Evaluation of myocardial injury through serum troponin I and echocardiography in anaphylaxis.

BACKGROUND: Anaphylaxis is an acute, lethal, multisystem syndrome that results from the sudden release of mast cell- and basophil-derived mediators. Although anaphylaxis can cause cardiac complications, the incidence of myocardial injury using troponin I (TnI) has not been characterized. In addition, patterns of cardiomyopathy have not been evaluated in patients with elevated TnI. Therefore, we studied the occurrence and patterns of myocardial injury with TnI and echocardiography in anaphylaxis.

METHODS: We conducted a retrospective review of 300 consecutive anaphylaxis cases that were diagnosed in the emergency department (ED) over 53 months (2011-2015). Myocardial injury was defined as elevation of TnI within 24hrs after arrival at the ED. We investigated systolic function and regional wall motion abnormality (RWMA) through echocardiography within 5 hours after arrival at the ED in patients with myocardial injury.

RESULTS: Among 300 patients (median age, 55 years), 22 patients demonstrated myocardial injury (7.3%). The median TnI was 0.222 ng/mL with a range from 0.057 ng/mL to 19.4 ng/mL. Three patients presented reduced systolic function and 4 patients showed RWMA. One patient showed reverse Takotsubo cardiomyopathy and other 2 patients had RWMA discordant to the distribution of coronary arteries. Another patient showed RWMA (inferior wall) with ST elevation of II, III, and aVF. All 4 patients were discharge after recovery of cardiomyopathy without any specific intervention for cardiomyopathy.

CONCLUSIONS: Myocardial injury developed in 7.3% of patients with anaphylaxis. Various cardiomyopathy, including Kounis syndrome and Takotsubo cardiomyopathy, has been observed in patients with myocardial injury.