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Transient Symptomatic Severe Mitral Regurgitation after Electric Cardioversion of Atrial Fibrillation
Author(s) -
Stampfli Tomoe,
Monnard Simon,
Müller Hajo
Publication year - 2013
Publication title -
echocardiography
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.404
H-Index - 62
eISSN - 1540-8175
pISSN - 0742-2822
DOI - 10.1111/echo.12055
Subject(s) - medicine , cardiology , cardiogenic shock , atrial fibrillation , mitral regurgitation , ventricle , cardioversion , mitral valve , shock (circulatory) , myocardial infarction
After electric cardioversion ( EC ), several cases of cardiac stunning with cardiogenic shock have been reported. Several hypotheses have been proposed, including stunning of the left ventricle ( LV ) and modifications in the LV conformation that could lead to severe mitral regurgitation ( MR ). We report 2 cases of cardiogenic shock with severe MR after EC for atrial fibrillation ( AF ). Case 1: A 75‐year‐old man presented with AF . A transesophageal echocardiography before the EC showed moderate MR . Shortly after successful EC , the patient developed a cardiogenic shock. The transthoracic and a transesophageal echocardiography showed severe MR . Four days later, an echocardiography showed recovery of MR to a moderate grade. Case 2: An 85‐year‐old woman with a history of percutaneous aortic valve replacement presented with AF . After EC , she developed a cardiogenic shock. The transthoracic echocardiography showed severe MR . After recovery, the echocardiography showed moderate MR . Discussion: Cardiac stunning after EC is well known and could explain the development of severe MR due to restrictive movement of leaflets. The transient character of the MR favors a functional origin with an alteration in the geometry of the mitral apparatus. Some cases of so‐called “eclipsed MR ” are described in the literature, however, independently to electric shocks. Conclusion: In some patients, flash pulmonary edema seems to be due to transient severe functional MR , although the exact underlying physiopathologic mechanism remains unclear. An ischemic origin with papillary muscle dysfunction due to transient low perfusion could also be advocated.