Unusual towering elevation of troponin I after ST-elevation myocardial infarction and intensive monitoring with echocardiography post-percutaneous coronary intervention: a case report

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• 作者：Fahad Javed (1)
  Shahzeb A Khan (1)
  Emad F Aziz (1)
  Taimur Abbasi (1)
  Ramya Suryadevara (1)
  Eyal Herzog (1)
  
• 刊名：Journal of Medical Case Reports
• 出版年：2010
• 出版时间：December 2010
• 年：2010
• 卷：4
• 期：1
• 全文大小：468KB
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• 作者单位：Fahad Javed (1)
  Shahzeb A Khan (1)
  Emad F Aziz (1)
  Taimur Abbasi (1)
  Ramya Suryadevara (1)
  Eyal Herzog (1)
  
  1. 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
  

文摘

Introduction 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. Case presentation 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. Conclusion 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.