Cramer G Etienne, Gommans D H Frank, Dieker Hendrik-Jan, Michels Michelle, Verheugt Freek, de Boer Menko-Jan, Bakker Jeannette, Fouraux Michael A, Timmermans Janneke, Kofflard Marcel, Brouwer Marc
Cardiology, Radboudumc, Nijmegen, Gelderland, The Netherlands
Cardiology, Radboudumc, Nijmegen, Gelderland, The Netherlands.
Heart. 2020 Aug;106(15):1169-1175. doi: 10.1136/heartjnl-2019-315818. Epub 2020 Jan 30.
Troponin and high signal intensity on T2-weighted (HighT2) cardiovascular magnetic resonance imaging (CMRi) are both markers of myocardial injury in hypertrophic cardiomyopathy (HCM). The interplay between exercise and disease development remains uncertain in HCM. We sought to assess the occurrence of postexercise troponin rises and its determinants.
Multicentre project on patients with HCM and mutation carriers without hypertrophy (controls). Participants performed a symptom limited bicycle test with hs-cTnT assessment pre-exercise and 6 hours postexercise. Pre-exercise CMRi was performed in patients with HCM to assess measures of hypertrophy and myocardial injury. Depending on baseline troponin (< or 13 ng/L), a rise was defined as a >50% or >20% increase, respectively.
Troponin rises occurred in 18% (23/127) of patients with HCM and 4% (2/53) in mutation carriers (p=0.01). Comparing patients with HCM with and without a postexercise troponin rise, maximum heart rates (157±19 vs 143±23, p=0.004) and maximal wall thickness (20 mm vs 17 mm, p=0.023) were higher in the former, as was the presence of late gadolinium enhancement (85% vs 57%, p=0.02). HighT2 was seen in 65% (13/20) and 19% (15/79), respectively (p<0.001). HighT2 was the only independent predictor of troponin rise (adjusted odds ratio 7.9; 95% CI 2.7 to 23.3; p<0.001).
Postexercise troponin rises were seen in about 20% of patients with HCM, almost five times more frequent than in mutation carriers. HighT2 on CMRi may identify a group of particularly vulnerable patients, supporting the concept that HighT2 reflects an active disease state, prone to additional injury after a short episode of high oxygen demand.
肌钙蛋白和T2加权（高T2）心血管磁共振成像（CMRi）上的高信号强度都是肥厚型心肌病（HCM）中心肌损伤的标志物。运动与疾病发展之间的相互作用在HCM中仍不确定。我们试图评估运动后肌钙蛋白升高的发生率及其决定因素。
针对HCM患者和无肥厚的突变携带者（对照组）开展的多中心项目。参与者进行了症状限制性自行车试验，在运动前和运动后6小时评估高敏肌钙蛋白T（hs-cTnT）。对HCM患者进行运动前CMRi检查，以评估肥厚和心肌损伤的指标。根据基线肌钙蛋白（<或13 ng/L），升高分别定义为升高>50%或>20%。
HCM患者中18%（23/127）出现肌钙蛋白升高，突变携带者中4%（2/53）出现肌钙蛋白升高（p=0.01）。比较运动后肌钙蛋白升高和未升高的HCM患者，前者的最大心率（157±19对143±23，p=0.004）和最大壁厚（20 mm对17 mm，p=0.023）更高，钆增强晚期的存在情况也是如此（85%对57%，p=0.02）。高T2分别在65%（13/20）和19%（15/79）的患者中出现（p<0.001）。高T2是肌钙蛋白升高的唯一独立预测因素（调整后的优势比为7.9；95%置信区间为2.7至23.3；p<0.001）。
约20%的HCM患者出现运动后肌钙蛋白升高，几乎是突变携带者的五倍。CMRi上的高T2可能识别出一组特别易损的患者，支持高T2反映活跃疾病状态的概念，即在短时间高需氧发作后易于发生额外损伤。
