Comparisons of multiple troponin assays for detecting chronic myocardial injury in the general population: redundant or complementary?
Comparisons of multiple troponin assays for detecting chronic myocardial injury in the general population: redundant or complementary?
复制标题
检测一般人群慢性心肌损伤的多种肌钙蛋白检测的比较：冗余还是互补？
DOI：
10.1093/eurheartj/ehad414
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发表时间：
2023
影响因子：
39.3
通讯作者：
Berry,JarettD
中科院分区：
文献类型：
--
作者：
deLemos,JamesA;Berry,JarettD
编辑部的急诊效率和防止不必要的住院，硬结果没有改善。更高的检测灵敏度和精确度也为高灵敏度肌钙蛋白的其他潜在应用打开了大门，最终可能被证明具有更大的临床影响。其中最有希望的是在没有心脏症状的流动个体中测量hs-cTnT或hs-cTnI。动态环境中的肌钙蛋白升高通常被归类为慢性心肌损伤，这一术语将肌钙蛋白持续低水平升高与心肌梗死或其他急性心肌损伤原因引起的急性肌钙蛋白升高区分开来。在慢性冠状动脉疾病（CAD）或心力衰竭（HF）门诊患者中使用hs-cTnT的早期研究发现，较高水平的hs-cTnT与全因死亡率和心血管死亡率以及发生或进展性HF的风险增加有关。在普通人群队列中进行的研究也报告了hs-cTnT与死亡和心衰的强烈关联，以及与CAD结局的显著但较小的关联。5,6特别是在hs-cTnT水平远低于第99个百分位阈值时，包括在接近检测极限的极低水平时，与HF的关联是明显的。这一点很重要，因为这些低于第99百分位阈值的低但可测量的肌钙蛋白值在指南中很少受到关注，并且在临床实践中经常被忽略。在深度表型队列中，hs-cTnT与心脏结构异常（如左室肥厚和纤维化）的相关性比与冠状动脉粥样硬化的相关性更强，这一发现可能解释了hs-cTnT与HF的相关性强于缺血结果。总的来说，这些发现表明，即使是轻微的慢性心肌损伤也可能暴露出预示未来HF风险的结构性心脏异常。随着hs-cTnI检测的出现，它们也在慢性CAD和普通人群队列中进行了评估，在某些情况下直接与hs-cTnT进行了比较。这些研究普遍表明hs-cTnI也与非致死性和致死性CVD结果密切相关。也许有些令人惊讶的是，这些研究只报道了hs-cTnT和hs-cTnI之间的适度相关性。最有趣的是，研究通常报告了hs-cTnT和hs-cTnI的互补而不是冗余的风险信息。8,9直接比较研究的范围从急诊科的“排除”研究，到慢性CAD和一般人群研究，在每个临床背景下，不同肌钙蛋白亚型提供的信息是互补的。8-10先前在普通人群队列中的研究比较了单一hs-cTnI检测与唯一可用的hs-cTnT检测。虽然hs-cTnT只有一家制造商，但不同制造商的多种检测方法可用于hs-cTnI，每种检测方法使用结合不同cTnI表位的不同抗体对。在这一期的《欧洲心脏杂志》上，McEvoy等人报道了一项研究，该研究比较了9180名美国NHANES普通人群中无心血管疾病（CVD）个体的四种不同的hs-cTn检测方法。在1999-2004年期间收集了11份血清标本，解冻后用罗氏Elecys法测定hs-cTnT，用三种不同的方法（Abbott Architect、siemens’s Centaur和Ortho Vitros）测定hs-cTnI。
EDITORIAL emergency department efficiency and prevents unnecessary hospital admissions, hard outcomes have not been improved. 2 Greater assay sensitivity and precision have also opened the door for other potential applications for high-sensitivity troponins, which may eventually prove to have even greater clinical impact. The most promising of these focus on measurement of hs-cTnT or hs-cTnI in ambulatory individuals without cardiac symptoms. Troponin elevations in the ambulatory environment are usually classified as chronic myocardial injury, a term that distinguishes persistent low-level troponin elevations from acute elevations seen with myocardial infarction or other causes of acute myocardial injury. 1 Early studies with hs-cTnT in outpatients with chronic coronary artery disease (CAD) or heart failure (HF) found that higher levels of hs-cTnT were associated with increased risk for allcause and cardiovascular mortality and incident or progressive HF. 3, 4 Studies performed in general population cohorts also reported strong associations of hs-cTnT with death and HF, and significant but smaller associations with CAD outcomes. 5, 6 Associations with HF, in particular, were evident at hs-cTnT levels well below the 99th percentile threshold, including at very low levels near the assay’s limit of detection. This is important as these low but measurable troponin values below the 99th percentile threshold receive little attention in guidelines and are often ignored in clinical practice.In deeply phenotyped cohorts, hs-cTnT associated more strongly with abnormalities in cardiac structure, such as left ventricular hypertrophy and fibrosis, than with measures of coronary atherosclerosis, 5, 7 a finding that probably explains the stronger associations of hs-cTnT with HF than ischaemic outcomes. 6 In aggregate, these findings suggest that even minor chronic myocardial injury may unmask structural cardiac abnormalities that presage future HF risk. As hs-cTnI assays became available, they were also evaluated in chronic CAD and general population cohorts, and in some cases directly compared with hs-cTnT. These studies have generally shown that hs-cTnI also associates robustly with non-fatal and fatal CVD outcomes. Perhaps somewhat surprisingly, these studies have reported only modest correlations between hs-cTnT and hs-cTnI. Most interesting is that studies have generally reported complementary, rather than redundant, risk information for hs-cTnT and hs-cTnI. 8, 9 The spectrum of direct comparison studies spans from emergency department ‘rule out’studies, to chronic CAD and general population studies, and in each clinical context the information provided by the different troponin subtypes has been complementary. 8–10 Prior studies in general population cohorts have compared a single hs-cTnI assay with the only available hs-cTnT assay. Although there is only one manufacturer for hs-cTnT, multiple assays from different manufacturers are available for hs-cTnI, each of which uses different antibody pairs that bind to different cTnI epitopes. In this issue of the European Heart Journal, McEvoy et al. report a study that compares four different hs-cTn assays in 9180 individuals without cardiovascular disease (CVD) in the US NHANES general population cohort. 11 Serum specimens had been collected in 1999–2004 and were thawed for measurement of hs-cTnT with the Roche Elecys assay, and of hs-cTnI with three different assays, namely Abbott Architect, Siemen’s Centaur, and Ortho Vitros.