2001 EVALUATING THE ROLE OF CARDIAC TROPONIN I IN CRITICALLY ILL

Dr CHIU Alexander
Intensive Care Unit, United Christian Hospital (December 2001 Critical Care Medicine Exit Assessment Exercise)
 
Critically ill patients are constantly exposed to a variety of physiological and pathological
stresses that can cause damage to their myocardium [1,2] Overt myocardial infarction is
uncommon however, and had been reported to occur in around 3% in one series [3]. Subclinical
myocardial damage on the other hand, is capable of causing cardiac dysfunction, hinder
hemodynamic stability and affect outcomes of these patients. Unfortunately, routine clinical
assessment and hemodynamic monitoring are difficult to recognize such damage. Conventional
diagnostic tools, such as electrocardiogram and MB isoenzyme of creatinine kinase (CKMB) [4-7]
are modalities of low sensitivity and specificity with much limitation in clinical use. Cardiac
troponin I (cTnI) is one of the most sensitive and specific marker for myocardial injury currently
available [8,9]. It has rapidly become the new "gold standard" marker for use in acute myocardial
infarction (AMI). Recently, several studies have raised the question of an unexpectedly high
percentage of elevated cTnI levels in critically ill patients without underlying coronary syndrome.
The potential diagnostic and prognostic uses of cTnI in these patients has been a topic of great
interest, notably in those suffering from sepsis, hypovolemic shock, and acute neurologic events
[10-22]. In the first part of this article, an overview of the development of cardiac troponin and its
association with adverse manifestations and outcomes is being reviewed. Different postulations
of the mechanism of troponin release were also presented. In the second part of this article, a
prospective observational study evaluating the role of cTnI in diagnosing myocardial dysfunction
is described.