Jacob VanHouten1, Gregory Fricker1, Bridget Collins1, Ritwik Bhatia1, Christopher Ellis2, Matthew Schrag3. 1. Vanderbilt University School of Medicine, Nashville, TN, USA. 2. Department of Cardiology, Vanderbilt University Medical Center, Nashville, TN, USA. 3. Department of Neurology, Vanderbilt University Medical Center, Medical Research Building III, Suite 6160/Office 6158c, 465 21st Avenue S, Nashville, TN, 37240, USA. matthew.schrag@vanderbilt.edu.
Abstract
PURPOSE OF REVIEW: Cardiac troponin levels in the blood are an important biomarker of acute coronary events, but may also be elevated in the context of acute ischemic stroke without an obvious concurrent myocardial insult. The objective of this study and systematic review is to determine how high the circulating troponin I level can rise due to ischemic stroke. RECENT FINDINGS: Anonymized medical records from Vanderbilt University Medical Center were reviewed identifying 151,972 unique acute ischemic stroke events, of which 1226 met criteria for inclusion in this study. Included patients had at least one measurement of troponin I level documented during the hospital visit when an acute ischemic stroke was diagnosed and were free of known cardiac/coronary disease, renal impairment, sepsis, or other confounders. In this group, 20.6% had a circulating troponin I level elevated over the reference range, but 99% were below 2.13 ng/mL. This is significantly lower than the distribution observed in a cohort of 89,423 unique cases of acute coronary syndrome (p < 2.2-16). A systematic review of published literature further supported the conclusion that troponin I level may increase due to an acute ischemic stroke, but rarely rises above 2 ng/mL. Because of the shared risk factors between stroke and coronary artery disease, clinicians caring for patients with acute ischemic stroke should always have a high index of suspicion for comorbid cardiac and cardiovascular disease. In general, troponin I levels greater than 2 ng/mL should not be attributed to an acute ischemic stroke, but should prompt a thorough evaluation for coronary artery disease.
PURPOSE OF REVIEW: Cardiac troponin levels in the blood are an important biomarker of acute coronary events, but may also be elevated in the context of acute ischemic stroke without an obvious concurrent myocardial insult. The objective of this study and systematic review is to determine how high the circulating troponin I level can rise due to ischemic stroke. RECENT FINDINGS: Anonymized medical records from Vanderbilt University Medical Center were reviewed identifying 151,972 unique acute ischemic stroke events, of which 1226 met criteria for inclusion in this study. Included patients had at least one measurement of troponin I level documented during the hospital visit when an acute ischemic stroke was diagnosed and were free of known cardiac/coronary disease, renal impairment, sepsis, or other confounders. In this group, 20.6% had a circulating troponin I level elevated over the reference range, but 99% were below 2.13 ng/mL. This is significantly lower than the distribution observed in a cohort of 89,423 unique cases of acute coronary syndrome (p < 2.2-16). A systematic review of published literature further supported the conclusion that troponin I level may increase due to an acute ischemic stroke, but rarely rises above 2 ng/mL. Because of the shared risk factors between stroke and coronary artery disease, clinicians caring for patients with acute ischemic stroke should always have a high index of suspicion for comorbid cardiac and cardiovascular disease. In general, troponin I levels greater than 2 ng/mL should not be attributed to an acute ischemic stroke, but should prompt a thorough evaluation for coronary artery disease.
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