Association between serum amyloid A levels and coronary heart disease: a systematic review and meta-analysis of 26 studies

2020 
The relationship between serum amyloid A (SAA) and coronary heart disease (CHD) remains inconsistent, and the correlation of SAA levels and some factors have not been thoroughly evaluated in CHD. The present study assessed the associations of SAA levels and CHD, and the correlation of SAA levels and CRP, fibrinogen, interleukin-6 (IL-6), and HDL-C levels in CHD patient. We systematically searched databases of Cochrane Library, PubMed, Embase, and ScienceDirect from their inception to 2018. Pooled standardized mean difference (SMD), correlation coefficient (r), and 95% confidence intervals (CI) were computed using random-effect model. A total of 26 studies were identified for analysis, involving a total of 6466 CHD cases and 16,184 participants. Compared with the control group, the case group had markedly higher SAA levels (SMD = 0.38, 95% CI 0.21, 0.56). Subgroup analysis manifested that SAA level difference between case group and control group were associated with age, continent, and study type. Moreover, meta-regression model suggested that different continent, sex, and publication year can explain the origin of 52.05%, 50.17%, 28.07% heterogeneity, respectively. By stratified analyses, we further found that the concentration of SAA increased gradually with the aggravation of CHD. Additionally, the meta-analysis of correlation showed that SAA levels were positively related with CRP (r = 0.45, 95% CI 0.19, 0.71), fibrinogen (r = 0.41, 95% CI 0.35, 0.47), and IL-6 (r = 0.48, 95% CI 0.41, 0.54) levels, but negatively linked with HDL-C levels (r = − 0.28, 95% CI − 0.38, − 0.18) in CHD patients. High levels of SAA are significantly associated with increased risk of CHD, especially for participants aged more than 55 years, subjects from Europe and Asia, or case–control study. Furthermore, we find that SAA concentrations increased with the severity of CHD. Importantly, our study suggests that high levels of SAA might play a role in CHD by increasing CRP, fibrinogen, IL-6 levels, or attenuating HDL-C levels.
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