Chest
Volume 111, Issue 5, May 1997, Pages 1340-1347
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Clinical Investigations in Critical Care
Clinically Recognized Cardiac Dysfunction: An Independent Determinant of Mortality Among Critically III Patients: Is There a Role for Serial Measurement of Cardiac Troponin I?

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Objective

To determine the relative importance of clinically recognized cardiac dysfunction and unrecognized cardiac injury to hospital mortality.

Design

Prospective, blinded, single-center study.

Setting

Medical ICU of Barnes-Jewish Hospital, St. Louis, a university-affiliated teaching hospital.

Patients

Two hundred sixty adult patients requiring admission to the medical ICU.

Interventions

Daily blood collection.

Main outcome measures

The presence of cardiac dysfunction (myocardial infarction, unstable angina, cardiac arrest, or congestive heart failure) as determined by the physicians responsible for the care of the patient. Daily measurement of levels of cardiac troponin I, a sensitive, highly specific, and long-lived marker of myocardial injury.

Results

Fifty-five (21.2%) patients had clinical evidence of cardiac dysfunction, among whom 22 (40%) had an elevated level of cardiac troponin I. A total of 41 (15.8%) patients had evidence of acute myocardial injury based on elevated levels of cardiac troponin I. Patients with clinically recognized cardiac dysfunction had a significantly greater hospital mortality rate compared to patients without clinically recognized cardiac dysfunction (45.5% vs 10.2%; p<0.001). Similarly, patients with elevated blood levels of cardiac troponin I had a greater hospital mortality rate compared to patients without elevated blood levels of cardiac troponin I (26.8% vs 16.0%; p=0.095). Multiple logistic-regression analysis controlling for potential confounding variables demonstrated that the presence of clinically recognized cardiac dysfunction was independently associated with hospital mortality (adjusted odds ratio=3.0; 95% confidence interval=1.9 to 4.8; p=0.016). However, having an elevated blood level of cardiac troponin I was not found to be an independent determinant of hospital mortality.

Conclusion

Among critically ill medical patients, clinically recognized cardiac dysfunction is an independent determinant of hospital mortality. The identification of unrecognized cardiac injury, using serial measurements of cardiac troponin I, did not independently contribute to the prediction of hospital mortality.

Section snippets

Study Location and Population

The study was conducted within the medical ICU (19 beds) of Barnes-Jewish Hospital, St. Louis, a private teaching hospital with 1,300 medical ICU admissions per year. All patients admitted to the medical ICU during a 3-month period (April 1995 to June 1995) were evaluated prospectively. The nursing staff and physicians providing care for the patients in the medical ICU were completely blinded to the nature of this investigation. The study protocol was approved by the Human Studies Committee of

Patient Population

A total of 260 eligible patients requiring medical ICU admission were evaluated during the study period. The mean age of the study population was 58.5±18.6 years and 49.2% were female. Baseline demographic information and hospital mortality according to the presence or absence of clinically recognized cardiac dysfunction are shown in Table 1. Patients with clinically recognized cardiac dysfunction were significantly older (p=0.007), had greater APACHE II scores (p<0.001), and were more likely

DISCUSSION

Our main observation was that the occurrence of clinically recognized cardiac dysfunction is common (21.2%) among critically ill medical patients and is an independent determinant of hospital mortality. The finding of acute cardiac injury, assessed using serial blood measurements of cardiac troponin I, was also common (15.8%) but did not independently contribute to hospital mortality. We also demonstrated that severity of illness as assessed by APACHE II was not a good discriminator for the

ACKNOWLEDGMENTS

The authors wish to thank Daniel P. Schuster, MD, for his review of this manuscript.

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  • Cited by (0)

    This work was supported in part by a grant from the American Lung Association of eastern Missouri.

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