A myocardial cytotoxic process is involved in the cardiac dysfunction of meningococcal septic shock

Myocardial dysfunction is a characteristic component of meningococcal septic shock and contributes to the persisting high mortality from the disease. Specific treatment of the myocardial failure has been hampered by the lack of understanding of its pathophysiology. We were interested to determine whether myocardial cell death was occurring in the presence of meningococcal septicemia and whether it correlated with the degree of left ventricular dysfunction and disease severity. We therefore investigated the release of cardiac troponin I (cTnI), a sensitive and specific marker of myocardial cell death, and related this to the severity of disease and cardiac dysfunction.

Prospective study

Pediatric intensive care unit

Patients admitted to the pediatric intensive care unit with a diagnosis of meningococcal septicemia.

Serum concentrations of cTnI were determined at admission to intensive care in 101 children with meningococcal septicemia and serially in 37 children. Changes in cTnI were related to disease severity as measured by the Pediatric Risk of Mortality score and two markers of cardiac dysfunction.

Serum concentrations of cTnI were elevated above the range for healthy children in 24% of children with meningococcal septicemia at admission and in 62% of patients within 48 hrs. The peak concentrations occurred between 12 and 36 hrs after admission. There were significant correlations between cTnI levels and disease severity and between cTnI levels and the degree of myocardial depression measured by quantitative transthoracic echocardiography and peak inotrope requirements.

The elevated serum concentrations of cTnI indicate that myocardial cell death is occurring in meningococcal septicemia. The relationship between cTnI and markers of myocardial function suggest that the cell death may have a role in the pathogenesis of myocardial dysfunction in meningococcal septicemia. Elucidation of the mechanism responsible for myocardial injury may lead to the development of therapeutic interventions to prevent or limit this cardiac damage.