Cardiac troponins I and T are biological markers of left ventricular dysfunction in septic shock.

BACKGROUND: Cardiac depression in severe sepsis and septic shock is characterized by left ventricular (LV) failure. To date, it is unclear whether clinically unrecognized myocardial cell injury accompanies, causes, or results from this decreased cardiac performance. We therefore studied the relationship between cardiac troponin I (cTnI) and T (cTnT) and LV dysfunction in early septic shock. METHODS: Forty-six patients were consecutively enrolled, fluid-resuscitated, and treated with catecholamines. Cardiac markers were measured at study entry and after 24 and 48 h. LV function was assessed by two-dimensional transesophageal echocardiography. RESULTS: Increased plasma concentrations of cTnI (>/=0.4 microgram/L) and cTnT (>/=0.1 microgram/L) were found in 50% and 36%, respectively, of the patients at one or more time points. cTnI and cTnT were significantly correlated (r = 0.847; P <0.0001). Compared with cTnI-negative patients, cTnI-positive subjects were older, presented higher Acute Physiology and Chronic Health Evaluation II scores at diagnosis, and tended to have a worse survival rate and a more frequent history of arterial hypertension or previous myocardial infarction. In contrast, the two groups did not differ in type of infection or pathogen, or in dose and type of catecholamine administered. Continuous electrocardiographic monitoring in all patients and autopsy in 12 nonsurvivors did not disclose the occurrence of acute ischemia during the first 48 h of observation. LV dysfunction was strongly associated with cTnI positivity (78% vs 9% in cTnI-negative patients; P <0.001). In multiple regression analysis, both cTnI and cTnT were exclusively associated with LV dysfunction (P <0.0001). CONCLUSIONS: These findings suggest that in septic shock, clinically unrecognized myocardial cell injury is a marker of LV dysfunction. The latter condition tends to occur more often in severely ill older patients with underlying cardiovascular disease. Further studies are needed to determine the extent to which myocardial damage is a cause or a consequence of LV dysfunction.

Analytic and clinical evaluation of the Abbott AxSYM cardiac troponin I assay.

We evaluated the AxSYM immunoassay for the quantification of cardiac troponin I (cTnI). Total assay imprecision, expressed as coefficient of variation, ranged between 5.6% and 8.3% for commercial control serum samples and between 4.2% and 13.9% for pooled patient samples. Linearity was verified up to 42 micrograms/L. Triglycerides (up to 1,000 mg/dL) did not interfere with the assay, but minor hemolysis and clinically relevant hyperbilirubinemia caused a negative bias. In 186 patient samples, AxSYM cTnI levels correlated significantly with data obtained with the Stratus II cTnI fluorometric enzyme immunoassay but were 3 to 4 times higher on AxSYM than on Stratus II. In 111 healthy blood donors, the reference range for cTnI levels on AxSYM was 0.0 to 0.4 microgram/L. After eccentric isokinetic exercise, healthy volunteers showed a rise in creatine kinase MB mass (AxSYM) but not in cTnI. On AxSYM and Stratus II, cTnI levels increased above the manufacturer's cutoff for acute myocardial infarction in all 17 patients followed up after onset of infarction-related chest pain but in only 1 of 91 control subjects. The AxSYM cTnI assay is a valid alternative for the detection of myocardial injury with diagnostic performance comparable to the established Stratus cTnI assay.