https://doi.org/10.1007/s00392-025-02625-4
1Universitätsklinikum Düsseldorf Klinik für Kardiologie, Pneumologie und Angiologie Düsseldorf, Deutschland; 2Universitätsklinikum Düsseldorf Institut für Molekulare Kardiologie Düsseldorf, Deutschland
Methods: From the prospective STEMI pathway, 61 patients (mean age: 63.0 years, 64% male) with CMR examination (3T Philips Ingenia) 5 days after STEMI and at follow-up after 6 months (n=5) were included. A control group of 32 healthy subjects (mean age: 49.9 years, 50% male) was established undergoing the same imaging protocol for sternum visualization. Established imaging sequences, including T1-/T2- mapping, T2*-weighted sequences as well as mDIXON for fat suppression were employed. The analysis was conducted in both the short axis and the transverse plane. The sternum signal was correlated with demographic factors (age, gender) and compared with signals from control bones (vertebral body, proximal humerus) as well as with the signal of other immune system related organs (spleen, liver).
Results: The mean T2 relaxation time in the transverse axis five days after infarction was significantly higher in the STEMI group than in the control group (113 ms vs. 104.5 ms, p=0.027). A comparison between T2 relaxation times at day 5 and the follow-up at 6-months indicated a tendency toward a decrease of the T2 relaxation time (113 ms vs. 107.6 ms, p=0.51), which, however, did not reach statistical significance due to the small sample size. T1 and T2* relaxation times did not differ between groups, neither in transverse plane nor in short axis (SAX) (T1 SAX: p=0.41: T1 transversal plane: p=0.95; T2* SAX: p=0.41; T2* transversal plane: p=0.45). The mDIXON analysis demonstrated that there was no significant difference in fat content between the STEMI group and the control group (65.8% vs. 63.8%, p=0.57). Comparative analysis of T2 relaxation times in control bones (humerus p=0.76, vertebra p=0.82) and immune system related organs (spleen p=0.11, liver p=0.91) revealed no significant differences as well. Additionally, no significant correlation was observed between T1, T2, and T2* relaxation times with respect to age, gender, or laboratory values. When considering sternal fat content and age, a significant positive correlation was found, in the control group (r=0.377, p=0.03) and the STEMI group (r=0.449, p < 0.001).
Conclusion: The sternal T2 relaxation time was significantly elevated in the STEMI group compared to the control group five days after the infarction. Importantly, mDIXON analysis showed no significant differences in fat content between groups, suggesting that the increased T2 relaxation time is not influenced by fat composition. This observation indicates a potential inflammatory response originating from the sternum following myocardial infarction, with T2 relaxation time possibly serving as a valuable marker for detecting associated myocardial inflammation. To enhance our understanding of the sternal response, further evaluation of additional patients, the integration of laboratory data, and the investigation of the effects of sternal activation on myocardial remodeling is warranted.