Myocardial injury and ventricular dysfunction related to training levels among nonelite participants in the Boston marathon
Myocardial injury and ventricular dysfunction related to training levels among nonelite participants in the Boston marathon
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DOI：
10.1161/circulationaha.106.647461
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发表时间：
2006-11-28
期刊：
影响因子：
37.8
通讯作者：
Wood, Malissa J.
中科院分区：
文献类型：
--
作者：
Neilan, Tomas G.;Januzzi, James L.;Wood, Malissa J.
背景-多项研究分别记录了耐力运动后心功能不全和心脏损伤的生化证据;然而，两者之间缺乏令人信服的联系。我们的目的是确定所观察到的短暂性心功能不全和生化证据的业余参与者在耐力运动的心脏损伤之间的关联，并引出观察到的损伤和dysfunction.Methods和Results的危险因素-我们筛选了60名非精英参与者，2004年和2005年波士顿马拉松赛前后，超声心动图和血清生物标志物。超声心动图包括常规测量以及组织多普勒衍生的应变和应变率成像。生物标志物包括心肌肌钙蛋白T（cTnT）和N-末端脑钠肽前体（NT-proBNP）。所有受试者均完成了比赛。比赛后的超声心动图异常包括舒张期充盈改变，肺动脉压和右心室内径增加，右心室收缩功能下降。基线时，所有患者的肌钙蛋白均不可测量。比赛结束后，> 60%的参与者的cTnT水平升高>正常值的第99百分位数（> 0.01 ng/ mL），而40%的参与者的cTnT水平等于或高于急性心肌坏死的决策限（>= 0.03 ng/mL）。比赛后，NT-proBNP浓度从63（四分位距[IQR] 21至81）pg/mL增加至131（IQR 82至193）pg/mL（P < 0.001）。生物标志物的增加与比赛后舒张功能障碍、肺动脉压升高和右心室功能障碍（右心室中应变，r =-0.70，P < 0.001）相关，与训练里程呈负相关（r =-0.71，P < 0.001）。与每周训练> 45英里的运动员相比，训练0.01 ng/mL的运动员，P < 0.001）和应激（NT-proBNP 182 vs 106 pg/mL，P < 0.001）。结论-完成马拉松与心功能不全和损伤的相关生化和超声心动图证据相关，并且这种风险在训练较少的参与者中增加。
Background - Multiple studies have individually documented cardiac dysfunction and biochemical evidence of cardiac injury after endurance sports; however, convincing associations between the two are lacking. We aimed to determine the associations between the observed transient cardiac dysfunction and biochemical evidence of cardiac injury in amateur participants in endurance sports and to elicit the risk factors for the observed injury and dysfunction.Methods and Results - We screened 60 nonelite participants, before and after the 2004 and 2005 Boston Marathons, with echocardiography and serum biomarkers. Echocardiography included conventional measures as well as tissue Doppler-derived strain and strain rate imaging. Biomarkers included cardiac troponin T (cTnT) and N-terminal pro-brain natriuretic peptide (NT-proBNP). All subjects completed the race. Echocardiographic abnormalities after the race included altered diastolic filling, increased pulmonary pressures and right ventricular dimensions, and decreased right ventricular systolic function. At baseline, all had unmeasurable troponin. After the race, > 60% of participants had increased cTnT > 99th percentile of normal (> 0.01 ng/ mL), whereas 40% had a cTnT level at or above the decision limit for acute myocardial necrosis (>= 0.03 ng/mL). After the race, NT-proBNP concentrations increased from 63 (interquartile range [IQR] 21 to 81) pg/mL to 131 (IQR 82 to 193) pg/mL (P < 0.001). The increase in biomarkers correlated with post-race diastolic dysfunction, increased pulmonary pressures, and right ventricular dysfunction (right ventricular mid strain, r = -0.70, P < 0.001) and inversely with training mileage (r = -0.71, P < 0.001). Compared with athletes training > 45 miles/ wk, athletes who trained 0.01 ng/mL, P < 0.001), and stress (NT-proBNP 182 versus 106 pg/mL, P < 0.001).Conclusions - Completion of a marathon is associated with correlative biochemical and echocardiographic evidence of cardiac dysfunction and injury, and this risk is increased in those participants with less training.