Document Detail

Cardiac troponins I and T are biological markers of left ventricular dysfunction in septic shock.
MedLine Citation:
PMID:  10794747     Owner:  NLM     Status:  MEDLINE    
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.
K M ver Elst; H D Spapen; D N Nguyen; C Garbar; L P Huyghens; F K Gorus
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Clinical chemistry     Volume:  46     ISSN:  0009-9147     ISO Abbreviation:  Clin. Chem.     Publication Date:  2000 May 
Date Detail:
Created Date:  2000-05-31     Completed Date:  2000-05-31     Revised Date:  2004-11-17    
Medline Journal Info:
Nlm Unique ID:  9421549     Medline TA:  Clin Chem     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  650-7     Citation Subset:  IM    
Department of Clinical Chemistry, Academic Hospital Vrije Universiteit Brussel (AZ-VUB), B-1090 Brussels, Belgium.
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MeSH Terms
Aged, 80 and over
Biological Markers / blood
C-Reactive Protein / metabolism
Calcitonin / blood
Creatine Kinase / blood
Echocardiography, Transesophageal
Middle Aged
Myocardium / metabolism
Prospective Studies
Protein Precursors / blood
Shock, Septic / blood*,  complications
Troponin I / blood*
Troponin T / blood*
Ventricular Dysfunction, Left / blood*,  etiology,  ultrasonography
Reg. No./Substance:
0/Biological Markers; 0/Isoenzymes; 0/Protein Precursors; 0/Troponin I; 0/Troponin T; 56645-65-9/procalcitonin; 9007-12-9/Calcitonin; 9007-41-4/C-Reactive Protein; EC Kinase

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