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Published on: June 20, 2014
Endomyocardial expression of SDF-1 predicts mortality in patients with suspected myocarditis
Christine S Zuern1, Britta Walker2, Martina Sauter3
1Department of Cardiology and Cardiovascular Medicine, University of Tuebingen, Otfried-Mueller-Str. 10, 72076, Tuebingen, Germany. christine.zuern@gmx.de.
Insights
Stromal cell-derived factor 1 (SDF-1) is elevated in inflammatory cardiomyopathy and predicts mortality in patients with suspected myocarditis. SDF-1 expression identifies high-risk individuals, aiding in risk stratification and treatment optimization.
Area of Science:
- Cardiology
- Immunology
- Pathology
Background:
- Risk stratification is crucial for managing suspected myocarditis.
- Stromal cell-derived factor 1 (SDF-1), an inflammatory chemokine, is found in inflamed heart muscle.
- Investigating SDF-1's role in identifying high-risk myocarditis patients is important.
Purpose of the Study:
- To determine if endomyocardial SDF-1 expression can identify high-risk patients with suspected myocarditis.
- To assess the correlation between SDF-1 expression, myocardial fibrosis, and patient outcomes.
Main Methods:
- 174 patients with non-ischemic heart failure and suspected myocarditis underwent endomyocardial biopsy.
- Biopsies were analyzed for histopathology, immunohistology, and SDF-1 staining.
- Patient follow-up averaged 27.5 months to assess mortality.
Main Results:
- SDF-1 was significantly higher in inflammatory cardiomyopathy (65.4%) versus non-inflammatory (19.1%).
- SDF-1 levels correlated with myocardial fibrosis (r=0.196, p=0.010).
- SDF-1 positivity was linked to higher 4-year mortality (26.0% vs. 9.5%, p=0.001) and was the strongest independent predictor of mortality (HR 6.1, p=0.018).
Conclusions:
- Endomyocardial SDF-1 expression is elevated in inflammatory cardiomyopathy.
- SDF-1 positively correlates with myocardial fibrosis.
- SDF-1 identifies high-risk patients with suspected myocarditis, aiding in risk stratification.
Background:
Risk stratification in patients with suspected myocarditis is pivotal for optimizing therapy. Stromal cell-derived factor 1 (SDF-1) is an inflammatory chemokine expressed in the inflamed and failing myocardium. Therefore, we aimed to investigate whether endomyocardial expression of SDF-1 identifies high-risk patients with suspected myocarditis.
Methods And Results:
We prospectively enrolled 174 patients with non-ischemic HF who underwent endomyocardial biopsy for suspected myocarditis. Biopsies were analyzed using established histopathological and immunohistological criteria together with SDF-1 staining. SDF-1 was significantly enhanced in patients with inflammatory cardiomyopathy (65.4 % positive biopsies) as compared to patients with non-inflammatory cardiomyopathy (19.1 %, p < 0.001). SDF-1 expression levels correlated significantly with the degree of myocardial fibrosis (correlation coefficient r = 0.196; p = 0.010) since patients with severe myocardial fibrosis displayed high myocardial SDF-1 expression. During a mean follow-up of 27.5 months, 20 patients (11.5 %) died. The 4-year mortality rate was 26.0 % among the 92 SDF-1-positive patients vs. 9.5 % among the 82 SDF-1-negative patients (p = 0.001). On multivariable analysis which considered clinical (NYHA functional class, left ventricular ejection fraction), laboratory (brain natriuretic peptide, troponin I) and biopsy staining, SDF-1 was the strongest independent predictor of mortality (hazard ratio 6.1; 95 % confidence interval 1.4-27.5; p = 0.018). Subgroup analysis revealed SDF-1 as a predictor of mortality in both patients with inflammatory and non-inflammatory cardiomyopathy.
Conclusions:
Endomyocardial expression of SDF-1 is enhanced in inflammatory cardiomyopathy, positively correlates with myocardial fibrosis and identifies high-risk patients with suspected myocarditis.
Related Concept Videos
Myocarditis I: Introduction
Myocarditis II: Clinical Features and Diagnostic Tests
Cardiomyopathy II: Dilated Cardiomyopathy
Cardiomyopathy III: Hypertrophic Cardiomyopathy
Myocarditis III: Medical Management

