Transient left ventricular dysfunction syndrome during anaphylactic shock

Abstract

Transient left ventricular dysfunction syndrome (TVLDS) has been rarely observed during anaphylactic shock and its pathophysiology remains still enigmatic. Multivessel epiicardial coronary spasm or coronary microvascular impairment were suggested as primary causative mechanism. Alternatively, the release of various inflammatory mediators including histamine could induce a coronary artery spasm or erosion/rupture of an atheromatous plaque contributing to TLVDS. Challenging this paradigm, a direct catecholamine acute toxicity was recently proposed as a causative mechanism of the stunned myocardium observed in TLVDS. We report a patient with severe TLVDS during anaphylactic shock. Whilst ECG depicted a drastic ST segment elevation in the anterior leads, cardiac catheterism confirms the co-existence of severe reduction of systemic vascular resistance and normal coronary angiogram. In the absence of any documented spasm or perfusion abnormalities, the defective uptake of 123I-metaiodobenzyl-guanidine (123I-mIBG) in the hypocontractile LV segments suggests that epinephrine-induced stunned myocardium is the main mechanism of LV systolic dysfunction. This report highlights that excess doses of epinephrine might contribute to TLVDS through direct myocardial stunning. The possible noxious contribution of other mediators such as histamine or cytokines released in the Kounis syndrome remains to be established.