DOI: 10.1161/circ.148.suppl_1.14592 ISSN: 0009-7322

Abstract 14592: Sepsis Cardiac Edema Related Reversible Injury (SCERRI)

Verity J Ford, Willard N Applefeld, Jeffrey Wang, Junfeng Sun, Jing Feng, VANDANA SACHDEV, Stanislav Sidenko, Zu-Xi YU, steven B solomon, Michael A Solomon, Marcus Y Chen, Charles Natanson, MD
  • Physiology (medical)
  • Cardiology and Cardiovascular Medicine

Background: In human septic shock, radionuclide cine angiograms found depression of LVEF and dilatation of the LV (EDV). Peaking at 48h after shock onset, the changes reversed by day 10. Nonsurvivors paradoxically had normal EFs and EDVs. Subsequent TTE studies have not consistently reproduced these findings. To investigate this paradox, we reviewed published clinical studies of cardiac function during sepsis and performed serial CMRIs in a canine model of sepsis-induced cardiac changes.

Methods: Clinical studies of sepsis reporting EFs and EDVs in survivors and nonsurvivors were identified from 1980 onward. Sedated purpose-bred beagles (25, 2 y/o) intra-bronchially challenged with S. aureus or saline had serial CMRIs and histology.

Results: Mean EF at 24h ranged from 31-69% across 20 clinical studies. Over these studies survivors vs. nonsurvivors, mean EF differences were only 1% (p=0.15; I 2 5%). Twelve clinical sepsis studies reported mean EDVs and showed that survivors had larger EDVs than nonsurvivors (SMD 0.36, p<0.0001; I 2 57%). Like clinical studies, EFs in our S. aureus challenged animal model was similarly depressed in both survivors and nonsurvivors (41% vs. 45%, p=0.34). In animals like humans, LV EDV was significantly higher at 48h in survivors vs . nonsurvivors (40 vs. 30 ml p=0.02) while CVPs and PAOPs were similar throughout (p=ns). From 48 to 96h the septic animals EF recovers towards normal in survivors. CMRIs in septic animals vs. controls showed LV wall thinning with a progressive significant loss of dry mass (~ 1g/24h over 96h) and increased LV wall edema (2-4% total over 96h). There was no histological or biochemical evidence of myocyte necrosis, elevated troponins or BNPs, only endothelial and myocyte edema with mild myofilament loss.

Conclusions: Septic shock results in ventricular wall changes not explained by loading conditions or myocardial necrosis. Sepsis-induced cardiac injury is associated with edema as demonstrated by both histopathology and CMRI. The unexpected, acute loss of LV dry mass occurred even as edema increased and the EF recovered, consistent with an adaptive, reparative process. Determining how dry mass is lost and which cells and tissues are affected may clarify mechanisms of cardiac injury and repair in septic shock.

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