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1
Department of Clinical Chemistry, Academic Hospital Vrije Universiteit Brussel (AZ-VUB), B-1090 Brussels, Belgium.
2
Department of Intensive Care, Academic Hospital Vrije Universiteit Brussel (AZ-VUB), B-1090 Brussels,
Belgium.
3
Department of Pathological Anatomy,
Academic Hospital Vrije Universiteit Brussel (AZ-VUB), B-1090 Brussels,
Belgium.
a Address correspondence to this author at: Academic Hospital Vrije Universiteit Brussel (AZ-VUB), Department of Clinical Chemistry, Laarbeeklaan 101, B-1090 Brussels, Belgium. Fax 32-2-4775047; e-mail bdr{at}vub.ac.be
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.
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