Abstract: Poster Presentations |

Elevation of Cardiac Troponin I Is a Marker of Developing Myocardial Hypoxia in Sepsis FREE TO VIEW

Nam D Nguyen, MD; Su Fuhong, MD; S Hachimi-Idrissi, MD; Luc Huyghens, MD
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Erasme Hospital, Brussels, Belgium


Chest. 2003;124(4_MeetingAbstracts):226S. doi:10.1378/chest.124.4_MeetingAbstracts.226S
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PURPOSE:  Cardiac depression occurs in sepsis despite a preservation of coronary blood flow in most patients and cardiac injury can be detected by an elevation of plasma cardiac troponin I (cTnI). The aim of our study is to determine, whether the release of cTnI from myocytes, is related to any modification of coronary perfusion pressure (COPP) or due to a direct toxic effect of different inflammatory mediators during sepsis.

METHODS:  For 4 consecutive days after admission, plasma cTnI, c-reactive- protein (CRP) and arterial lactate were charted in 185 patients with severe sepsis and septic shock and tumor necrosis factor alpha (TNF) in 30 patients. cTnI was considered elevated if its value was more than 0.4 micrograms /L.. Cardiac dysfunction was detected by Echocardiography in all patients and Hemodynamics was assessed, especially to evaluate COPP and left ventricular stroke work index (LVSWI). ANOVA tests were used for statistics.

RESULTS:  cTnI was elevated in a total of 62% of 185 patients after 4 days. A higher incidence of cardiac dysfunction, multiple organ failure, as well as a higher mortality rate were associated with patients that had elevated cTnI (p<0.005).In the latter, LVSWI was also significantly reduced during 4 days, but COPP only decreased after 72 hours (p<0.005), despite a normalization of cardiac index after 24 hours. Cardiac dysfunction was not associated with arterial lactate and TNF, but significantly associated with the elevation of cTnI and the maximum value of CRP occurred (p<0.005).

CONCLUSION:  Elevation of cTnI and cardiac dysfunction occurred during severe sepsis and septic shock, which both were associated with a lower COPP and a higher risk of developing myocardial hypoxia, rather than a direct injury effect under inflammatory mediators like TNF.

DISCLOSURE:  N. D Nguyen, None.

Wednesday, October 29, 2003

12:30 PM - 2:00 PM




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