TY - JOUR
T1 - Stress-induced cardiomyopathy
AU - Boland, Torrey A.
AU - Lee, Vivien H.
AU - Bleck, Thomas P
N1 - Publisher Copyright:
Copyright © 2015 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.
PY - 2015/3/4
Y1 - 2015/3/4
N2 - Objectives: Reversible stress-induced cardiac dysfunction is frequently seen as a complication of a multitude of acute stress states, in particular neurologic injuries. This dysfunction may be difficult to distinguish between that caused by myocardial ischemia and may impact both the treatment strategies and prognosis of the underlying condition. Critical care practitioners should have an understanding of the epidemiology, pathophysiology, clinical characteristics, precipitating conditions, differential diagnosis, and proposed treatments for stress-induced cardiomyopathy. Data Sources: MEDLINE database search conducted from inception to August 2014, including the search terms "tako-tsubo,""stress-induced cardiomyopathy," "neurogenic cardiomyopathy,""neurogenic stress cardiomyopathy," and "transient left ventricular apical ballooning syndrome". In addition, references from pertinent articles were used for a secondary search. Study Selection and Data Extraction: After review of peer-reviewed original scientific articles, guidelines, and reviews resulting from the literature search described above, we made final selections for included references and data based on relevance and author consensus. Data Synthesis: Stress-induced cardiomyopathy occurs most commonly in postmenopausal women. It can be precipitated by emotional stress, neurologic injury, and numerous other stress states. Patients may present with symptoms indistinguishable from acute coronary syndrome or with electrocardiogram changes and wall motion abnormalities on echocardiogram following neurologic injury. Nearly all patients will have an elevated cardiac troponin. The underlying etiology is likely related to release of catecholamines, both locally in the myocardium and in the circulation. Differential diagnosis includes myocardial infarction, myocarditis, neurogenic pulmonary edema, and nonischemic cardiomyopathy. Although the natural course of stress-induced cardiomyopathy is resolution, treatment strategies include sympathetic blockade and supportive care. Conclusions: Stress-induced cardiomyopathy may mimic myocardial infarction and is an important condition to recognize in patients with underlying stress states, particularly neurologic injuries.
AB - Objectives: Reversible stress-induced cardiac dysfunction is frequently seen as a complication of a multitude of acute stress states, in particular neurologic injuries. This dysfunction may be difficult to distinguish between that caused by myocardial ischemia and may impact both the treatment strategies and prognosis of the underlying condition. Critical care practitioners should have an understanding of the epidemiology, pathophysiology, clinical characteristics, precipitating conditions, differential diagnosis, and proposed treatments for stress-induced cardiomyopathy. Data Sources: MEDLINE database search conducted from inception to August 2014, including the search terms "tako-tsubo,""stress-induced cardiomyopathy," "neurogenic cardiomyopathy,""neurogenic stress cardiomyopathy," and "transient left ventricular apical ballooning syndrome". In addition, references from pertinent articles were used for a secondary search. Study Selection and Data Extraction: After review of peer-reviewed original scientific articles, guidelines, and reviews resulting from the literature search described above, we made final selections for included references and data based on relevance and author consensus. Data Synthesis: Stress-induced cardiomyopathy occurs most commonly in postmenopausal women. It can be precipitated by emotional stress, neurologic injury, and numerous other stress states. Patients may present with symptoms indistinguishable from acute coronary syndrome or with electrocardiogram changes and wall motion abnormalities on echocardiogram following neurologic injury. Nearly all patients will have an elevated cardiac troponin. The underlying etiology is likely related to release of catecholamines, both locally in the myocardium and in the circulation. Differential diagnosis includes myocardial infarction, myocarditis, neurogenic pulmonary edema, and nonischemic cardiomyopathy. Although the natural course of stress-induced cardiomyopathy is resolution, treatment strategies include sympathetic blockade and supportive care. Conclusions: Stress-induced cardiomyopathy may mimic myocardial infarction and is an important condition to recognize in patients with underlying stress states, particularly neurologic injuries.
KW - Catecholamines
KW - Heart failure
KW - Neurogenic stress cardiomyopathy
KW - Stress-induced cardiomyopathy
KW - Tako-tsubo cardiomyopathy
KW - Transient left ventricular apical ballooning syndrome
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U2 - 10.1097/CCM.0000000000000851
DO - 10.1097/CCM.0000000000000851
M3 - Review article
C2 - 25565459
AN - SCOPUS:84924340257
SN - 0090-3493
VL - 43
SP - 686
EP - 693
JO - Critical care medicine
JF - Critical care medicine
IS - 3
ER -