Sandesara Pratik B, O'Neal Wesley T, Tahhan Ayman Samman, Hayek Salim S, Lee Suegene K, Khambhati Jay, Topel Matthew L, Hammadah Muhammad, Alkhoder Ayman, Ko Yi-An, Gafeer Mohamad Mazen, Beshiri Agim, Murtagh Gillian, Kim Jonathan H, Wilson Peter, Shaw Leslee, Epstein Stephen E, Sperling Laurence S, Quyyumi Arshed A
Emory Clinical Cardiovascular Research Institute, Division of Cardiology, Emory University School of Medicine, Atlanta, Georgia.
Emory Clinical Cardiovascular Research Institute, Division of Cardiology, Emory University School of Medicine, Atlanta, Georgia.
Am J Cardiol. 2018 Jun 15;121(12):1461-1466. doi: 10.1016/j.amjcard.2018.02.039. Epub 2018 Mar 14.
It is unknown whether the association of high-sensitivity troponin I (hs-TnI) with adverse cardiovascular outcomes varies by the presence of chronic kidney disease (CKD). We examined the association of hs-TnI with adverse cardiovascular outcomes in those with and without CKD in 4,107 (mean age, 64 years; 63% men; 20% black) patients from the Emory Cardiovascular Biobank who underwent coronary angiography. CKD (n = 1,073) was defined as estimated glomerular filtration rate <60 ml/min/1.73 m or urine albumin/creatinine ratio >30 mg/g at baseline. Cox regression was used to compute hazard ratios (HR) for the association between hs-TnI levels (per doubling of hs-TnI: log[hs-TnI] + 1) and death, cardiovascular death, and major adverse cardiac events (MACE), separately. Hs-TnI was a stronger predictor of death (CKD: HR 1.23, 95% confidence interval [CI] 1.15 to 1.31; no CKD: HR 1.11, 95% CI 1.05 to 1.17, p-interaction = 0.023), cardiovascular death (CKD: HR 1.24, 95% CI 1.14 to 1.34; no CKD: HR 1.15, 95% CI 1.07 to 1.22, p-interaction = 0.12), and MACE (CKD: HR 1.18, 95% CI 1.11 to 1.25; no CKD: HR 1.11, 95% CI 1.06 to 1.16, p-interaction = 0.095) in CKD compared with non-CKD. The association between hs-TnI and death in patients with CKD was stronger for patients without obstructive coronary artery disease (no obstructive coronary artery disease: HR 1.60, 95% CI 1.27 to 2.01; obstructive coronary artery disease: HR 1.19, 95% CI 1.11 to 1.27, p-interaction = 0.041). In conclusion, hs-TnI is a stronger predictor of adverse cardiovascular events in patients who have CKD than those without, even in the absence of obstructive coronary artery disease. Hs-TnI may identify CKD patients who are high risk for adverse cardiovascular outcomes in whom aggressive risk factor modification strategies are warranted.
高敏肌钙蛋白I（hs-TnI）与不良心血管结局之间的关联是否因慢性肾脏病（CKD）的存在而有所不同尚不清楚。我们在4107名（平均年龄64岁；63%为男性；20%为黑人）接受冠状动脉造影的埃默里心血管生物样本库患者中，研究了hs-TnI与有无CKD患者不良心血管结局之间的关联。CKD（n = 1073）定义为基线时估计肾小球滤过率<60 ml/min/1.73 m²或尿白蛋白/肌酐比值>30 mg/g。采用Cox回归分别计算hs-TnI水平（hs-TnI每增加一倍：log[hs-TnI]+1）与死亡、心血管死亡和主要不良心脏事件（MACE）之间关联的风险比（HR）。与无CKD患者相比，hs-TnI对CKD患者的死亡（CKD：HR 1.23，95%置信区间[CI] 1.15至1.31；无CKD：HR 1.11，95% CI 1.05至1.17，p交互作用 = 0.023）、心血管死亡（CKD：HR 1.24，95% CI 1.14至1.34；无CKD：HR 1.15，95% CI 1.07至1.22，p交互作用 = 0.12）和MACE（CKD：HR 1.18，95% CI 1.11至1.25；无CKD：HR 1.11，95% CI 1.06至1.16，p交互作用 = 0.095）的预测更强。在无阻塞性冠状动脉疾病的CKD患者中，hs-TnI与死亡之间的关联更强（无阻塞性冠状动脉疾病：HR 1.60，95% CI 1.27至2.01；阻塞性冠状动脉疾病：HR 1.19，95% CI 1.11至1.27，p交互作用 = 0.041）。总之，即使在无阻塞性冠状动脉疾病的情况下，hs-TnI对有CKD患者不良心血管事件的预测也比无CKD患者更强。Hs-TnI可能识别出有不良心血管结局高风险的CKD患者，对这些患者有必要采取积极的危险因素修正策略。
