J Cardiovasc Ultrasound.  2016 Mar;24(1):79-83. 10.4250/jcu.2016.24.1.79.

Stress-Induced Cardiomyopathy Presenting as Shock

Affiliations
  • 1Division of Cardiology, Department of Internal Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea. kcmd.sung@samsung.com
  • 2Department of Cardiovascular Surgery, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea.

Abstract

Stress-induced cardiomyopathy has become a more recognized and reported entity. It can be caused by emotional or physical stress, which causes excessive catecholamine release. Typically, the clinical course is benign with conservative treatment being effective. However, stress-induced cardiomyopathy can be fatal. A 41-year-old female presented with cardiogenic shock followed by sudden back pain. Initial echocardiographic finding showed severely decreased ejection fraction with akinesia at all mid-to-apical walls with relatively preserved basal wall contractility. The coronary artery was intact on coronary angiography. Cardiac resuscitation and extra-corporeal membrane oxygenation was needed to manage the cardiogenic shock. Recovery was complete after 2 weeks.

Keyword

Takotsubo cardiomyopathy; Extracorporeal membrane oxygenation; Shock; Cardiogenic; Echocardiography

MeSH Terms

Adult
Back Pain
Cardiomyopathies*
Coronary Angiography
Coronary Vessels
Echocardiography
Extracorporeal Membrane Oxygenation
Female
Humans
Membranes
Oxygen
Resuscitation
Shock*
Shock, Cardiogenic
Takotsubo Cardiomyopathy
Oxygen

Figure

  • Fig. 1 Electrocardiographic findings revealed sinus tachycardia with ST segment elevation in precordial leads at initial admission (A) and normalized ST segment on follow up electrocardiogram at 1 month after discharge (B).

  • Fig. 2 Transthoracic echocardiography, parasternal long axis view (A at diastolic period, B at systolic period), and apical 4-chamber view (C at diastolic period, D at systolic period), showed dilated cavity, akinesia at all mid to apical left ventricular (LV) walls and relatively preserved contractility in basal walls, with severe LV systolic dysfunction (estimated LV ejection fraction, 15–20%) (B).

  • Fig. 3 Coronary angiography showing normal coronary arteries, without significant stenosis. LAD: left anterior descending artery, LCX: left circumflex artery, RCA: right coronary artery.

  • Fig. 4 Cardiac magnetic resonance imaging showing no evidence of LV wall motion abnormality on white blood cine image (A), myocardial perfusion defect in gadolinium-based contrast enhanced first-pass perfusion image (B). There was no evidence of delayed enhancement of LV myocardium (C). LA: left atrium, LV: left ventricle, RA: right atrium, RV: right ventricle.


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