Association Between Extracellular Volume Assessed by Cardiac MRI and New-Onset Atrial Fibrillation in Patients With ST-Segment Elevation Myocardial Infarction

Abstract

Objective: Although left ventricular (LV) fibrosis has been strongly linked to atrial fibrillation (AF), its relationship with new-onset AF (NOAF) following ST-segment elevation myocardial infarction (STEMI) remains unclear. This study aimed to investigate the association between different extracellular volume (ECV) measurements in the LV and NOAF during acute-phase STEMI.

Materials and methods: This retrospective study included 517 patients diagnosed with acute STEMI (440 males, 77 females; mean age, 57.2 ± 12.4 years). All patients underwent cardiac magnetic resonance (CMR) imaging with T1 mapping sequences during hospitalization. Blood samples were collected within 24 hours of the CMR examination. ECV was assessed in three regions of the left ventricle: the non-myocardial infarction region (NMI-ECV), the myocardial infarction region (MI-ECV), and the entire myocardium (integral ECV). Multi-variable logistic regression was used to evaluate the associations between these ECV parameters and NOAF. Receiver operating characteristic (ROC) analysis was performed to assess the predictive value of ECV measurements, both alone and in combination with two conventional risk factors-N-terminal pro-B-type natriuretic peptide and infarct-related artery (right coronary artery).

Results: During hospitalization, 40 (7.7%) patients developed NOAF. After adjusting for confounding factors, including left atrial strain, MI-ECV, NMI-ECV, and integral ECV were independently associated with NOAF. The area under the ROC curve for predicting NOAF was 0.702 (95% confidence interval: 0.615-0.789), 0.625 (0.531-0.719), and 0.712 (0.627-0.798) for MI-ECV, NMI-ECV, and integral ECV, respectively. The addition of integral ECV and MI-ECV to conventional factors significantly improved the predictive performance for NOAF.

Conclusion: ECV measured using CMR was independently and significantly associated with NOAF occurrence in acute-phase STEMI. Incorporating ECV into risk assessment models could significantly improve NOAF prediction.

Keywords: Atrial fibrillation; Cardiac magnetic resonance; Extracellular volume; Myocardial fibrosis; Myocardial infarction.

Fig. 1. Study flowchart. STEMI = ST-segment elevation myocardial infarction, AF = atrial fibrillation

Fig. 2. The measurement of ECV. A-D: Native T1 map (A), enhanced T1 map (B), generate ECV images (C), the distribution coefficient λ generates the image (D); red circle marks the endocardium, green circle marks the epicardium, ROI (yellow) marks the blood pool, ROI (pink) marks the non-myocardial infarction sites, ROI (blue) marks the myocardial infarction site. ECV = extracellular volume, ROI = region of interest

Fig. 3. Dose-response relationship between ECV and NOAF in patients with STEMI. A-C: A dose-response relationship between integral ECV and NOAF (A), a dose-response relationship between MI-ECV and NOAF (B), a dose-response relationship between NMI-ECV and NOAF (C). ECV = extracellular volume, NOAF = new-onset atrial fibrillation, STEMI = ST-segment elevation myocardial infarction, MI = myocardial infarction, NMI = non-myocardial infarction, CI = confidence interval

Fig. 4. Receiver operating characteristic analysis of combined parameters for identifying new-onset atrial fibrillation. IRA = infarct-related artery, RCA = right coronary artery, NT-proBNP = N-terminal pro-B-type natriuretic peptide, AUC = area under the curve, MI = myocardial infarction, ECV = extracellular volume, NMI = non-myocardial infarction