Of 152 patients with STEMI included in our prospective observational study, 135 patients (mean age 60.72 years; 12.70% female, median follow-up of 510 days) underwent the standardized CMR protocol at least twice (Fig. 1). Overall, 86 patients with MVO and 49 patients without MVO were followed up for three years. Participants were dichotomized according to whether they were complicated with MVO (86 patients with MVO).

Study flowchart. A total of 135 participants were available at the end of our present analysis. Fifty normal participants were recruited as the control group

The patients’ baseline characteristics are summarized in Table 1. Patients with MVO tended to have higher peaks of CK-MB (p = 0.006), cTnI (p < 0.001), BNP (p = 0.020), and CRP (p < 0.001) and were more likely to have MACE (25.60% vs. 8.20%, p = 0.013). The obstruction of culprit vessels occurred more often in the proximal segments in patients with MVO than without MVO (p = 0.002). TIMI flow grade was lower in patients with MVO during pre (p = 0.030)- and post-PCI (p = 0.040).

Patients with MVO tended to have lower LVEF on three occasions: within 1 week (p = 0.001), 30 days (p = 0.001), and 6 months (p = 0.003). They were also more likely to have higher LGE volume on three occasions: within 1 week (p < 0.001), 30 days (p < 0.001), and 6 months (p = 0.002) (Table 2). Transmural infarction (p < 0.001), pericardial effusion (p < 0.001), and IMH (p < 0.001) occurred more often in patients with MVO.

Native T1 values of remote myocardium in patients with and without MVO changed from 1 week to 6 months after MI dynamically. The native T1 value of remote myocardium in the first week was higher than those of 1 month. Compensatory thickening of the basal left ventricular septum was greater in patients with MVO than those without MVO (Fig. 2). At 1 week and 30 days, remote myocardium T1 values of group with MVO were higher than those without MVO (p = 0.030 and p = 0.001, respectively), while differences were not significant at 6 months (p = 0.09). In patients with and without MVO, remote T1 values were lowest at 30 days and highest at 6 months (Fig. 3A). In patients with and without MACE, remote T1 values were lowest at 30 days (Fig. 3B). Patients with MACE tended to have higher native T1 values (Additional file 1: Table S2).

Native T1 values of remote myocardium in patients with and without MVO changed from 1 week to 6 months after MI dynamically. The native T1 value of remote myocardium in the first week was higher than those of 1 month. Inflammation of remote myocardium increased in the acute phase while diminished gradually during follow-up, and fibrosis of remote myocardium increased gradually. Native T1 values were determined by myocardial fibrosis in the chronic stage. The first patient had mural thrombosis in the apical during the first week. Compensatory thickening of the basal left ventricular septum was greater in patients with MVO than those without MVO

The box-plots (25th percentile, median, and 75th percentile) represent dynamic changes in native T1 values of remote myocardium on three occasions. In patients with and without MVO, remote T1 values were lowest at 30 days and highest at 6 months (A). In patients with and without MACE, remote T1 values were lowest at 30 days (B)

During a median (510 days) follow-up, a total of 26 (19.26%) MACE (death, n = 2 [1.48%]; myocardial reinfarction, n = 4 [2.96%]; ventricular tachycardia, n = 1 [0.74%]; and hospitalization for heart failure, n = 19 [14.07%]) were observed.

In the univariable Cox regression analysis (Table 3), patients with the following characteristics were significantly associated with MACE: higher Killip class (HR 2.47, 95%CI 1.53–4, p < 0.001), higher cTnImax (HR 1.01, 95%CI 1.001–1.02, p = 0.030), higher CRPmax (HR 1.02, 95%CI 1.01–1.03, p = 0.004), lower TIMI flow grade of post-PCI (HR 0.37, 95%CI 0.20–0.70, p = 0.002), lower LVEF1w (HR 0.93, 95%CI 0.90–0.97, p < 0.001), lower LVEF6M (HR 0.95, 95%CI 0.92–0.99, p = 0.013), higher LGE1w (HR 1.10, 95%CI 1.06–1.14, p < 0.001), higher LGE30D (HR 1.12, 95%CI 1.08–1.17, p < 0.001), higher LGE6M (HR 1.05, 95%CI 1.01–1.09, p < 0.001), higher remote native1w T1 (HR 1.02, 95%CI 1.004–1.03, p = 0.009), higher remote native30D T1 (HR 1.04, 95%CI 1.03–1.05, p < 0.001), higher remote native6M T1 (HR 1.02, 95%CI 1.01–1.03, p = 0.004), higher frequency of transmural infarction (HR 5.26, 95%CI 1.24–22.27, p = 0.024), IMH (HR 3.57, 95%CI 1.07–11.93, p = 0.038), and MVO (HR 2.95, 95%CI 1.01–8.56, p = 0.047).

For univariable Cox regression analysis, p ≤ 0.1 was included into stepwise multivariable Cox regression analysis. Native1w T1 (HR 1.03, 95%CI 1.01–1.04, p = 0.002), Native30D T1 (HR 1.05, 95%CI 1.03–1.07, p < 0.001), and LGE (HR 1.10, 95%CI 1.05–1.15, p < 0.001) were joint independent predictors of MACE during mid-term follow-up for all patients with STEMI after PPCI (Table 4). In multivariable cox regression analysis of 86 patients with MVO, native30D T1 (HR 1.05, 95%CI 1.04–1.07, p < 0.001) and LGE (HR 1.10, 95%CI 1.05–1.15, p < 0.001) were joint independent predictors of MACE (Additional file 1: Table S4). Native T1 of remote myocardium surpasses predictive value of MVO or LGE in C-statistics of all patients (p < 0.001). And native30D T1 value was stronger independent predictor than native1w T1 in C-statistics of patients with MVO (p < 0.001) (Fig. 4).

Kaplan–Meier curve for the MACE-free survival rate of three groups. a MVO present versus absent (p = 0.037). b Native T11w > 1261 ms versus ≤ 1261 ms (p < 0.001); c Native T130D > 1245 ms versus ≤ 1245 ms (p < 0.001)