|Year : 2014 | Volume
| Issue : 6 | Page : 799-801
Adiponectin & inflammatory biomarkers in coronary artery disease
Jaewon Oh, Seok-Min Kang
Cardiology Division, Severance Cardiovascular Hospital & Cardiovascular Research Institute Yonsei University College of Medicine Seoul, Korea
|Date of Web Publication||4-Aug-2014|
Cardiology Division, Severance Cardiovascular Hospital & Cardiovascular Research Institute Yonsei University College of Medicine Seoul
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Oh J, Kang SM. Adiponectin & inflammatory biomarkers in coronary artery disease. Indian J Med Res 2014;139:799-801
Inflammation plays a pivotal role in the initiation and progression of atherothrombosis and triggering of atherosclerotic cardiovascular disease (ASCVD). Clinical studies have demonstrated that chronic inflammation is associated with the future cardiovascular (CV) events, and the emerging biomarkers related to inflammation have been investigated to improve identification of at-risk asymptomatic patients. Conventional CV risk factors in the Framingham risk score (FRS), such as age, male sex, hypercholesterolaemia, hypertension, diabetes mellitus and smoking have been the cornerstone in the assessment of ASCVD risk for decades  . However, approximately one-third of low-risk individuals with 0 or 1 FRS risk factor have been known to develop ASCVD in the future  . m0 any researchers have tried to assess accurately ASCVD risk beyond FRS by identification of chronic and subclinical inflammation status. The Justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER) trial, targeted to apparently healthy persons without hyperlipidaemia but with elevated high sensitive C-reactive protein (hsCRP), demonstrated the clinical beneficial effect of rosuvastatin therapy  . In lines with this background, the recent 2013 American Heart Association (AHA) / American College of Cardiology (ACC) guidelines have recommended the usage of hsCRP for stratifying the high risk patients for ASCVD in addition to revising FRS to pooled cohort equation (PCE)  . However, the risk-stratification using hsCRP cannot go without any limitations  . t0 here is a great variability in the hsCRP levels among individuals based on gender, ethnicity, etc . Though the hsCRP levels are reported to be higher in women than in men, the association between hsCRP and ASCVD may be less in women compared with men  . The highest hsCRP levels were generally found in African Americans, followed by Hispanics, South Asians, Whites, and East Asians, respectively  . So, we need to find more specific inflammatory biomarker or multi-panel biomarkers approach for predicting ASCVD risk.
Adiponectin is an adipokine secreted specifically from the adipose tissue. Adiponectin modulates glucose metabolism and insulin resistance. Thus, adiponectin may act as a potential link between diabetes mellitus and its CV consequences. Hypoadiponectinaemia has already been shown to be associated with obesity, diabetes mellitus, insulin resistance, coronary artery disease (CAD), and heart failure ,, . A high serum adiponectin level is associated with favourable cardiovascular risk profiles. However, previous epidemiological studies have reported conflicting results in clinical outcomes , . Paradoxically, a high serum adiponectin level was associated with an increased mortality risk in healthy people, as well as in patients with ASCVD and heart failure, so called as 'adiponectin paradox'  . In this issue, Kumpatla et al have shown the associations among inflammatory biomarkers including adiponectin and CAD in India. Though the concept of this study is not new, but it has an important clinical implication considering this clinical study conducted in India. According to this study, adiponectin and other inflammatory markers such as sE-selectin and TNF-α showed significant associations with CAD.
In western countries, many researchers have focused on the ethnic disparity between Caucasians and African Americans in the assessment of ASCVD risk. The ethnic disparities in ASCVD risk may be the result of differences in circulating adipokines and inflammatory markers. A recent study confirmed the existence of ethnic differences in adiponectin and CRP levels among Caucasians, Japanese Americans, Latinos, African Americans and native Hawaiians  . According to this study, Japanese Americans had lower hsCRP and adiponectin levels compared to Caucasians. Another recent study from Korea reported that hsCRP concentrations were lower in Koreans than those reported for Caucasian population  . Thus, Koreans may need lower cut-off value of hsCRP for high risk group selection than Caucasians (2.0 mg/l). These findings suggest that there are variations in biomarkers such hsCRP, adiponectin, etc. between Asia and the other parts of the world. Recently, the inter Asian disconcordance has been paid attention. Mediators of ethnic differences in insulin resistance differed markedly depending on the ethnic groups. General adiposity explained the difference in insulin resistance between Chinese and Malays, whereas abdominal fat distribution, inflammation and unexplained factors contributed to excess insulin resistance in Asian Indians as compared with Chinese and Malays  . One could speculate that there might be disparities in biomarkers between East Asian and South Asian such as India. In the context of these disparities, the study by Kumpatla and group  should be paid more attention in Asia.
However, they did not demonstrate that adiponectin could be a better biomarker than other inflammatory biomarkers including hsCRP in the assessment of ASCVD in Indians  . Further, whether these biomarkers are additive to conventional risk factors in India by using advanced statistical methods such as net reclassification improvement, integrated discrimination improvement and comparing C-statics is not known. What is the cut-off point of hsCRP for Indian? Are there any differences between adiponectin and hsCRP in predicting CV events? The superiority of adiponectin over CRP in this study could just be a coincidental finding when considering small sample-sized cross-sectional study design. Therefore, it should be confirmed in prospectively designed larger sample-sized clinical study, which could compare the prognostic power of biomarkers for predicting future CV events in India.
Considering the ethnic disparities in inflammatory biomarkers, each country should try to find more reliable, reproducible, and more specific biomarker for its own people especially in Asian countries.
| References|| |
|1.||Batsis JA, Lopez-Jimenez F. Cardiovascular risk assessment--from individual risk prediction to estimation of global risk and change in risk in the population. BMC Med 2010; 8 : 29. |
|2.||Khot UN, Khot MB, Bajzer CT, Sapp SK, Ohman EM, Brener SJ, et al. Prevalence of conventional risk factors in patients with coronary heart disease. JAMA 2003; 290 : 898-904. |
|3.||Ridker PM, Danielson E, Fonseca FA, Genest J, Gotto AM Jr, Kastelein JJ, et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med 2008; 359 : 2195-207. |
|4.||Stone NJ, Robinson JG, Lichtenstein AH, Bairey Merz CN, Blum CB, Eckel RH, et al. 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: A report of the American College of Cardiology/American Heart Association Task Force on practice guidelines. Circulation 2014; 129 (Suppl 2) : S1-S45. |
|5.||Yousuf O, Mohanty BD, Martin SS, Joshi PH, Blaha MJ, Nasir K, et al. High-sensitivity C-reactive protein and cardiovascular disease: a resolute belief or an elusive link? J Am Coll Cardiol 2013; 62 : 397-408. |
|6.||Woloshin S, Schwartz LM. Distribution of C-reactive protein values in the United States. N Engl J Med 2005; 352 : 1611-3. |
|7.||Kaptoge S, Di Angelantonio E, Pennells L, Wood AM, White IR, Gao P, et al. C-reactive protein, fibrinogen, and cardiovascular disease prediction. N Engl J Med 2012; 367 : 1310-20. |
|8.||Vaiopoulos AG, Marinou K, Christodoulides C, Koutsilieris M. The role of adiponectin in human vascular physiology. Int J Cardiol 2012; 155 : 188-93. |
|9.||Oh J, Kim JY, Park S, Youn JC, Son NH, Shin DJ, et al. The relationship between insulin-like growth factor-1 and metabolic syndrome, independent of adiponectin. Clin Chim Acta 2012; 413 : 506-10. |
|10.||Won H, Kang SM, Shin MJ, Oh J, Hong N, Park S, et al. Plasma adiponectin concentration and its association with metabolic syndrome in patients with heart failure. Yonsei Med J 2012; 53 : 91-8. |
|11.||Cavusoglu E, Ruwende C, Chopra V, Yanamadala S, Eng C, Clark LT, et al. Adiponectin is an independent predictor of all-cause mortality, cardiac mortality, and myocardial infarction in patients presenting with chest pain. Eur Heart J 2006; 27 : 2300-9. |
|12.||Singer JR, Palmas W, Teresi J, Weinstock R, Shea S, Luchsinger JA. Adiponectin and all-cause mortality in elderly people with type 2 diabetes. Diabetes Care 2012; 35 : 1858-63. |
|13.||Kizer JR, Benkeser D, Arnold AM, Mukamal KJ, Ix JH, Zieman SJ, et al. Associations of total and high-molecular-weight adiponectin with all-cause and cardiovascular mortality in order persons: the Cardiovascular Health Study. Circulation 2012; 126 : 2951-61. |
|14.||Kumpatla S, Karuppiah K, Immaneni S, Muthukumaran P, Krishnan J, Narayanamoorthy SK, et al. Comparison of plasma adiponectin & certain inflammatory markers in angiographically proven coronary artery disease patients with & without diabetes - A study from India. Indian J Med Res 2014; 139 : 841-50. |
|15.||Morimoto Y, Conroy SM, Ollberding NJ, Kim Y, Lim U, Cooney RV, et al. Ethnic differences in serum adipokine and C-reactive protein levels: the multiethnic cohort. Int J Obes (Lond) 2014. Feb13.doi.10.1038/ijo.2014.25[Epub ahead of print]. |
|16.||Sung KC, Ryu S, Chang Y, Byrne CD, Kim SH. C-reactive protein and risk of cardiovascular and all-cause mortality in 268 803 East Asians. Eur Heart J 2014. Feb 25 [Epub ahead of print]. |
|17.||Gao H, Salim A, Lee J, Tai ES, van Dam RM. Can body fat distribution, adiponectin levels and inflammation explain differences in insulin resistance between ethnic Chinese, Malays and Asian Indians? Int J Obes (Lond) 2012; 36 : 1086-93. |