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| IJCEM Copyright © 2008-All rights reserved. Published by e-Century Publishing Corporation, Madison, WI 53711 |
Int J Clin Exp Med 1(2),171-180;2008
Review Article
trauma-shock-induced acute heart failure
Marlon A. Lee, Atsuko Yatani, Justin T. Sambol, Edwin A. Deitch
Department of Surgery, New Jersey Medical School, Newark, NJ 07103
Received March 15, 2008; accepted March, 2008; available online March, 2008
Abstract: Acute injury-induced cardiac contractile dysfunction occurs even in young and otherwise healthy individuals after major
injuries, and significantly contributes to morbidity and mortality in patients with pre-existent cardiac diseases as well as in patients who
develop multiple organ dysfunction syndrome. Recent studies indicate that post-injury acute cardiac failure is the result of an
exaggerated cardiac inflammatory response resulting in an inflammatory cardiomyopathy characterized by decreased cardiac
contractility. Over the past decade, many of the effector molecules involved in this process have been identified as having some
involvement in generating a myocardial inflammatory response. However, less is known about the agents and processes involved in
triggering this inflammation-induced decrease in cardiac contractility. Consequently, in this review, the concept of the heart responding
to major injury like an innate immune organ will be presented, the various effector molecules and mechanisms leading to myocyte
contractile dysfunction will be reviewed and data indicating that the acute cardiac contractile dysfunction observed after trauma is due to
gut-derived intestinal lymph factors will be reviewed. (IJCEM803001).
Key Words: mesenteric lymph, trauma-hemorrhage, burn, cardiac dysfunction
Full Text PDF
Address all correspondence to: Edwin A. Deitch, MD, 185 South Orange Avenue, MSB-G518, Newark, NJ 07103, USA.. Tel:
973-972-5045, Fax: 973-972-6801, E-mail: edeitch@umdnj.edu
Review Article
trauma-shock-induced acute heart failure
Marlon A. Lee, Atsuko Yatani, Justin T. Sambol, Edwin A. Deitch
Department of Surgery, New Jersey Medical School, Newark, NJ 07103
Received March 15, 2008; accepted March, 2008; available online March, 2008
Abstract: Acute injury-induced cardiac contractile dysfunction occurs even in young and otherwise healthy individuals after major
injuries, and significantly contributes to morbidity and mortality in patients with pre-existent cardiac diseases as well as in patients who
develop multiple organ dysfunction syndrome. Recent studies indicate that post-injury acute cardiac failure is the result of an
exaggerated cardiac inflammatory response resulting in an inflammatory cardiomyopathy characterized by decreased cardiac
contractility. Over the past decade, many of the effector molecules involved in this process have been identified as having some
involvement in generating a myocardial inflammatory response. However, less is known about the agents and processes involved in
triggering this inflammation-induced decrease in cardiac contractility. Consequently, in this review, the concept of the heart responding
to major injury like an innate immune organ will be presented, the various effector molecules and mechanisms leading to myocyte
contractile dysfunction will be reviewed and data indicating that the acute cardiac contractile dysfunction observed after trauma is due to
gut-derived intestinal lymph factors will be reviewed. (IJCEM803001).
Key Words: mesenteric lymph, trauma-hemorrhage, burn, cardiac dysfunction
Full Text PDF
Address all correspondence to: Edwin A. Deitch, MD, 185 South Orange Avenue, MSB-G518, Newark, NJ 07103, USA.. Tel:
973-972-5045, Fax: 973-972-6801, E-mail: edeitch@umdnj.edu
