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• W1889237735 abstract "SummaryBackground:Osteoprotegerin (OPG) is a secretory glycoprotein which belongs to the tumor necrosis factor receptor family. OPG immunoreactivity was demonstrated in normal blood vessels and in early atherosclerotic lesions. In a previous study, we showed that high serum OPG levels are associated with progression of coronary artery disease (CAD). Objectives:The present study was designed to assess the association between serum OPG level and long‐term prognosis in patients with stable coronary artery disease. Methods:We performed a prospective, observational cohort study in 225 subjects to examine whether serum OPG levels can predict cardiovascular mortality. The median OPG levels were 1.02 ng mL−1 at baseline. Results: During the follow‐up (61 ± 25 months), 27 deaths occurred including 13 cardiovascular deaths. When the subjects were divided into three groups according to serum OPG level, the group with high serum OPG showed a higher risk for cardiovascular mortality. A Multivariate Cox proportional hazards model indicated that the higher risk of cardiovascular death in the high OPG level group remained significant (hazards ratio of 7.44, 95%CI 0.92–60.30, highest vs. lowest OPG tertile). In contrast, serum OPG levels were not associated with non‐cardiovascular mortality. Conclusions:Our data show that serum OPG levels are an independent predictor of cardiovascular mortality in patients with stable coronary artery disease. Background:Osteoprotegerin (OPG) is a secretory glycoprotein which belongs to the tumor necrosis factor receptor family. OPG immunoreactivity was demonstrated in normal blood vessels and in early atherosclerotic lesions. In a previous study, we showed that high serum OPG levels are associated with progression of coronary artery disease (CAD). Objectives:The present study was designed to assess the association between serum OPG level and long‐term prognosis in patients with stable coronary artery disease. Methods:We performed a prospective, observational cohort study in 225 subjects to examine whether serum OPG levels can predict cardiovascular mortality. The median OPG levels were 1.02 ng mL−1 at baseline. Results: During the follow‐up (61 ± 25 months), 27 deaths occurred including 13 cardiovascular deaths. When the subjects were divided into three groups according to serum OPG level, the group with high serum OPG showed a higher risk for cardiovascular mortality. A Multivariate Cox proportional hazards model indicated that the higher risk of cardiovascular death in the high OPG level group remained significant (hazards ratio of 7.44, 95%CI 0.92–60.30, highest vs. lowest OPG tertile). In contrast, serum OPG levels were not associated with non‐cardiovascular mortality. Conclusions:Our data show that serum OPG levels are an independent predictor of cardiovascular mortality in patients with stable coronary artery disease. Osteoprotegerin (OPG), a member of the tumor necrosis factor (TNF) receptor family, has been identified as a regulator of bone resorption [1Simonet W.S. Lacey D.L. Dunstan C.R. Kelley M. Chang M.S. Luthy R. Nguyen H.Q. Wooden S. Bennett L. Boone T. Shimamoto G. DeRose M. Elliott R. Colombero A. Tan H.L. Trail G. Sullivan J. Davy E. Bucay N. Renshaw‐Gegg L. et al.Osteoprotegerin: a novel secreted protein involved in the regulation of bone density.Cell. 1997; 89: 309-19Abstract Full Text Full Text PDF PubMed Google Scholar]. Recently, it has been demonstrated that OPG is produced by a variety of tissues including the cardiovascular system (heart, arteries and veins), lung, kidney and immune tissues, as well as bone [1Simonet W.S. Lacey D.L. Dunstan C.R. Kelley M. Chang M.S. Luthy R. Nguyen H.Q. Wooden S. Bennett L. Boone T. Shimamoto G. DeRose M. Elliott R. Colombero A. Tan H.L. Trail G. Sullivan J. Davy E. Bucay N. Renshaw‐Gegg L. et al.Osteoprotegerin: a novel secreted protein involved in the regulation of bone density.Cell. 1997; 89: 309-19Abstract Full Text Full Text PDF PubMed Google Scholar, 2Yun T.J. Chaudhary P.M. Shu G.L. Frazer J.K. Ewings M.K. Schwartz S.M. Pascual V. Hood L.E. Clark E.A. OPG/FDCR‐1, a TNF receptor family member, is expressed in lymphoid cells and is up‐regulated by ligating CD40.J Immunol. 1998; 161: 6113-21PubMed Google Scholar], and that the expression and production of OPG are regulated by various cytokines and hormones [3Hofbauer L.C. Khosla S. Dunstan C.R. Lacey D.L. Boyle W.J. Riggs B.L. The roles of osteoprotegerin and osteoprotegerin ligand in the paracrine regulation of bone resorption.J Bone Miner Res. 2000; 15: 2-12Crossref PubMed Google Scholar]. OPG‐deficient mice develop severe osteoporosis and medial arterial calcification of the aorta and renal arteries [4Bucay N. Sarosi I. Dunstan C.R. Morony S. Tarpley J. Capparelli C. Scully S. Tan H.L. Xu W. Lacey D.L. Boyle W.J. Simonet W.S. osteoprotegerin‐deficient mice develop early onset osteoporosis and arterial calcification.Genes Dev. 1998; 12: 1260-8Crossref PubMed Google Scholar], and the development of osteoporosis and arterial calcification are completely prevented by restoration of the gene [5Min H. Morony S. Sarosi I. Dunstan C.R. Capparelli C. Scully S. Van G. Kaufman S. Kostenuik P.J. Lacey D.L. Boyle W.J. Simonet W.S. Osteoprotegerin reverses osteoporosis by inhibiting endosteal osteoclasts and prevents vascular calcification by blocking a process resembling osteoclastogenesis.J Exp Med. 2000; 192: 463-74Crossref PubMed Scopus (483) Google Scholar]. OPG is also expressed in vascular cells such as coronary smooth muscle cells and endothelial cells in vitro [6Hofbauer L.C. Shui C. Riggs B.L. Dunstan C.R. Spelsberg T.C. O’Brien T. Khosla S. Effects of immunosuppressants on receptor activator of NF‐kappaB ligand and osteoprotegerin production by human osteoblastic and coronary artery smooth muscle cells.Biochem Biophys Res Commun. 2001; 280: 334-9Crossref PubMed Scopus (0) Google Scholar]. In endothelial cells, OPG acts as an anti‐apoptotic factor [7Malyankar U.M. Scatena M. Suchland K.L. Yun T.J. Clark E.A. Giachelli C.M. Osteoprotegerin is an alpha vbeta 3‐induced, NF‐kappa B‐dependent survival factor for endothelial cells.J Biol Chem. 2000; 275: 20959-62Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar]. OPG immunoreactivity was demonstrated in the normal vessel wall, and also in early atherosclerotic lesions in human tissues [8Dhore C.R. Cleutjens J.P. Lutgens E. Cleutjens K.B. Geusens P.P. Kitslaar P.J. Tordoir J.H. Spronk H.M. Vermeer C. Daemen M.J. Differential expression of bone matrix regulatory proteins in human atherosclerotic plaques.Arterioscler Thromb Vasc Biol. 2001; 21: 1998-2003Crossref PubMed Google Scholar]. These findings suggest that OPG may play an important role in the development of vascular disease. In a previous study, we showed that there is a significant correlation between elevated serum OPG levels and the severity of coronary artery disease [9Jono S. Ikari Y. Shioi A. Mori K. Miki T. Hara K. Nishizawa Y. Serum osteoprotegerin levels are associated with the presence and severity of coronary artery disease.Circulation. 2002; 106: 1192-4Crossref PubMed Scopus (453) Google Scholar]. Serum OPG levels have also been found to be associated with the progression of carotid atherosclerosis and onset of cardiovascular disease [10Kiechl S. Schett G. Wenning G. Redlich K. Oberhollenzer M. Mayr A. Santer P. Smolen J. Poewe W. Willeit J. Osteoprotegerin is a risk factor for progressive atherosclerosis and cardiovascular disease.Circulation. 2004; 109: 2175-80Crossref PubMed Scopus (457) Google Scholar]. The present report is a cohort study of 225 patients that evaluated the possible association between serum OPG levels and cardiovascular mortality in coronary artery disease (CAD) patients. The present study comprised a cohort of 225 patients who underwent elective coronary angiography between October 1999 and June 2000. All patients fulfilled the clinical indication for cardiac catheterization with stable chest pain and/or signs of myocardial ischemia on exercise electrocardiography. Patients with acute coronary syndrome or with chronic kidney disease were excluded. Written informed consent was obtained from all patients. During the study period, there were 363 eligible patients with stable coronary artery disease. Patients undergoing hemodialysis (n = 45) and with chronic kidney disease (n = 91) were excluded. Only two patients refused to participate in the study. Thus, the number of patients included in the study was 225. Physical examination, blood pressure, body mass index (BMI) and a hematological and biochemical profile were obtained. Age and history of tobacco use were assessed through an interview preceding the physical examination. Diabetes was considered present if a patient was being treated with insulin or oral agents for blood glucose control or had a fasting glucose level of ≥ 126 mg dL−1 (7.0 mmol L−1). Hypertension was defined by a systolic blood pressure of ≥ 140 mmHg and diastolic blood pressure of ≥ 90 mmHg, current antihypertensive treatment or a combination of them all. Hyperlipidemia was defined as a total cholesterol level of > 240 mg dL−1 (6.2 mmol L−1), current use of lipid‐lowering agents or both. Quantitative coronary angiography (QCA) was performed, using an automated edge detection system CMS (MEDIS, Leiden, the Netherland), by experienced cardiologists who were unaware of the clinical and biological data of patients. Significant coronary stenosis was defined as a ≥ 50% diameter narrowing based on the QCA measurement. The variability in repeat measurements of percent diameter stenosis was 2.7%. The severity of CAD was represented as the number of diseased vessels. Fasting serum samples were collected and stored at −80 °C until use. Serum OPG levels were determined using a sandwich enzyme‐linked immunosorbent assay (Cosmo Bio, Tokyo, Japan) as previously described [9Jono S. Ikari Y. Shioi A. Mori K. Miki T. Hara K. Nishizawa Y. Serum osteoprotegerin levels are associated with the presence and severity of coronary artery disease.Circulation. 2002; 106: 1192-4Crossref PubMed Scopus (453) Google Scholar]. Briefly, a monoclonal antibody against human OPG, designated clone OI‐19, was used to capture OPG from serum. Captured OPG was detected with peroxidase‐labeled antihuman OPG monoclonal antibody, designated clone OI‐4, and color was developed with tetramethylbenzidine substrate. All samples were measured in duplicate and averaged. The detection limit of this assay was 0.03 ng mL−1 and the intra‐ and interassay coefficients of variation were < 3.2% and < 5.4%, respectively. All patients were followed‐up until December 2007 with a median follow‐up of 70.6 months. Data and cause of death were obtained by reviewing the clinical records. For patients who were transferred to other hospitals, we reviewed the questionnaire forms completed by the attending physicians at those hospitals. All data are presented as mean ± standard deviation (SD). Comparisons between groups for study variables were done using the unpaired Student’s t‐test for normally distributed parameters and the Mann–Whitney U‐test for non‐normally distributed data. Survival curves were plotted using the Kaplan–Meier method with log rank test. Prognostic variables for survival were determined using the univariate or multivariate Cox proportional hazard regression models. Serum OPG level at baseline showed a skewed distribution with a median of 1.015 ng mL−1 (IQR 0.818–1.262). Serum OPG levels showed positive correlation with age. For every 10 year increase in age, the OPG level had increased by 0.082 ng mL−1 (95% CI 0.028–0.136). We found no association of serum OPG levels with other CAD risk factors including gender, hypertension, diabetes, hyperlipidemia and current smoking. Table 1 summarizes baseline characteristics of the subjects divided by baseline OPG levels. When baseline OPG levels in the study population were divided into tertiles, we found that patients with high OPG levels were older. Number of coronary artery vessels involved in disease was higher in the high OPG group. Left ventricular ejection fraction < 50% was frequently observed in the high OPG group. Heart rate was higher in the high OPG group. Diabetes, hypertension and hyperlipidemia were similar among the three groups. Use of angiotensin converting enzyme inhibitor/angiotensin receptor blocker, Ca channel blockers, beta blockers or statins was also similar among the three groups.Table 1Characteristics at baselineTertile groupP valueLowMediumHighNumber of subjects757575OPG (ng mL−1)median0.741.021.42range0.22–0.870.88–1.181.19–3.08Age (years)60.5 SD 9.564.0 SD 10.164.8 SD 10.50.02Gender (male/female)60/1561/1465/100.51Diabetes (%)2835440.12Hypertension (%)6977760.49Hyperlipidemia (%)6977760.49Smoking (%)4132370.49Number of vessel disease on CAG1.0 SD 1.01.3 SD 1.01.5 SD 1.10.003Ejection fraction on LVG (%)65.9 SD 10.565.3 SD 10.863.4 SD 13.10.37Ejection fraction < 50%7 (9.3%)3 (4.0%)14 (18.7%)0.013Height (cm)162.2 SD 8.3161.6 SD 7.8161.8 SD 7.10.91Weight (kg)64.8 SD 10.960.4 SD 10.862.2 SD 11.80.06Body mass index (kg m−2)24.5 SD 2.923.0 SD 3.123.6 SD 3.50.02Blood urea nitrogen (mg dL−1)15.8 SD 5.916.7 SD5.216.4 SD 5.60.61Creatinin (mg dL−1)1.03 SD 2.160.84 SD 0.301.03 SD 0.990.71Systolic blood pressure (mmHg)126 SD 15129 SD 16130 SD 160.37Diastolic blood pressure (mmHg)75 SD 975 SD 1075 SD 110.98Heart rate (beats/min)66 SD 1171 SD 872 SD 90.0003Na (mEq L−1)143.7 SD 1.9143.7 SD 2.3143.6 SD 2.70.93K (mEq L−1)4.5 SD 0.34.4 SD 0.44.5 SD 0.40.51Cl (mEq L−1)106.2 SD 2.3105.8 SD 2.6105.5 SD 2.60.28Phosphate (mg dL−1)3.4 SD 1.33.3 SD 0.43.2 SD 0.60.69Alkaline phosphatase (IU L−1)238 SD 70230 SD 67268 SD 790.01Fibrinogen (mg dL−1)272 SD 70285 SD 54287 SD 580.39eGFR (mL min−1 m−2)75.3 SD 20.671.4 SD 21.366.7 SD 20.70.06Total cholesterol (mg dL−1)195.3 33.3199.5 29.5189.3 33.90.2Triglyceride (mg dL−1)166 SD 80145 SD 83161 SD 970.33HDL‐Cholesterol (mg dL−1)50.7 SD 13.454.9 SD 16.551.7 SD 13.10.22ACEI/ARB (%)2331220.35Calcium channel blocker (%)6064680.63Nitro (%)4957410.14Beta blocker (%)1524230.28Diuretics (%)47110.27Statin (%)2428260.82OPG, osteoprotegerin; CAG, coronary angiography; eGFR, estimated glomerular filtration rate; HDL, high density lipoprotein; ACEI, angiotesin converting enzyme inhigitor; ARB, angiotensin receptor blocker; LVG, left ventriculography. Open table in a new tab OPG, osteoprotegerin; CAG, coronary angiography; eGFR, estimated glomerular filtration rate; HDL, high density lipoprotein; ACEI, angiotesin converting enzyme inhigitor; ARB, angiotensin receptor blocker; LVG, left ventriculography. During the follow‐up period (median 70.6.months), 198 patients were confirmed to be alive and there were 27 deaths. Of these 27 deaths, 13 were considered to be due to cardiac causes and the other 14 deaths were considered to be due to noncardiovascular causes. Seven heart failures were reported during the follow‐up. A total of 60 percutaneous coronary intervention (PCI) procedures and 18 coronary artery bypass surgeries were performed. Ten myocardial infarctions, 11 strokes, nine abdominal aortic aneurysms, four peripheral artery diseases and nine carotid stenoses were reported. Chronic hemodialysis was started in six patients during the follow‐up and seven patients were hospitalized as a result of heart failure. Kaplan–Meier survival curves according to OPG tertiles at baseline are presented in Fig. 1, showing the cumulative incidence of both cardiovascular and non‐cardiovascular mortalities of the subjects in the tertiles of serum OPG concentration. From the Kaplan–Meier curve, 5‐year cardiovascular mortality free rate was 98.3% in the lowest tertile, 95.4% in the medium tertile and 87.9% in the highest tertile. The patients in the highest tertile of serum OPG showed higher cardiovascular mortality. In contrast, serum OPG was not associated with non‐cardiovascular mortality. Univariate analysis showed diabetes (HR 3.86, 95%CI 1.18–12.54), dyslipidemia (HR 3.76, 95%CI 1.03–13.66) and higher serum OPG levels (HR 8.85, 95%CI 1.12–69.87, highest vs. lowest tertile) were prognostic in these patients. However, ejection fraction or number of coronary artery disease was not statistically significant. Multivariate Cox proportional hazard analyses were performed to determine whether there was an association between high circulating OPG and cardiovascular mortality adjusted for age, gender, hypertension, diabetes, dyslipidemia and smoking (Table 2). Serum OPG levels and the presence of diabetes (HR 3.59 95%CI 1.08–11.95) were associated with cardiovascular mortality. We also analyzed major adverse cardiovascular events (MACE) as an end point including cardiovascular death + myocardial infarction + PCI + bypass surgery. An association between MACE and serum OPG levels was not observed (HR 1.047, 95%CI 0.579–1.892, lowest vs. highest tertile).Table 2Analysis for cardiovascular mortalityTertile groupLowMediumHighNumber of subjects757575Person years364.4394.2369.4Cardiovascular mortalitynumber of events139incident rates (/person years)0.0030.0080.024Univariate analysisHR (95%CI) (vs. lowest tertile)N/A2.80 (0.29–26.92)8.85 (1.12–69.87)Multivariate analysis*HR (95%CI) (vs. lowest tertile)N/A2.33 (0.24–22.90)7.44 (0.92–60.30)*Cox proportional hazard model adjusted for age, gender, hypertension, diabetes, dyslipidemia and smoking. Open table in a new tab *Cox proportional hazard model adjusted for age, gender, hypertension, diabetes, dyslipidemia and smoking. It has been proposed that OPG is significantly involved in the progression of cardiovascular disease [11Van Campenhout A. Golledge J. Osteoprotegerin, vascular calcification and atherosclerosis.Atherosclerosis. 2009; 204: 321-9Abstract Full Text Full Text PDF PubMed Scopus (240) Google Scholar]. We have shown that there is a positive correlation between serum OPG levels and the severity of coronary artery disease [9Jono S. Ikari Y. Shioi A. Mori K. Miki T. Hara K. Nishizawa Y. Serum osteoprotegerin levels are associated with the presence and severity of coronary artery disease.Circulation. 2002; 106: 1192-4Crossref PubMed Scopus (453) Google Scholar]. In the present study, we demonstrated that serum OPG levels predicted cardiovascular mortality in a cohort of 225 patients with stable coronary artery disease. OPG functions as a soluble decoy receptor for receptor activator of nuclear factor‐κB (RANK) ligand (RANKL or OPG ligand). RANKL is produced by osteoblastic lineage cells and activated T lymphocytes and stimulates its receptor, RANK, which is located on osteoclasts and dendritic cells, and thus, modulates various biological functions such as osteoclast formation and survival [12Kong Y.Y. Yoshida H. Sarosi I. Tan H.L. Timms E. Capparelli C. Morony S. Oliveira‐dos‐Santos A.J. Van G. Itie A. Khoo W. Wakeham A. Dunstan C.R. Lacey D.L. Mak T.W. Boyle W.J. Penninger J.M. OPGL is a key regulator of osteoclastogenesis, lymphocyte development and lymph‐node organogenesis.Nature. 1999; 397: 315-23Crossref PubMed Scopus (0) Google Scholar]. OPG, RANKL and RANK act as key regulators of bone metabolism and the immune system. OPG has been shown to play a role in the regulation of the immune response and it is regulated by several cytokines involved in the inflammatory response. As atherosclerosis has recently been considered as an inflammatory disease [13Ross R. Atherosclerosis – an inflammatory disease.N Engl J Med. 1999; 340: 115-26Crossref PubMed Scopus (19136) Google Scholar], OPG may be involved in the progression of atherosclerosis. OPG is also a receptor for the cytotoxic ligand, TNF‐related apoptosis inducing ligand (TRAIL), a potent activator of apoptosis [14Emery J.G. McDonnell P. Burke M.B. Deen K.C. Lyn S. Silverman C. Dul E. Appelbaum E.R. Eichman C. DiPrinzio R. Dodds R.A. James I.E. Rosenberg M. Lee J.C. Young P.R. Osteoprotegerin is a receptor for the cytotoxic ligand TRAIL.J Biol Chem. 1998; 273: 14363-7Abstract Full Text Full Text PDF PubMed Scopus (1051) Google Scholar]. One possibility is that OPG influences vascular disease by inhibiting TRAIL‐induced apoptosis of vascular cells. Although the mechanism for the vascular effects of OPG is elusive, emerging evidence indicates that OPG may act as a protective factor for vascular diseases. One hypothesis is that increased serum OPG levels may be a compensatory self‐defensive response to the progression of atherosclerosis. We and another group have reported that OPG levels increase with an increase in severity of CAD in humans [9Jono S. Ikari Y. Shioi A. Mori K. Miki T. Hara K. Nishizawa Y. Serum osteoprotegerin levels are associated with the presence and severity of coronary artery disease.Circulation. 2002; 106: 1192-4Crossref PubMed Scopus (453) Google Scholar, 15Schoppet M. Sattler A.M. Schaefer J.R. Herzum M. Maisch B. Hofbauer L.C. Increased osteoprotegerin serum levels in men with coronary artery disease.J Clin Endocrinol Metab. 2003; 88: 1024-8Crossref PubMed Scopus (0) Google Scholar]. In addition, elevated OPG levels were independently associated with the progression of carotid atherosclerosis and with the incidence of cardiovascular mortality but not with non‐cardiovascular mortality [10Kiechl S. Schett G. Wenning G. Redlich K. Oberhollenzer M. Mayr A. Santer P. Smolen J. Poewe W. Willeit J. Osteoprotegerin is a risk factor for progressive atherosclerosis and cardiovascular disease.Circulation. 2004; 109: 2175-80Crossref PubMed Scopus (457) Google Scholar]. A cohort study of elderly women showed that those who died of a stroke or any other vascular cause had higher OPG levels at study baseline [16Browner W.S. Lui L.Y. Cummings S.R. Associations of serum osteoprotegerin levels with diabetes, stroke, bone density, fractures, and mortality in elderly women.J Clin Endocrinol Metab. 2001; 86: 631-7Crossref PubMed Scopus (479) Google Scholar]. A recent large cohort study showed that OPG is associated with the risk of future CAD in apparently healthy men and women, independent of established cardiovascular risk factors [17Semb A.G. Ueland T. Aukrust P. Wareham N.J. Luben R. Gullestad L. Kastelein J.J. Khaw K.T. Boekholdt S.M. Osteoprotegerin and soluble receptor activator of nuclear factor‐kappaB ligand and risk for coronary events: a nested case‐control approach in the prospective EPIC‐Norfolk population study 1993–2003.Arterioscler Thromb Vasc Biol. 2009; 29: 975-80Crossref PubMed Scopus (0) Google Scholar]. OPG measured at admission due to an acute ischemic stroke is associated with long‐term mortality [18Jensen J.K. Ueland T. Atar D. Gullestad L. Mickley H. Aukrust P. Januzzi J.L. Osteoprotegerin concentrations and prognosis in acute ischaemic stroke.J Intern Med. 2009; PubMed Google Scholar]. OPG also predicted all cause mortality in patients with chronic kidney disease [19Sigrist M.K. Levin A. Er L. McIntyre C.W. Elevated osteoprotegerin is associated with all‐cause mortality in CKD stage 4 and 5 patients in addition to vascular calcification.Nephrol Dial Transplant. 2009; 24: 3157-62Crossref PubMed Scopus (0) Google Scholar]. In the present study, we found that cardiovascular mortality is associated with a higher serum OPG concentration and with some of the common risk factors, such as diabetes and dyslipidemia. Subjects with high circulating OPG had a higher cardiovascular risk that was independent of the other potential confounders including age, gender, hypertension, diabetes, dyslipidemia and smoking. After adjustment for other predictors of cardiovascular mortality, serum OPG levels were independently associated with high cardiovascular mortality. Although the analysis was based on tertiles, we also found a monotonous increase in cardiovascular mortality risk based on quintiles. However, the OPG level was not related to non‐cardiovascular mortality. Thus, OPG appears not to be a non‐specific marker of disease or poor health. The strong association between high OPG and cardiovascular mortality could indicate that OPG is a potentially stable and reliable marker of cardiovascular disease. Ueland et al. [20Ueland T. Jemtland R. Godang K. Kjekshus J. Hognestad A. Omland T. Squire I.B. Gullestad L. Bollerslev J. Dickstein K. Aukrust P. Prognostic value of osteoprotegerin in heart failure after acute myocardial infarction.J Am Coll Cardiol. 2004; 44: 1970-6Crossref PubMed Scopus (173) Google Scholar] reported that the serum OPG level predicted mortality and heart failure development in patients with acute coronary syndrome. In the present study, OPG predicted mortality and a significant correlation between baseline OPG and frequency of low ejection fraction was observed. However, OPG did not predict heart failure development. Only seven heart failures were reported during the follow‐up (median 70.6 months) despite of a total of 27 deaths in this study. The lack of statistical power in this analysis because of the limited number of patients with heart failure could explain the non‐significance of the results with respect to OPG levels and heart failure. Alternatively, a difference of target disease; stable coronary artery disease, or acute coronary syndrome may explain the findings. There are a few limitations in this study. We studied subjects presenting with chest pain consistent with stable angina and patients with acute coronary syndrome were excluded. The sample size in our study is relatively small. This study was designed to survey the predictors for cardiovascular mortality and the number of fatal events was relatively small. Large population‐based studies should be undertaken to confirm our findings. In conclusion, the present study demonstrated that an increase in serum OPG level is a predictor of cardiovascular mortality in a cohort of patients with stable coronary artery disease. The authors state that they have no conflict of interest. This work was supported in part by a grant‐in‐aid for Scientific Research from Japan Society for the Promotion of Science (12671121)." @default.
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• W1889237735 title "Serum osteoprotegerin levels and long‐term prognosis in subjects with stable coronary artery disease" @default.
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