全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...

Anti-Apolipoprotein A-1 IgG Levels Predict Coronary Artery Calcification in Obese but Otherwise Healthy Individuals

DOI: 10.1155/2012/243158

Full-Text   Cite this paper   Add to My Lib

Abstract:

We aimed at determining whether anti-apolipoprotein (apo) A-1 IgG levels are independent predictors of coronary artery calcification (CAC) and coronary endothelial dysfunction in obese and nonobese subjects without cardiovascular disease. 48 nonobese and 43 obese subjects were included. CAC score was measured by thorax scanner and defined by an Agatston score >?0. Coronary endothelial dysfunction was determined by measuring myocardial blood flow responses to cold pressor test (CPT) on PET/CT. Serum anti-apoA-1 IgG levels were measured by ELISA. Prevalence of coronary calcification was similar between the two study groups, but the prevalence of coronary endothelial dysfunction was higher in obese subjects. Anti-apoA-1 IgG levels and positivity rate were higher in obese than in nonobese individuals. CAC score was higher in anti-apoA-1 IgG positive subjects. ROC analyses indicated that anti-apoA-1 IgG levels were significant predictors of CAC?>?0, but not of coronary endothelial dysfunction with a negative predictive value of 94%. Anti-apoA-1 IgG positivity was associated with a 17-fold independent increased risk of CAC?>?0. In conclusion, those preliminary results indicate that anti-apoA-1 IgG autoantibodies are raised in obese subjects and independently predict the presence of coronary calcification in this population but not the presence of coronary endothelial dysfunction. 1. Introduction Despite significant progress related to evidence-based preventive and medical strategies, atherosclerosis-related cardiovascular diseases still account for the majority of morbidity and mortality in Western countries [1, 2]. Cardiovascular risk stratification mostly relies on the assessment of the traditional cardiovascular risk factors, allowing clinicians to derive different cardiovascular risk stratification tools, such as the widespread Framingham risk score (FRS) [1–4]. Nevertheless, the FRS predictive accuracy for major adverse cardiovascular event occurrence has been shown to be suboptimal, especially for screening purpose [5–8], and prompted the medical community to improve current cardiovascular risk stratification strategies. Among emerging candidates, coronary artery calcium (CAC) scoring, using noncontrast computed tomography, has been shown to be a very promising screening tool to rule out both coronary artery disease and major adverse cardiovascular events in different populations, outperforming conventional cardiovascular risk stratification tools [9–13]. However, its widespread use as a screening tool is likely to be impeded by its financial costs and

References

[1]  D. Lloyd-Jones, R. Adams, M. Carnethon et al., “Heart disease and stroke statistics—2009 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee,” Circulation, vol. 119, no. 3, pp. e21–e181, 2009.
[2]  E. S. Ford, U. A. Ajani, J. B. Croft et al., “Explaining the decrease in U.S. deaths from coronary disease, 1980–2000,” New England Journal of Medicine, vol. 356, no. 23, pp. 2388–2398, 2007.
[3]  P. W. F. Wilson, R. B. D'Agostino, D. Levy, A. M. Belanger, H. Silbershatz, and W. B. Kannel, “Prediction of coronary heart disease using risk factor categories,” Circulation, vol. 97, no. 18, pp. 1837–1847, 1998.
[4]  R. B. D'Agostino, R. S. Vasan, M. J. Pencina et al., “General cardiovascular risk profile for use in primary care: the Framingham heart study,” Circulation, vol. 117, no. 6, pp. 743–753, 2008.
[5]  T. P. Murphy, R. Dhangana, M. J. Pencina, A. M. Zafar, and R. B. D'Agostino, “Performance of current guidelines for coronary heart disease prevention: optimal use of the Framingham-based risk assessment,” Atherosclerosis, vol. 216, no. 2, pp. 452–457, 2011.
[6]  J. A. Hanley and B. J. McNeil, “The meaning and use of the area under a receiver operating characteristic (ROC) curve,” Radiology, vol. 143, no. 1, pp. 29–36, 1982.
[7]  K. Nasir, E. D. Michos, R. S. Blumenthal, and P. Raggi, “Detection of high-risk young adults and women by coronary calcium and national cholesterol education program panel III guidelines,” Journal of the American College of Cardiology, vol. 46, no. 10, pp. 1931–1936, 2005.
[8]  K. M. Johnson and D. A. Dowe, “The detection of any coronary calcium outperforms framingham risk score as a first step in screening for coronary atherosclerosis,” American Journal of Roentgenology, vol. 194, no. 5, pp. 1235–1243, 2010.
[9]  M. Blaha, M. J. Budoff, L. J. Shaw et al., “Absence of coronary artery calcification and all-cause mortality,” Journal of the American College of Cardiology, vol. 2, no. 6, pp. 692–700, 2009.
[10]  T. S. Polonsky, R. L. McClelland, N. W. Jorgensen et al., “Coronary artery calcium score and risk classification for coronary heart disease prediction,” Journal of the American Medical Association, vol. 303, no. 16, pp. 1610–1616, 2010.
[11]  A. Sarwar, L. J. Shaw, M. D. Shapiro et al., “Diagnostic and prognostic value of absence of coronary artery calcification,” Journal of the American College of Cardiology, vol. 2, no. 6, pp. 675–688, 2009.
[12]  T. H. Schindler, H. R. Schelbert, A. Quercioli, and V. Dilsizian, “Cardiac PET imaging for the detection and monitoring of coronary artery disease and microvascular health,” Journal of the American College of Cardiology, vol. 3, no. 6, pp. 623–640, 2010.
[13]  P. Greenland, J. S. Alpert, G. A. Beller et al., “2010 ACCF/AHA guideline for assessment of cardiovascular risk in asymptomatic adults,” Journal of the American College of Cardiology, vol. 56, no. 25, pp. e50–e103, 2010.
[14]  C. J. Binder, M. K. Chang, P. X. Shaw et al., “Innate and acquired immunity in atherogenesis,” Nature Medicine, vol. 8, no. 11, pp. 1218–1226, 2002.
[15]  C. Blasi, “The autoimmune origin of atherosclerosis,” Atherosclerosis, vol. 201, no. 1, pp. 17–32, 2008.
[16]  R. R. S. Packard and P. Libby, “Inflammation in atherosclerosis: from vascular biology to biomarker discovery and risk prediction,” Clinical Chemistry, vol. 54, no. 1, pp. 24–38, 2008.
[17]  P. Roux-Lombard, S. Pagano, F. Montecuco, N. Satta, and N. Vuilleumier, “Auto-antibodies as emergent prognostic markers and possible mediators of ischemic cardiovascular diseases,” Clinical Reviews in Allergy and Immunology. In press.
[18]  N. Vuilleumier, M. F. Rossier, S. Pagano et al., “Anti-apolipoprotein A-1 IgG as an independent cardiovascular prognostic marker affecting basal heart rate in myocardial infarction,” European Heart Journal, vol. 31, no. 7, pp. 815–823, 2010.
[19]  N. Vuilleumier, S. Bas, S. Pagano et al., “Anti-apolipoprotein A-1 IgG predicts major cardiovascular events in patients with rheumatoid arthritis,” Arthritis and Rheumatism, vol. 62, no. 9, pp. 2640–2650, 2010.
[20]  A. Finckh, D. S. Courvoisier, S. Pagano et al., “Evaluation of cardiovascular risk in patients with rheumatoid arthritis: do cardiovascular biomarkers offer added predictive ability over established clinical risk scores?” Arthritis Care and Research, vol. 64, no. 6, pp. 817–825, 2012.
[21]  P.-F. Keller, S. Pagano, P. Roux-Lombard et al., “Autoantibodies against apolipoprotein A-1 and phosphorylcholine for diagnosis of non-ST-segment elevation myocardial infarction,” Journal of Internal Medicine, vol. 271, no. 5, pp. 451–462, 2012.
[22]  F. Montecucco, N. Vuilleumier, S. Pagano et al., “Anti-Apolipoprotein A-1 auto-antibodies are active mediators of atherosclerotic plaque vulnerability,” European Heart Journal, vol. 32, no. 4, pp. 412–421, 2011.
[23]  A. Quercioli, Z. Pataky, G. Vincenti et al., “Elevated endocannabinoid plasma levels are associated with coronary circulatory dysfunction in obesity,” European Heart Journal, vol. 32, no. 11, pp. 1369–1378, 2011.
[24]  A. Quercioli, F. Mach, M. Bertolotto et al., “Receptor activator of NF-κB ligand (RANKL) increases the release ofneutrophil products associated with coronary vulnerability,” Thrombosis and Haemostasis, vol. 107, no. 1, pp. 124–139, 2012.
[25]  J. Davignon and P. Ganz, “Role of endothelial dysfunction in atherosclerosis,” Circulation, vol. 109, no. 23, supplement 1, pp. III27–III32, 2004.
[26]  P. Tounian, Y. Aggoun, B. Dubern et al., “Presence of increased stiffness of the common carotid artery and endothelial dysfunction in severely obese children: a prospective study,” The Lancet, vol. 358, no. 9291, pp. 1400–1404, 2001.
[27]  A. Quercioli, Z. Pataky, F. Montecucco et al., “Coronary vasomotor control in obesity and morbid obesity: contrasting flow responses with endocannabinoids, leptin, and inflammation,” Journal of the American College of Cardiology, vol. 5, no. 8, pp. 805–815, 2012.
[28]  I. Valenta, A. Quercioli, G. Vincenti et al., “Structural epicardial disease and microvascular function are determinants of an abnormal longitudinal myocardial blood flow difference in cardiovascular risk individuals as determined with PET/CT,” Journal of Nuclear Cardiology, vol. 17, no. 6, pp. 1023–1033, 2010.
[29]  T. C. Villines, E. A. Hulten, L. J. Shaw et al., “Prevalence and severity of coronary artery disease and adverse events among symptomatic patients with coronary artery calcification scores of zero undergoing coronary computed tomography angiography: results from the CONFIRM (Coronary CT Angiography Evaluation for Clinical Outcomes: an International Multicenter) registry,” Journal of the American College of Cardiology, vol. 58, no. 24, pp. 2533–2540, 2011.
[30]  V. Dilsizian and J. Narula, Atlas of Nuclear Cardiology, Current Medicine Group, 3rd edition, 2009.
[31]  T. H. Schindler, R. Campisi, D. Dorsey et al., “Effect of hormone replacement therapy on vasomotor function of the coronary microcirculation in post-menopausal women with medically treated cardiovascular risk factors,” European Heart Journal, vol. 30, no. 8, pp. 978–986, 2009.
[32]  E. R. DeLong, D. M. DeLong, and D. L. Clarke-Pearson, “Comparing the areas under two or more correlated receiver operating characteristic curves: a nonparametric approach,” Biometrics, vol. 44, no. 3, pp. 837–845, 1988.
[33]  M.-A. Cornier, J.-P. Després, N. Davis et al., “Assessing adiposity: a scientific statement from the american heart association,” Circulation, vol. 124, no. 18, pp. 1996–2019, 2011.
[34]  A. Stofkova, “Leptin and adiponectin: from energy and metabolic dysbalance to inflammation and autoimmunity,” Endocrine Regulations, vol. 43, no. 4, pp. 157–168, 2009.
[35]  J. R. Batuca, P. R. J. Ames, M. Amaral, C. Favas, D. A. Isenberg, and J. Delgado Alves, “Anti-atherogenic and anti-inflammatory properties of high-density lipoprotein are affected by specific antibodies in systemic lupus erythematosus,” Rheumatology, vol. 48, no. 1, pp. 26–31, 2009.
[36]  P. R. J. Ames, E. Matsuura, J. R. Batuca et al., “High-density lipoprotein inversely relates to its specific autoantibody favoring oxidation in thrombotic primary antiphospholipid syndrome,” Lupus, vol. 19, no. 6, pp. 711–716, 2010.
[37]  D. Farbstein and A. P. Levy, “HDL dysfunction in diabetes: causes and possible treatments,” Expert Review of Cardiovascular Therapy, vol. 10, no. 3, pp. 353–361, 2012.
[38]  V. P. W. Scholtes, D. Versteeg, J. P. P. M. De Vries et al., “Toll-like receptor 2 and 4 stimulation elicits an enhanced inflammatory response in human obese patients with atherosclerosis,” Clinical Science, vol. 121, no. 5, pp. 205–214, 2011.
[39]  S. J. Kim, Y. Choi, Y. H. Choi, and T. Park, “Obesity activates toll-like receptor-mediated proinflammatory signaling cascades in the adipose tissue of mice,” Journal of Nutritional Biochemistry, vol. 23, pp. 113–122, 2012.
[40]  S. Pagano, N. Satta, D. Werling et al., “Anti-apolipoprotein A-1 IgG in patients with myocardial infarction promotes inflammation through TLR2/CD14 complex,” Journal of Internal Medicine, vol. 272, no. 4, pp. 344–357, 2012.

Full-Text

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133