Javed Fahad, Khan Shahzeb A, Aziz Emad F, Abbasi Taimur, Suryadevara Ramya, Herzog Eyal
Division of Cardiology, St, Luke's Roosevelt Hospital Center, University Hospital for College of Physicians and Surgeons of Columbia University, Amsterdam Avenue, 10025, New York, USA.
J Med Case Rep. 2010 May 18;4:137. doi: 10.1186/1752-1947-4-137.
The elevation of troponin levels directly corresponds to the extent of myocardial injury. Here we present a case of a robust rise in cardiac biomarkers that correspond to extensive damage to the myocardium but did not spell doom for our patient. It is important to note that, to the best of our knowledge, this is the highest level of troponin I ever reported in the literature after a myocardial injury in an acute setting.
A 53-year-old African American man with an unknown medical history presented to the emergency room of our hospital with chest pain associated with diaphoresis and altered mental status. He required emergency intubation due to acute respiratory failure and circulatory collapse within 10 minutes of his arrival. He was started on heparin and eptifibatide (Integrilin) drips but he was taken immediately for cardiac catheterization, which showed a total occlusion of his proximal left anterior descending, diffuse left circumflex disease and severe left ventricular dysfunction with segmental wall motion abnormality. He remained hypotensive throughout the procedure and an intra-aortic balloon pump was inserted for circulatory support. His urinary toxicology examination result was positive for cocaine metabolites. Serial echocardiograms showed an akinetic apex, a severely hypokinetic septum, and severe systolic dysfunction of his left ventricle. Our patient stayed at the Coronary Care Unit for a total of 15 days before he was finally discharged.
Studies demonstrate that an increase of 1 ng/ml in the cardiac troponin I level is associated with a significant increase in the risk ratio for death. The elevation of troponin I to 515 ng/ml in our patient is an unusual robust presentation which may reflect a composite of myocyte necrosis and reperfusion but without short-term mortality. Nevertheless, prolonged close monitoring is required for better outcome. We also emphasize the need for the troponin assays to be standardized and have universal cutoffs for comparisons across available data.
肌钙蛋白水平的升高与心肌损伤程度直接相关。在此,我们报告一例心脏生物标志物显著升高的病例,该升高与心肌广泛损伤相对应,但患者并未因此而预后不良。需要注意的是,据我们所知,这是文献中报道的急性心肌损伤后肌钙蛋白I的最高水平。
一名53岁的非裔美国男性,既往病史不明,因胸痛伴多汗及精神状态改变就诊于我院急诊科。他在到达后10分钟内因急性呼吸衰竭和循环衰竭需要紧急插管。他开始接受肝素和依替巴肽(Integrilin)静脉滴注,但立即接受了心脏导管检查,结果显示左前降支近端完全闭塞、左旋支弥漫性病变以及严重的左心室功能障碍伴节段性室壁运动异常。在整个手术过程中他一直处于低血压状态,并插入了主动脉内球囊泵以提供循环支持。他的尿液毒理学检查结果显示可卡因代谢物呈阳性。系列超声心动图显示心尖运动减弱、室间隔严重运动减弱以及左心室严重收缩功能障碍。我们的患者在冠心病监护病房共住院15天,最终出院。
研究表明,心脏肌钙蛋白I水平每升高1 ng/ml,死亡风险比就会显著增加。我们的患者肌钙蛋白I升高至515 ng/ml是一种异常显著的表现,这可能反映了心肌细胞坏死和再灌注的综合情况,但并未导致短期死亡。尽管如此,为了获得更好的预后,仍需要进行长期密切监测。我们还强调肌钙蛋白检测需要标准化,并具有通用的临界值以便对现有数据进行比较。