Circulating serum amyloid A levels but not SAA1 variants predict long-term outcomes of angiographically confirmed coronary artery disease

• Published in: Ci ji yi xue za zhi 2022-10, Vol.34 (4), p.423-433
• Main Authors: Yeh, Kuan-Hung, Hsu, Lung-An, Juang, Jyh-Ming Jimmy, Chiang, Fu-Tien, Teng, Ming-Sheng, Tzeng, I-Shiang, Wu, Semon, Lin, Jeng-Feng, Ko, Yu-Lin
• Format: Article
• Language: English
• Subjects: coronary artery disease; genome-wide association study; long-term outcomes; Original; saa1 gene; serum amyloid a
• ISSN: 1016-3190; 2223-8956
• DOI: 10.4103/tcmj.tcmj_219_21

Circulating serum amyloid A (SAA) levels are strongly associated with atherosclerotic cardiovascular disease risk and severity. The association between genetic variants, SAA levels, inflammatory marker levels, and coronary artery disease (CAD) prognosis has not been fully understood. In total, 2199 Taiwan Biobank (TWB) participants were enrolled for a genome-wide association study (GWAS), and the long-term outcomes in 481 patients with CAD were analyzed. The primary endpoint was all-cause mortality, and the secondary endpoint was the combination of all-cause death, myocardial infarction, stroke, and hospitalization for heart failure. Through GWAS, rs11024600 and rs7112278 were independently associated with SAA levels ( = 3.84 × 10 and = 1.05 × 10 , respectively). SAA levels were positively associated with leukocyte counts and multiple inflammatory marker levels in CAD patients and with body mass index, hemoglobin, high-density lipoprotein cholesterol, and alanine aminotransferase levels in TWB participants. By stepwise linear regression analysis, gene variants contributed to 27.53% and 8.07% of the variation of the SAA levels in TWB and CAD populations, respectively, revealing a stronger influence of these two variants in TWB participants compared to CAD patients. Kaplan-Meier survival analysis revealed that SAA levels, but not gene variants, were associated with long-term outcomes in patients with CAD. Cox regression analysis also indicated that high circulating SAA levels were an independent predictor of both the primary and secondary endpoints. genotypes contributed significantly to SAA levels in the general population and in patients with CAD. Circulating SAA levels but not genetic variants could predict long-term outcomes in patients with angiographically confirmed CAD.