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Cardiac Magnetic Resonance Studies in a Large Animal Model That Simulates the Cardiac Abnormalities of Human Septic Shock

Authors :
Verity J. Ford
Willard N. Applefeld
Jeffrey Wang
Junfeng Sun
Steven B. Solomon
Stanislav Sidenko
Jing Feng
Cynthia Sheffield
Harvey G. Klein
Zu‐Xi Yu
Parizad Torabi‐Parizi
Robert L. Danner
Vandana Sachdev
Michael A. Solomon
Marcus Y. Chen
Charles Natanson
Source :
Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, Vol 13, Iss 15 (2024)
Publication Year :
2024
Publisher :
Wiley, 2024.

Abstract

Background Septic shock is associated with increases in end‐diastolic volume (EDV) and decreases in ejection fraction that reverse within 10 days. Nonsurvivors do not develop EDV increases. The mechanism is unknown. Methods and Results Purpose‐bred beagles (n=33) were randomized to receive intrabronchial Staphylococcus aureus or saline. Over 96 hours, cardiac magnetic resonance imaging and echocardiograms were performed. Tissue was obtained at 66 hours. From 0 to 96 hours after bacterial challenge, septic animals versus controls had significantly increased left ventricular wall edema (6%) and wall thinning with loss of mass (15%). On histology, the major finding was nonocclusive microvascular injury with edema in myocytes, the interstitium, and endothelial cells. Edema was associated with significant worsening of biventricular ejection fractions, ventricular‐arterial coupling, and circumferential strain. Early during sepsis, (0–24 hours), the EDV decreased; significantly more in nonsurvivors (ie, greater diastolic dysfunction). From 24 to 48 hours, septic animals' biventricular chamber sizes increased; in survivors significantly greater than baseline and nonsurvivors, whose EDVs were not different from baseline. Preload, afterload, or heart rate differences did not explain these differential changes. Conclusions The cardiac dysfunction of sepsis is associated with wall edema. In nonsurvivors, at 0 to 24 hours, sepsis induces a more severe diastolic dysfunction, further decreasing chamber size. The loss of left ventricular mass with wall thinning in septic survivors may, in part, explain the EDV increases from 24 to 48 hours because of a potentially reparative process removing damaged wall tissue. Septic cardiomyopathy is most consistent with a nonocclusive microvascular injury resulting in edema causing reversible systolic and diastolic dysfunction with more severe diastolic dysfunction being associated with a decreased EDV and death.

Details

Language :
English
ISSN :
20479980
Volume :
13
Issue :
15
Database :
Directory of Open Access Journals
Journal :
Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
Publication Type :
Academic Journal
Accession number :
edsdoj.f495b8bb43042a29f124e2468971206
Document Type :
article
Full Text :
https://doi.org/10.1161/JAHA.123.034026