Background: The pathophysiology of stress-induced cardiomyopathy (SCM) remains poorly understood. Recent evidences suggested that inflammatory status such as elevated C-reactive protein (CRP) is related to the impairments of left ventricular function in SCM. But, it is obscure whether elevated CRP can predict the clinical outcomes of SCM or not. Method: We enrolled 65 patients of SCM from 4 tertiary hospitals. All patients met the Mayo criteria of the diagnosis of SCM. hs-CRP was measured at initial presentation of hospitals by immunoturbidimetric assay. Major adverse event was defined as composites of any death, cardiogenic shock, and thromboembolic complication. Results: Twenty-one patients (26%) were experienced major adverse event (5 of death, 15 of cardiogenic shock, 1 of thromboembolic complication). Baseline demographics were similar between adverse event group and non-event group, except younger age in adverse event group (58.8 vs. 69.3 years, p=0.013). There were significantly higher level of hs-CRP at admission (7.4 짹 8.5 vs. 2.9 짹 3.8 mg/dL, p=0.026) and peak troponin-I levels (9.3 짹 15.2 vs. 2.1 짹 2.1 ng/mL, p=0.040) Multivariate regression analysis (adjusted for age, sex, LV ejection fraction and peak troponin-I) identified elevated hs-CRP as a predictor of increased risk of the clinical event (Hazard ratio: 1.20, 95% confidence interval: 1.03 to 1.40, p=0.023). The receiver operator characteristic curve area for the hs-CRP was 0.69 (p=0.017). At a cutoff value of 1.42mg/dL, sensitivity and specificity were 77% and 53%, respectively. Conclusion: hs-CRP is an independent predictor of adverse clinical event in patients with stress-induced cardiomyopathy. Our results suggest that systemic inflammation is a crucial value of pathogenesis and prognosis of SCM.