Troponin I in the intensive care unit setting: from the heart to the heart
Chiara Lazzeri1, Manuela Bonizzoli, Giovanni Cianchi
1Intensive Cardiac Care Unit, Heart and Vessel Department, Azienda Ospedaliero-Universitaria Careggi, University of Florence, Florence, Italy.
When measured in the plasma, cardiac troponins T (cTnT) and I (cTnI) are considered to be highly specific markers of myocardial cell damage; however, research has demonstrated that troponin elevation may associated with causes other than coronary artery disease. In the intensive care unit (ICU) setting, increased cTnI levels are quite common findings and when documented, even on admission, intensivists should bear in mind that this laboratory finding holds a prognostic role independent of the reason for ICU admission. The mechanism(s) (such as demand ischemia, myocardial strain, etc.) and not simply the cause (i.e., renal failure) of the increment in serum cTnI should be investigated to better tailor the therapeutical regimen in the single patient. In this review, we therefore consider the nonthrombotic causes of troponin elevation in the critical setting.
When measured in the plasma, cardiac troponins T (cTnT) and I (cTnI) are considered to be highly specific markers of myocardial cell damage; however, research has demonstrated that troponin elevation may associated with causes other than coronary artery disease. In the intensive care unit (ICU) setting, increased cTnI levels are quite common findings and when documented, even on admission, intensivists should bear in mind that this laboratory finding holds a prognostic role independent of the reason for ICU admission. The mechanism(s) (such as demand ischemia, myocardial strain, etc.) and not simply the cause (i.e., renal failure) of the increment in serum cTnI should be investigated to better tailor the therapeutical regimen in the single patient. In this review, we therefore consider the nonthrombotic causes of troponin elevation in the critical setting.
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