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

Objective: Myocardial dysfunction is a characteristic component of meningoc occal septic shock and contributes to the persisting high mortality from th e disease. Specific treatment of the myocardial failure has been hampered b y the lack of understanding of its pathophysiology. We were interested to d etermine whether myocardial cell death was occurring in the presence of men ingococcal septicemia and whether it correlated with the degree of left ven tricular dysfunction and disease severity. We therefore investigated the re lease of cardiac troponin I (cTnI), a sensitive and specific marker of myoc ardial cell death, and related this to the severity of disease and cardiac dysfunction. Design: Prospective study Setting: Pediatric intensive care unit Subjects: Patients admitted to the pediatric intensive care unit with a dia gnosis of meningococcal septicemia. Interventions: 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 measure d by the Pediatric Risk of Mortality score and two markers of cardiac dysfu nction. Measurements and Main Results: Serum concentrations of cTnI were elevated a bove the range for healthy children in 24% of children with meningococcal s epticemia at admission and in 62% of patients within 48 hrs. The peak conce ntrations occurred between 12 and 36 hrs after admission. There were signif icant correlations between cTnI levels and disease severity and between cTn I levels and the degree of myocardial depression measured by quantitative t ransthoracic echocardiography and peak inotrope requirements. Conclusions: The elevated serum concentrations of cTnI indicate that myocar dial 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 meningoco ccal septicemia. Elucidation of the mechanism responsible for myocardial in jury may lead to the development of therapeutic interventions to prevent or limit this cardiac damage.