• Yumiko Hosoya, Masafumi Watanabe, Masahiro Terashima, Eisuke Amiya, Tomoko Nakao, Akiko Hasegawa, Hironobu Hyodo, Jiro Ando, Tomoyuki Fujii, Ryozo Nagai, and Issei Komuro.
• Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Bunkyo, Tokyo, Japan.
• Int Heart J. 2013 Jan 1; 54 (2): 119-22.

AbstractAmniotic fluid embolism (AFE) is a rare but devastating complication of pregnancy. Acute circulatory failure and obstetric disseminated intravascular coagulopathy are often associated with AFE and lead to poor prognosis of this syndrome. Although many reports of AFE and its cardiopulmonary complications exist, their etiology remains unknown. Classically, it was believed that the fatal cardiopulmonary complication in AFE is due to acute and severe pulmonary hypertension caused by critical obstruction of the pulmonary vessels by embolized amniotic fluid. However, recent hypotheses are suggesting that anaphylactic reaction or a cytokine effect induced by amniotic fluid is the main pathophysiological mechanism. We report a case in which cardiac magnetic resonance imaging was performed at the chronic stage of AFE. Late gadolinium enhancement (LGE) was detected at the mid-wall of the left ventricle with no evidence of pulmonary hypertension. This finding suggests that the pathophysiological mechanism of severe cardiac complications in AFE may include direct left ventricular myocardial injury through an immune reaction or cytokine release, rather than pulmonary embolism.

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