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.
ver Elst
K M
KM
Department of Clinical Chemistry, Academic Hospital Vrije Universiteit Brussel (AZ-VUB), B-1090 Brussels, Belgium.
Spapen
H D
HD
Nguyen
D N
DN
Garbar
C
C
Huyghens
L P
LP
Gorus
F K
FK
D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D002116:Calcitonin / Q000097:blood; D003402:Creatine Kinase / Q000097:blood; D017548:Echocardiography, Transesophageal; D006801:Humans; D007527:Isoenzymes; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism; D011446:Prospective Studies; D011498:Protein Precursors / Q000097:blood; D012151:Resuscitation; D012772:Shock, Septic / Q000097:blood* / Q000150:complications; D019210:Troponin I / Q000097:blood*; D020107:Troponin T / Q000097:blood*; D018487:Ventricular Dysfunction, Left / Q000097:blood* / Q000000981:diagnostic imaging / Q000209:etiology
D015415:Biomarkers; D007527:Isoenzymes; D011498:Protein Precursors; D019210:Troponin I; D020107:Troponin T; D002116:Calcitonin; D002097:C-Reactive Protein; D003402:Creatine Kinase