF treatment strategy is proposed that addresses HFpEF-specific signaling and phenotypic diversity. In HFpEF, extracardiac comorbidities such as metabolic risk, arterial hypertension, and renal insufficiency drive left ventricular remodeling and dysfunction through systemic inflammation and coronary microvascular endothelial dysfunction. The latter affects left ventricular diastolic dysfunction through macrophage infiltration, resulting in interstitial fibrosis, and through altered paracrine signaling to cardiomyocytes, which become hypertrophied and stiff because of low nitric oxide and cyclic guanosine monophosphate. Systemic inflammation also affects other organs such as lungs, skeletal muscle, and kidneys, leading, respectively, to pulmonary hypertension, muscle weakness, and sodium retention. Individual steps of these signaling cascades can be targeted by specific interventions: metabolic risk by caloric restriction, systemic inflammation by statins, pulmonary hypertension by phosphodiesterase 5 inhibitors, muscle weakness by exercise training, sodium retention by diuretics and monitoring devices, myocardial nitric oxide bioavailability by inorganic nitrate-nitrite, myocardial cyclic guanosine monophosphate content by neprilysin or phosphodiesterase 9 inhibition, and myocardial fibrosis by spironolactone. Because of phenotypic diversity in HFpEF, personalized therapeutic strategies are proposed, which are configured in a matrix with HFpEF presentations in the abscissa and HFpEF predispositions in the ordinate.
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            Carotid intima-media thickness and plaque in cardiovascular risk assessment.

            Carotid intima-media thickness (CIMT) has been shown to predict cardiovascular (CV) risk in multiple large studies. Careful evaluation of CIMT studies reveals discrepancies in the comprehensiveness with which CIMT is assessed-the number of carotid segments evaluated (common carotid artery [CCA], internal carotid artery [ICA], or the carotid bulb), the type of measurements made (mean or maximum of single measurements, mean of the mean, or mean of the maximum for multiple measurements), the number of imaging angles used, whether plaques were included in the intima-media thickness (IMT) measurement, the report of adjusted or unadjusted models, risk association versus risk prediction, and the arbitrary cutoff points for CIMT and for plaque to predict risk. Measuring the far wall of the CCA was shown to be the least variable method for assessing IMT. However, meta-analyses suggest that CCA-IMT alone only minimally improves predictive power beyond traditional risk factors, whereas inclusion of the carotid bulb and ICA-IMT improves prediction of both cardiac risk and stroke risk. Carotid plaque appears to be a more powerful predictor of CV risk compared with CIMT alone. Quantitative measures of plaques such as plaque number, plaque thickness, plaque area, and 3-dimensional assessment of plaque volume appear to be progressively more sensitive in predicting CV risk than mere assessment of plaque presence. Limited data show that plaque characteristics including plaque vascularity may improve CV disease risk stratification further. IMT measurement at the CCA, carotid bulb, and ICA that allows inclusion of plaque in the IMT measurement or CCA-IMT measurement along with plaque assessment in all carotid segments is emerging as the focus of carotid artery ultrasound imaging for CV risk prediction.
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              Calcified coronary artery plaque measurement with cardiac CT in population-based studies: standardized protocol of Multi-Ethnic Study of Atherosclerosis (MESA) and Coronary Artery Risk Development in Young Adults (CARDIA) study.

              Calcified coronary artery plaque, measured at cardiac computed tomography (CT), is a predictor of cardiovascular disease and may play an increasing role in cardiovascular disease risk assessment. The Multi-Ethnic Study of Atherosclerosis (MESA) and the Coronary Artery Risk Development in Young Adults (CARDIA) study of the National Heart, Lung, and Blood Institute are population-based studies in which calcified coronary artery plaque was measured with electron-beam and multi-detector row CT and a standardized protocol in 6814 (MESA) and 3044 (CARDIA study) participants. The studies were approved by the appropriate institutional review board from the study site or agency, and written informed consent was obtained from each participant. Participation in the CT examination was high, image quality was good, and agreement for the presence of calcified plaque was high (kappa = 0.92, MESA; kappa = 0.77, CARDIA study). Extremely high agreement was observed between and within CT image analysts for the presence (kappa > 0.90, all) and amount (intraclass correlation coefficients, >0.99) of calcified plaque. Measurement of calcified coronary artery plaque with cardiac CT is well accepted by participants and can be implemented with consistently high-quality results with a standardized protocol and trained personnel. If predictive value of calcified coronary artery plaque for cardiovascular events proves sufficient to justify screening a segment of the population, then a standardized cardiac CT protocol is feasible and will provide reproducible results for health care providers and the public. (c) RSNA, 2005.
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                Author and article information

                Contributors
                m-cuttica@northwestern.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
                10 December 2018
                18 December 2018
                : 7
                : 24 ( doiID: 10.1002/jah3.2018.7.issue-24 )
                : e010672
                Affiliations
                [ 1 ] Division of Pulmonary and Critical Care Medicine Feinberg School of Medicine Northwestern University Chicago IL
                [ 2 ] Department of Preventive Medicine Feinberg School of Medicine Northwestern University Chicago IL
                [ 3 ] Division of Pulmonary, Allergy and Critical Care Medicine University of Alabama School of Medicine Birmingham AL
                [ 4 ] Division of Cardiology Kaiser Permanente Northern California Oakland CA
                [ 5 ] Division of Epidemiology and Community Health School of Public Health University of Minnesota Minneapolis MN
                [ 6 ] Division of Research Kaiser Permanente Northern California Oakland CA
                [ 7 ] Division of Preventive Medicine Department of Medicine University of Alabama at Birmingham AL
                [ 8 ] Division of Pulmonary and Critical Care Medicine Brigham and Women's Hospital Boston MA
                Author notes
                [*] [* ] Correspondence to: Michael J. Cuttica, MD, MS, 676 Saint Clair Street, Suite 1400, Chicago IL 60611. Email: m-cuttica@ 123456northwestern.edu
                Article
                JAH33701
                10.1161/JAHA.118.010672
                6405620
                30561252
                314de033-8cc6-4dfb-94ca-43431f260868
                © 2018 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-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                : 18 September 2018
                : 25 October 2018
                Page count
                Figures: 1, Tables: 4, Pages: 14, Words: 8577
                Funding
                Funded by: National Heart, Lung, and Blood Institute (NHLBI);
                Award ID: HHSN268201300025C
                Award ID: HHSN268201300026C
                Award ID: HHSN268201300027C
                Award ID: HHSN268201300028C
                Award ID: HHSN268201300029C
                Award ID: HHSN268200900041C
                Award ID: R01 HL122477
                Funded by: Intramural Research Program of the National Institute on Aging (NIA);
                Categories
                Original Research
                Original Research
                Epidemiology
                Custom metadata
                2.0
                jah33701
                18 December 2018
                Converter:WILEY_ML3GV2_TO_NLMPMC version:version=5.5.4 mode:remove_FC converted:18.12.2018

                Cardiovascular Medicine
                cardiac disease,heart failure,lung,pulmonary,pulmonary heart disease,cardiovascular disease,aging,epidemiology

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