Reflection on Diagnosis and Treatment Status for Stress Cardiomyopathy from Misdiagnosed Cases：A Report of 3 Cases

LI Ming-feng; CHEN Hua; LIU Xin; LIU Jie; MENG Qing-yi

doi:10.3969/j.issn.1002-3429.2016.02.002

Abstract：Objective To discuss the diagnosis and treatment status of stress cardiomyopathy from misdiagnosed pa-tients in order to reduce misdiagnosis and mistreatment rates. Methods Clinical data of three patients with stress cardiomy-opathy were retrospectively analyzed and related literature was also reviewed. Results The first patient mainly complained of heart palpitation and syncope for 20 days. The diagnosis of acute myocardial infarction was made because the patient's ECG showed the significant ST elevation in lead V2 ~V5 . After the appropriate treatment, the condition of the patient remained sta-ble and was transferred to the higher level hospital. The diagnosis of stress cardiomyopathy was made with coronary angiogra-phy and echocardiography, and after symptomatic treatment, the disease remissed and the patient was discharged. After 2 years of follow up, left ventricle shrink was found with the daily activity limitation. And the patient was found with the left ven-tricle enlargement, after non-limitation of activities. Again activity restriction made left ventricle begin to shrink. The second patient was admitted for chest pain for 1 week, and was diagnosed with "acute anterior wall myocardial infarction" with the ECG ST segment in V2 ~V4 leads at first. The angiography showed coronary vessels were normal, and enhanced movement in the base segment of left ventricle with the disappearing movement in the apical region. The diagnosis of stress cardiomyopathy was made, and after the symptomatic treatment, the patient was discharged. Electrocardiogram and cardiac function recovered in 3 months after discharge from hospital. The third patient was admitted for body injury for 3 h. The ECG showed ST eleva-tion in V2 ~V5 leads with the lower blood pressure during the treatment, and acute anterior myocardial infarction was suspec-ted. After checking normal troponin T, ECG returned to normal 9 h after injury. The diagnosis of stress cardiomyopathy was then made. The echocardiography showed that left ventricular wall motion decreased 12 h after injury. The patient was in a stable condition after symptomatic treatment and then was transferred for bone treatment. Conclusion The clinical manifesta-tions of stress cardiomyopathy are complex, very similar to that of acute myocardial infarction, and its diagnostic criteria are not identical. To avoid misdiagnosis and mistherapy, the clinicians should improve the awareness and vigilance of this disease.