Association of exhaled carbon monoxide with subclinical cardiovascular disease and their conjoint impact on the incidence of cardiovascular outcomes

European Heart Journal

Volumn 35, Issue 42, 2014, Pages 2980-2987

  Cheng, Susan ^a,b   Enserro, Danielle ^c   Xanthakis, Vanessa ^a,c,d   M Sullivan, Lisa ^c   Murabito, Joanne M ^a,d   Benjamin, Emelia J ^a,d   Polak, Joseph F ^e   O'Donnell, Christopher J ^a,f   Wolf, Philip A ^a,d   O'Connor, George T ^a,d   Keaney, John F ^g   Vasan, Ramachandran S ^a,d  

^a FRAMINGHAM HEART STUDY   (United States)

^b BRIGHAM AND WOMEN S HOSPITAL   (United States)

^c BOSTON UNIVERSITY   (United States)

^d BOSTON UNIVERSITY SCHOOL OF MEDICINE   (United States)

^e TUFTS MEDICAL CENTER   (United States)

^f NATIONAL HEART LUNG AND BLOOD INSTITUTE   (United States)

^g UNIVERSITY OF MASSACHUSETTS MEDICAL SCHOOL   (United States)

Author keywords

Carbon monoxide; Cardiovascular outcomes; Subclinical vascular disease

Indexed keywords

CARBON MONOXIDE; BIOLOGICAL MARKER;

ADULT; ARTICLE; CARBON MONOXIDE BLOOD LEVEL; CARDIOMETABOLIC RISK; CARDIOVASCULAR DISEASE; CARDIOVASCULAR FUNCTION; CARDIOVASCULAR RISK; DIAGNOSTIC TEST; DISEASE COURSE; EXPIRED AIR; FEMALE; FOLLOW UP; HUMAN; INCIDENCE; MAJOR CLINICAL STUDY; MALE; OUTCOME ASSESSMENT; SEX DIFFERENCE; SMOKING; SUBCLINICAL CARDIOVASCULAR DISEASE; VASCULAR DISEASE; BLOOD; BREATH ANALYSIS; CARDIOVASCULAR DISEASES; MIDDLE AGED; PROGNOSIS;

BIOMARKERS; BREATH TESTS; CARBON MONOXIDE; CARDIOVASCULAR DISEASES; FEMALE; HUMANS; INCIDENCE; MALE; MIDDLE AGED; PROGNOSIS;

EID: 84912099292     PISSN: 0195668X     EISSN: 15229645     Source Type: Journal    
DOI: 10.1093/eurheartj/ehu052     Document Type: Article

References (38)

1. Durante W. Carbon monoxide and bile pigments: surprising mediators of vascular function. Vasc Med 2002;7:195-202.
2. Wang X, Wang Y, Kim HP, Nakahira K, Ryter SW, Choi AM. Carbon monoxide protects against hyperoxia-induced endothelial cell apoptosis by inhibiting reactive oxygen species formation. J Biol Chem 2007;282:1718-1726.
3. Ndisang JF, Tabien HE, Wang R. Carbon monoxide and hypertension. J Hypertens 2004;22:1057-1074.
4. Chan KH, Ng MK, Stocker R. Haem oxygenase-1 and cardiovascular disease: mechanisms and therapeutic potential. Clin Sci (Lond) 2011;120:493-504.
5. Ryter SW, Morse D, Choi AM. Carbon monoxide and bilirubin: potential therapies for pulmonary/vascular injuryand disease. Am J Respir Cell Mol Biol 2007;36:175-182.
6. Johnson FK, Johnson RA, Durante W, Jackson KE, Stevenson BK, Peyton KJ. Metabolic syndrome increases endogenous carbon monoxide production to promote hypertension and endothelial dysfunction in obese Zucker rats. Am J Physiol Regul Integr Comp Physiol 2006;290:R601-R608.
7. Owens EO. Endogenous carbon monoxide productionin disease. Clin Biochem 2010; 43:1183-1188.
8. Paredi P, Biernacki W, Invernizzi G, Kharitonov SA, Barnes PJ. Exhaled carbon monoxide levels elevatedindiabetes and correlated with glucose concentrationinblood: a new test for monitoring the disease? Chest 1999;116:1007-1011.
9. Cheng S, Lyass A, Massaro JM, O'Connor GT, Keaney JF Jr, Vasan RS. Exhaled carbon monoxide and riskof metabolic syndrome and cardiovascular diseaseinthe community. Circulation 2010;122:1470-1477.
10. Kuller LH, Shemanski L, Psaty BM, Borhani NO, Gardin J, Haan MN, O'Leary DH, Savage PJ, Tell GS, Tracy R. Subclinical disease as an independent risk factor for cardiovascular disease. Circulation 1995;92:720-726.
11. Jones RH, Ellicott MF, Cadigan JB, Gaensler EA. The relationship between alveolar and blood carbon monoxide concentrations during breathholding; simple estimation of COHb saturation. J Lab Clin Med 1958;51:553-564.
12. Hedblad B, Ogren M, Engstrom G, Wollmer P, Janzon L. Heterogeneity ofcardiovas-cular risk among smokersis related to degreeof carbon monoxide exposure. Atherosclerosis 2005;179:177-183.
13. Kharitonov SA, Barnes PJ. Exhaled markersofpulmonary disease. Am JRespir Crit Care Med 2001;163:1693-1722.
14. Woodman G, Wintoniuk DM, Taylor RG, Clarke SW. Time course of end-expired carbon monoxide concentration is important in studies of cigarette smoking. Clin Sci (Lond) 1987;73:553-555.
15. Ingelsson E, Sullivan LM, Murabito JM, Fox CS, Benjamin EJ, Polak JF, Meigs JB, Keyes MJ, O'Donnell CJ, Wang TJ, D'Agostino RB Sr, Wolf PA, Vasan RS. Prevalence and prognostic impact of subclinical cardiovascular disease in individuals with the metabolic syndrome and diabetes. Diabetes 2007;56:1718-1726.
16. Kannel WB, Wolf PA, Garrison RJ. The Framingham Study: An Epidemiological Investigation of Cardiovascular Disease. Section 34. Some Risk Factors Related to the Annual Incidence of Cardiovascular Disease and Death Using Pooled Repeated Biennial Measurements: Framingham Heart Study, 30-year follow-up. Bethesda, MD: National Heart, Lung, and Blood Institute; 1987 (NIH publication no. 87-2703).
17. Bauer I, Pannen BH. Bench-to-bedside review: Carbon monoxide-from mitochon-drial poisoning to therapeutic use. Crit Care 2009;13:220.
18. Wu L, Wang R. Carbon monoxide: endogenous production, physiological functions, and pharmacological applications. Pharmacol Rev 2005;57:585-630.
19. Ryter SW, Alam J, Choi AM. Heme oxygenase-1/carbon monoxide: from basic science to therapeutic applications. Physiol Rev 2006;86:583-650.
20. Joe Y, Zheng M, Kim SK, Kim S, Uddin JM, Min TS, Ryu do G, Chung HT. The role of carbon monoxide in metabolic disease. Ann N Y Acad Sci 2011;1229:156-161.
21. Henningsson R, Alm P, Ekstrom P, Lundquist I. Hemeoxygenase andcarbon monoxide: regulatory roles in islet hormone release: a biochemical, immunohistochemical, and confocal microscopic study. Diabetes 1999;48:66-76.
22. Li M, Kim DH, Tsenovoy PL, Peterson SJ, Rezzani R, Rodella LF, Aronow WS, Ikehara S, Abraham NG. Treatment of obese diabetic mice with a heme oxygenase inducer reduces visceral and subcutaneous adiposity, increases adiponectin levels, and improves insulin sensitivity and glucose tolerance. Diabetes 2008;57: 1526-1535.
23. Morita T, Mitsialis SA, Koike H, Liu Y, Kourembanas S. Carbon monoxide controls the proliferation of hypoxic vascular smooth muscle cells. J Biol Chem 1997;272: 32804-32809.
24. Marazioti A, Bucci M, Coletta C, Vellecco V, Baskaran P, Szabo C, Cirino G, Marques AR, Guerreiro B, Goncalves AM, Seixas JD, Beuve A, Romao CC, Papapetropoulos A. Inhibition of nitric oxide-stimulated vasorelaxation by carbon monoxide-releasing molecules. Arterioscler Thromb Vasc Biol 2011;31:2570-2576.
25. Lin HH, Chen YH, Yet SF, Chau LY. After vascular injury, heme oxygenase-1/carbon monoxide enhances re-endothelialization via promoting mobilization of circulating endothelial progenitor cells. J Thromb Haemost 2009;7:1401-1408.
26. Lakkisto P, Kyto V, Forsten H, Siren JM, Segersvard H, Voipio-Pulkki LM, Laine M, Pulkki K, Tikkanen I. Heme oxygenase-1 and carbon monoxide promote neovascu-larization after myocardial infarction by modulating the expression of HIF-1alpha, SDF-1alpha and VEGF-B. Eur J Pharmacol 2010;635:156-164.
27. Wu BJ, Kathir K, Witting PK, Beck K, Choy K, Li C, Croft KD, Mori TA, Tanous D, Adams MR, Lau AK, Stocker R. Antioxidants protect from atherosclerosis by a heme oxygenase-1 pathway that is independent of free radical scavenging. J Exp Med 2006;203:1117-1127.
28. Orozco LD, Kapturczak MH, Barajas B, Wang X, Weinstein MM, Wong J, Deshane J, Bolisetty S, Shaposhnik Z, Shih DM, Agarwal A, Lusis AJ, Araujo JA. Heme oxygenase-1 expression in macrophages plays a beneficial role in atherosclerosis. Circ Res 2007;100:1703-1711.
29. Lee TS, Chang CC, Zhu Y, Shyy JY. Simvastatin induces heme oxygenase-1: a novel mechanism of vessel protection. Circulation 2004;110:1296-1302.
30. True AL, Olive M, Boehm M, San H, Westrick RJ, Raghavachari N, Xu X, Lynn EG, Sack MN, Munson PJ, Gladwin MT, Nabel EG. Heme oxygenase-1 deficiency accelerates formation of arterial thrombosis through oxidative damage to the endothe-lium, which is rescued by inhaled carbon monoxide. Circ Res 2007;101:893-901.
31. Brunt KR, Fenrich KK, Kiani G, Tse MY, Pang SC, Ward CA, Melo LG. Protection of human vascular smooth muscle cells from H2O2-induced apoptosis through functional codependence between HO-1 and AKT. Arterioscler Thromb Vasc Biol 2006; 26:2027-2034.
32. Yet SF, Layne MD, Liu X, Chen YH, Ith B, Sibinga NE, Perrella MA. Absence of heme oxygenase-1 exacerbates atherosclerotic lesion formation and vascular remodeling. FASEB J 2003;17:1759-1761.
33. Cheng C, Noordeloos AM, Jeney V, Soares MP, Moll F, Pasterkamp G, Serruys PW, Duckers HJ. Heme oxygenase 1 determines atherosclerotic lesion progression into a vulnerable plaque. Circulation 2009;119:3017-3027.
34. Thorup C, Jones CL, Gross SS, Moore LC, Goligorsky MS. Carbon monoxide induces vasodilation and nitric oxide release but suppresses endothelial NOS. Am J Physiol 1999;277:F882-F889.
35. Stec DE, Ishikawa K, Sacerdoti D, Abraham NG. The emerging role of heme oxyge-nase and its metabolites in the regulation of cardiovascular function. Int J Hypertens 2012;2012:593530.
36. Stevenson DK, Ostrander CE, Johnson JD. Effect of erythrocyte destruction on the pulmonary excretion rate of carbon monoxide in adult male Wistar rats. J Lab Clin Med 1979;94:649-654.
37. Chau CK, Tu EY, Chan DW, Burnett J. Estimating the total exposureto air pollutants for different population age groups in Hong Kong. Environ Int 2002;27:617-630.
38. EPA. Regional Trends in CO Levels. http://www.epa.gov/airtrends/carbon.html#coreg (5 November 2013).