https://doi.org/10.1007/s00392-025-02625-4
1Universitätsklinikum Heidelberg Klinik für Innere Med. III, Kardiologie, Angiologie u. Pneumologie Heidelberg, Deutschland
Aims Myocardial infarction (MI) leads to varying degrees of myocardial remodeling influenced by different clinical factors (e.g., age and comorbidities). To date, the impact of the culprit lesion and initial infarct size on cardiac remodeling remains unclear. This study aims to identify differences in remodeling depending on the localization of the culprit lesion, focusing on changes in the myocardial scar and cardiac function, including myocardial strain.
Methods and Results This single-center study included retrospectively 93 patients after ST-segment elevation or non-ST-segment elevation Type 1 MI. Patients underwent an initial cardiac magnetic resonance (CMR) examination within 10 days of MI and a follow-up CMR examination after a mean of 317 ± 104 days. Cardiac function was assessed using left ventricular ejection fraction (LV-EF), stroke volume (SV), and global longitudinal (GLS) and circumferential (GCS) strains derived from CMR feature-tracking. Myocardial scar quantification was performed on Late Gadolinium Enhancement (LGE) images. In addition, high-sensitivity cardiac troponin T (hs-cTnT) and NT-proBNP levels were recorded.
The study population consisted of 44 patients with left anterior descending artery (LAD) infarction, 18 with left circumflex artery (LCX) infarction, and 31 with right coronary artery (RCA) infarction. Demographic characteristics such as age, sex, and body mass index were comparable between the three groups, as were both cardiac biomarkers. Patients in the LAD group had a slightly larger myocardial scar area in the baseline CMR examination and a marginally higher hs-cTnT level; but these findings were not significantly different from the other groups. At baseline, patients in the LAD group showed a significantly greater impairment of cardiac function compared to the LCX and RCA groups, with reduced LV-SV (LAD 78.9 ± 16.4 ml; LCX 90.2 ± 17.2 ml; p = 0.018) and LV-GLS (LAD 10.7 ± 2.5 %; RCA 13.6 ± 2.3 %; p < 0.001).
Follow-up CMR showed significant improvements of LV-SV (+6.7 ± 13.7 ml; p = 0.012), LV-EF (+4.3 ± 7.2 %; p = 0.003), and LV-GLS (+2.3 ± 2.6 %; p < 0.001) in the overall cohort. Significant reductions in LV mass (-15.1 ± 23.5 g; p = 0.002) and in myocardial scar and microvascular obstruction (MVO) mass (myocardial scar -6.0 ± 10.9 g; MVO -1.2 ± 3.6 g; both p < 0.001) were observed. Further analysis revealed a significantly greater improvement of LV-EF in the LAD group compared to the LCX group (LAD +7.6 ± 6.9 %; LCX -1.2 ± 6.1 %; p < 0.001) and the RCA group (LAD +7.6 ± 6.9 %; RCA +2.6 ± 5.9 %; p = 0.002). The LV-SV showed a greater improvement in patients in the LAD group compared to patients in the LCX group (LAD +10.5 ± 11.5 ml; LCX +0.3 ± 15.2 ml; p = 0.006). In addition, LV-GLS showed a greater improvement in the LAD group than in the RCA group (LAD +3.0 ± 2.5 %; RCA +1.5 ± 1.9 %; p = 0.005), as did LV-GCS in the LAD group compared to both the LCX group (LAD +3.1 ± 2.0 %; LCX +1.6 ± 3.8 %; p = 0.045) and the RCA group (LAD +3.1 ± 2.0 %; RCA +1.7 ± 2.2 %; p = 0.005). There were no significant differences in the decrease of infarct or MVO mass between the three groups.
Conclusions In our study cohort myocardial scar remodeling did not differ significantly depending on the localization of the culprit lesion. Of note, our data shows that patients after revascularized LAD infarction may have greater improvement in cardiac functional parameters compared to patients after RCA or LCX infarction.