Cardiac Troponins I and T Are Biological Markers of Left Ventricular Dysfunction in Septic Shock

Abstract

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 μg/L) and cTnT (≥0.1 μg/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.

Cardiac troponin I does not independently predict mortality in critically ill patients with severe sepsis

“…However, most studies reporting the use of troponin in sepsis patients had a sample size of fewer than 50 patients. 11,14,[16][17][18]…”

“…9 The prognostic effects of elevated troponins in patients with sepsis have been studied by several investigators. [10][11][12][13][14][15] Some investigators found troponin to be an independent predictor, and others found troponin to be elevated in patients with sepsis but did not independently predict mortality. This variation in the published results might be resulting from the differences in the assays used to quantify troponin and the variability in the cut-off levels to define 'elevated' troponin in the published results.…”

“…Furthermore, most of these studies are relatively small with a sample size ranging between 15 and 46 patients. 11,14,[16][17][18] Given this variability in the published literature possibly resulting from small sample sizes, our aim was to evaluate the prognostic value of troponin I in a larger sample of critically ill patients admitted to our ICU with severe sepsis.…”

Cardiac troponins

“…74,90 While the exact mechanisms are unknown, cardiac oxygen demand exceeding supply, septic microemboli, toxic effects from bacterial endotoxins, and cardiac depressant effects from cytokines such as tumor necrosis factor-a are postulated mechanisms. 74,91 Ischemia and reperfusion injury secondary to microvascular dysfunction may also be involved. In humans, elevated cTn values during sepsis are associated with left ventricular dysfunction.…”

Prospective Clinical Evaluation of Serum Cardiac Troponin T in Dogs Admitted to a Veterinary Teaching Hospital

“…In humans, measurement of serum cardiac troponin concentration is most commonly used in the diagnosis of myocardial infarction secondary to coronary heart disease. [4][5][6] However, other causes of myocardial injury more commonly encountered in veterinary medicine, such as myocardial trauma, 7,8 myocarditis, 9,10 advanced congestive heart failure, 11,12 sepsis, 13,14 and anthracycline chemotherapy, [15][16][17][18] also cause increases in circulating cardiac troponin in humans. Several recent experimental studies also have identified increases in cTnT as a specific marker of myocardial damage secondary to myocardial infarction in dogs 2,19 and doxorubicin cardiotoxicosis in rats and mice.…”