Department of Medicine, Karolinska Institutet, Solna, Stockholm, Sweden; Functional Area of Emergency Medicine, Karolinska University Hospital, Huddinge, Stockholm, Sweden.
Department of Clinical Sciences, Karolinska Institutet, Solna, Stockholm, Sweden; Department of Cardiology, Danderyd University Hospital, Danderyd, Stockholm, Sweden.
J Am Coll Cardiol. 2017 Oct 31;70(18):2226-2236. doi: 10.1016/j.jacc.2017.08.064.
There is a paucity of data on the association between high-sensitivity cardiac troponin (hs-cTn) levels and outcomes in patients with chest pain but no myocardial infarction (MI), or any other condition that may lead to acutely elevated troponin levels.
The authors hypothesized that any detectable high-sensitivity cardiac troponin T (hs-cTnT) level is associated with adverse outcomes.
All patients (N = 22,589) >25 years of age with chest pain and hs-cTnT analyzed concurrently in the emergency department of Karolinska University Hospital, Stockholm, Sweden from 2011 to 2014 were eligible for inclusion. After excluding all patients with acute conditions that may have affected hs-cTnT, or MI associated with the visit, or insufficient information to determine whether troponin levels were stable, Cox regression was used to estimate risks for all-cause, cardiovascular, and noncardiovascular mortality, MI, and heart failure at different levels of troponins.
A total of 19,460 patients with a mean age of 54 ± 17 years were included. During a mean follow-up of 3.3 ± 1.2 years, 1,349 (6.9%) patients died. Adjusted hazard ratios (with 95% confidence intervals) for all-cause mortality were 2.00 (1.66 to 2.42), 2.92 (2.38 to 3.59), 4.07 (3.28 to 5.05), 6.77 (5.22 to 8.78), and 9.68 (7.18 to 13.00) in patients with hs-cTnT levels of 5 to 9, 10 to 14, 15 to 29, 30 to 49, and ≥50 ng/l, respectively, compared with patients with hs-cTnT levels <5 ng/l. There was a strong and graded association between all detectable levels of hs-cTnT and risk for MI, heart failure, and cardiovascular and noncardiovascular mortality.
Among patients with chest pain and stable troponin levels, any detectable level of hs-cTnT is associated with an increased risk of death and cardiovascular outcomes and should merit further attention.
目前关于高敏心肌肌钙蛋白（hs-cTn）水平与胸痛但无心肌梗死（MI）或任何其他可能导致肌钙蛋白水平急性升高的患者结局之间的关联的数据很少。
作者假设任何可检测到的高敏心肌肌钙蛋白 T（hs-cTnT）水平都与不良结局相关。
2011 年至 2014 年，在瑞典斯德哥尔摩卡罗林斯卡大学医院急诊科对年龄>25 岁、胸痛且 hs-cTnT 同时进行分析的所有患者均符合纳入标准。排除所有可能影响 hs-cTnT 的急性情况、与就诊相关的 MI 或无足够信息确定肌钙蛋白水平是否稳定的患者后，采用 Cox 回归估计不同水平的肌钙蛋白与全因、心血管和非心血管死亡率、MI 和心力衰竭相关的风险。
共纳入 19460 例平均年龄为 54±17 岁的患者。在平均 3.3±1.2 年的随访期间，1349 例（6.9%）患者死亡。全因死亡率的调整后危险比（95%置信区间）分别为 2.00（1.66 至 2.42）、2.92（2.38 至 3.59）、4.07（3.28 至 5.05）、6.77（5.22 至 8.78）和 9.68（7.18 至 13.00），与 hs-cTnT 水平<5ng/l 的患者相比，hs-cTnT 水平分别为 5 至 9ng/l、10 至 14ng/l、15 至 29ng/l、30 至 49ng/l 和≥50ng/l 的患者。所有可检测的 hs-cTnT 水平与 MI、心力衰竭和心血管及非心血管死亡率的风险之间存在强且分级关联。
在胸痛且肌钙蛋白水平稳定的患者中，任何可检测到的 hs-cTnT 水平都与死亡和心血管结局风险增加相关，应引起进一步关注。
