RESUMEN
Aims: Recent studies have shown that extracellular volume (ECV) can also be obtained without blood sampling by the linear relationship between haematocrit (HCT) and blood pool R1 (1/T1). However, whether this relationship holds for patients with myocardial infarction is still unclear. This study established and validated an ECV model without blood sampling in ST-segment elevation myocardial infarction (STEMI) patients. Methods and results: A total of 398 STEMI patients who underwent cardiac magnetic resonance (CMR) examination with T1 mapping and venous HCT within 24â h were retrospectively analysed. All patients were randomly divided into a derivation group and a validation group. The mean CMR scan time was 3â days after primary percutaneous coronary intervention. In the derivation group, a synthetic HCT formula was obtained by the linear regression between HCT and blood pool R1 (R 2 = 0.45, P < 0.001). The formula was used in the validation group; the results showed high concordance and correlation between synthetic ECV and conventional ECV in integral (bias = -0.12; R 2 = 0.92, P < 0.001), myocardial infarction site (bias = -0.23; R 2 = 0.93, P < 0.001), and non-myocardial infarction sites (bias = -0.09; R 2 = 0.94, P < 0.001). Conclusion: In STEMI patients, synthetic ECV without blood sampling had good consistency and correlation with conventional ECV. This study might provide a convenient and accurate method to obtain the ECV from CMR to identify myocardial fibrosis.
RESUMEN
BACKGROUND: Epicardial adipose tissue(EAT) is associated with inflammation in previous studies but is unknown in patients with ST-segment elevation myocardial infarction(STEMI).This study investigated the correlation between epicardial fat and inflammatory cells obtained by cardiac magnetic resonance (CMR) and the effect on atrial arrhythmias in patients with STEMI. METHODS: This was a single-center, retrospective study. We consecutively selected patients who all completed CMR after Percutaneous Coronary Intervention (PCI) from January 2019 to December 2022 and then had regular follow-ups at 1, 3, 6, 9, and 12 months. The enrolled patients were grouped according to the presence or absence of atrial arrhythmia and divided into atrial and non-atrial arrhythmia groups. RESULTS: White blood cell, neutrophil, lymphocyte, C-reactive protein, EATV, LVES, LVED were higher in the atrial arrhythmia group than in the non-atrial arrhythmia group, and LVEF was lower than that in the non-atrial arrhythmia group (p < 0.05); EATV was significantly positively correlated with each inflammatory indices (white blood cell: r = 0.415 p < 0.001, neutrophil:r = 0.386 p < 0.001, lymphocyte:r = 0.354 p < 0.001, C-reactive protein:r = 0.414 p < 0.001); one-way logistic regression analysis showed that risk factors for atrial arrhythmias were age, heart rate, white blood cell, neutrophil, lymphocyte, C-reactive protein, EATV, LVES, LVED; multifactorial logistic regression analysis showed that neutrophil, lymphocyte, C-reactive protein, EATV, and LVES were independent risk factors for atrial arrhythmias; ROC analysis showed that the area under the curve (AUC) for neutrophil was 0.862; the AUC for lymphocyte was 1.95; and the AUC for C-reactive protein was 0.862. reactive protein was 0.852; AUC for LVES was 0.683; and AUC for EATV was 0.869. CONCLUSION: In patients with STEMI, EAT was significantly and positively correlated with inflammatory indices; neutrophil, lymphocyte, C-reactive protein, EATV, and LVES were independent risk factors for atrial arrhythmias and had good predictive value.
