- Meeting abstract
The use of cardiac troponin I to diagnose myocardial dysfunction in the critically ill
Critical Care volume 6, Article number: P159 (2002)
Myocardial dysfunction in the critically ill is characterized by decreased contractility, increased compliance and progressive ventricular dilatation. The phenomenon is global but the clinical consequences are demonstrated predominantly by the left ventricle. The condition is most commonly seen in patients with sepsis and acute neurologic events, but has also been recognized in patients with trauma and other diseases giving rise to systemic inflammatory response syndrome. The pathophysiology is uncertain, but myocyte damage attributed to either micro-ischemia or circulating myocardial depressant substances are prevailing postulations. Electrocardiogram and conventional cardiac markers like CK-MB are modalities of low sensitivity and specificity to diagnose this condition. Cardiac troponin I (cTnI) is a highly tissue specific protein that is detectable in circulation even with minor myocardial injury. Given these properties, it appeared reasonable to use a biochemical assay of cTnI to detect myocardial dysfunction in these patients.
The purpose of the present study is threefold: to address the incidence of abnormal cTnI levels in critically ill patients; to evaluate the association of cTnI elevation with left ventricular dysfunction; and to assess whether cTnI elevation presages a poorer clinical outcome.
A prospectively designed study that recruited all admissions to our intensive care unit from June 2000 through September 2000. Patients suffered from myocardial infarction or undergone cardiopulmonary resuscitation was excluded. Blood samples for measurement of cTnI levels were obtained on admission and upon 72 hours. Transthoracic echocardiogram was performed within the first 3 days of admission to assess left ventricular ejection fraction using method described by Simpson. Extensive clinical evaluations and electrocardiograms were also obtained. In-ICU mortality was documented and surviving patients were followed up for a 6-month period.
Fifty-one patients (30%) of 170 admissions in the final cohort had elevated cTnI levels. The median cTnI level on admission was 3.0 ng/ml (1.2–6.0 ng/ml) and the median level at 72 hours was 3.7 ng/ml (1.5–8.8 ng/ml). Patients with elevated cTnI levels had lower systolic arterial pressure, higher creatinine levels, worse oxygenation index, greater APACHE II scores as well as more frequently suffered from sepsis (P < 0.05 in all conditions). Multiple logistic regression demonstrated cTnI status to be an independent predictor of left ventricular dysfunction with an adjusted odds ratio of 10.34 (2.31–46.21) and a P value of 0.002. Cumulative survival at 6 months revealed significant difference in mortality rates between cTnI-positive and cTnI-negative patients (log rank 4.55, P = 0.03). cTnI status however was not shown to be an independent predictor for in-ICU mortality by multivariate analysis.
There is a high incidence of cTnI elevation in the intensive care unit setting. cTnI is a surrogate marker for myocardial dysfunction and is also useful for risk stratification in those that are critically ill.
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Chiu, A. The use of cardiac troponin I to diagnose myocardial dysfunction in the critically ill. Crit Care 6 (Suppl 1), P159 (2002). https://doi.org/10.1186/cc1617