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Troponin I Levels Increase After Experimental Pneumococcal Pneumonia Infection in a Nonhuman Primate Model FREE TO VIEW

Marcos Restrepo, MD; Luis Reyes, MD; Cecilia Hinojosa; Jessica Perry; Robert Shade; Nilam Soni, MD; Melissa De La Garza; Luis Giavedoni, PhD; Carlos Orihuela, PhD
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University of Texas Health Science Center at San Antonio, San Antonio, TX

Chest. 2015;148(4_MeetingAbstracts):228A. doi:10.1378/chest.2278247
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SESSION TITLE: Critical Care Posters I

SESSION TYPE: Original Investigation Poster

PRESENTED ON: Wednesday, October 28, 2015 at 01:30 PM - 02:30 PM

PURPOSE: Cardiac complications during pneumococcal pneumonia could explain up to 40% of deaths related with pneumonia. Our research group have described recently that Streptococcus pneumoniae is able to translocate into the heart of experimentally infected mice and disrupt its normal function during invasive pneumococcal disease. To translate these findings to humans there is a need to identify non-invasive methods that could assess cardiac injury during and post-infection. Cardiac troponins are highly sensitive and specific markers of myocardial injury. Our aim was to test the kinetics of troponin I levels in an experimental non-human primate model of pneumococcal pneumonia.

METHODS: Healthy young baboons (n=3, 12-13 years old) were assessed at baseline with transthoracic 2D echocardiogram and 12-lead electrocardiogram evaluation. Baboons were tethered to allow for continuous electrocardiogram (ECG), heart rate, blood sampling, and temperature monitoring during infection. Anesthetized baboons were bronchoscopically infected with S. pneumoniae (108 CFU). Myocardial injury was tested by daily ultrasensitive troponin I ELISA. Baboons were euthanized when they developed a moribund state or 10 days post-infection. Pneumococcal myocardial invasion was assessed by fluorescent microscopy.

RESULTS: Baboons developed mild, moderate and severe pneumonia. The baboon with mild pneumonia had transient bacteremia and only one foci of bronchopneumonia. Baboons with moderate and severe pneumonia progressed to have extensive lobar and multilobar pneumonia, respectively. The baboon with severe pneumonia died four days post-infection. Pneumococcal invasion to the myocardium was observed in the baboons with moderate and severe disease. Among the three baboons there was a progressive incremental troponin I levels from baseline to day 4 post-infection. The highest level of troponin was observed among the baboons with moderate and severe pneumonia (0.066 vs. 0.015; p=0.03). Continues ECG revealed sinus tachycardia and non-specific changes of myocardial injury.

CONCLUSIONS: Troponin elevation increased in baboons with pneumonia in the presence of S. pneumoniae myocardial translocation.

CLINICAL IMPLICATIONS: The mechanism of myocardial invasion and cardiac complications during pneumococcal pneumonia needs to be elucidated to identify possible therapeutic targets.

DISCLOSURE: The following authors have nothing to disclose: Marcos Restrepo, Luis Reyes, Cecilia Hinojosa, Jessica Perry, Robert Shade, Nilam Soni, Melissa De La Garza, Luis Giavedoni, Carlos Orihuela

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