Guangdong Provincial Key Laboratory of Digestive Cancer Research, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, China.
Department of Nutrition, School of Public Health, Guangdong Medical University, Dongguan, China.
Am J Clin Nutr. 2021 Oct 4;114(4):1360-1370. doi: 10.1093/ajcn/nqab210.
S-adenosylmethionine (SAM) as methyl donors participates in methylation and is converted into S-adenosylhomocysteine (SAH), which is a precursor of homocysteine. Increased plasma SAH and homocysteine are associated with increased risk of cardiovascular disease. However, the relation of plasma SAM with cardiovascular risk is still unclear.
To determine the relation between plasma SAM and risk of mortality among patients with coronary artery disease (CAD).
Baseline plasma SAM concentrations were measured in 1553 patients with CAD from the Guangdong Coronary Artery Disease Cohort between October 2008 and December 2011. Proportional hazards Cox analyses were performed to ascertain associations between SAM and risk of all-cause and cardiovascular mortality.
After a median follow-up of 9.2 (IQR: 8.5-10.2) y, of 1553 participants, 321 had died, including 227 deaths from cardiovascular diseases. Patients in the lowest quartile of SAM concentrations had a higher risk of all-cause death (HR, 1.59; 95% CI: 1.14, 2.21) and cardiovascular death (HR, 2.14; 95% CI: 1.41, 3.27) than those in the highest quartile in multivariable adjusted analysis. Each 1-SD decrease in the SAM concentration remained associated with a 42% greater risk of total death (HR, 1.42; 95% CI: 1.23, 1.64) and a 66% higher risk of cardiovascular death (HR, 1.66; 95% CI: 1.37, 2.01) after fully adjusting for other cardiovascular risk factors. Furthermore, each 1-SD decrease in plasma SAM/SAH ratio, as the methylation index, was also inversely associated with the risk of all-cause (HR, 1.80; 95% CI: 1.42, 2.29) and cardiovascular mortality (HR, 1.68; 95% CI: 1.29, 2.19) in fully adjusted analyses.
Our data show a significant inverse relation between plasma SAM and risk of mortality in patients with CAD after adjustment for homocysteine, SAH, and other cardiovascular disease risk factors.
S-腺苷甲硫氨酸(SAM)作为甲基供体参与甲基化,并转化为 S-腺苷同型半胱氨酸(SAH),SAH 是同型半胱氨酸的前体。增加的血浆 SAH 和同型半胱氨酸与心血管疾病风险增加相关。然而,血浆 SAM 与心血管风险的关系尚不清楚。
确定冠心病(CAD)患者血浆 SAM 与死亡率之间的关系。
在 2008 年 10 月至 2011 年 12 月期间,从广东冠状动脉疾病队列中招募了 1553 名 CAD 患者,测量了他们的基线血浆 SAM 浓度。采用比例风险 Cox 分析来确定 SAM 与全因和心血管死亡率之间的关系。
在中位随访 9.2(IQR:8.5-10.2)年后,1553 名参与者中有 321 人死亡,其中 227 人死于心血管疾病。在多变量调整分析中,SAM 浓度最低四分位数的患者全因死亡风险(HR,1.59;95%CI:1.14,2.21)和心血管死亡风险(HR,2.14;95%CI:1.41,3.27)均高于最高四分位数的患者。SAM 浓度每降低 1-SD,全因死亡风险增加 42%(HR,1.42;95%CI:1.23,1.64),心血管死亡风险增加 66%(HR,1.66;95%CI:1.37,2.01)。此外,在充分调整其他心血管危险因素后,血浆 SAM/SAH 比值(作为甲基化指标)每降低 1-SD,全因死亡率(HR,1.80;95%CI:1.42,2.29)和心血管死亡率(HR,1.68;95%CI:1.29,2.19)的风险也呈负相关。
我们的数据表明,在调整同型半胱氨酸、SAH 和其他心血管疾病危险因素后,CAD 患者的血浆 SAM 与死亡率之间存在显著的负相关关系。