Introduction

ST-segment elevation myocardial infarction (STEMI) remains a major cause of morbidity and mortality worldwide. Effective risk stratification is crucial for the management of STEMI patients1,2. Percutaneous coronary intervention (PCI) is the preferred treatment strategy for STEMI. Knowledge of coronary angiographic findings may help formulate more rational therapeutic strategies to improve the clinical outcomes of these patients3,4. Previous studies have shown that culprit lesions in the left anterior descending artery (LAD), especially in the left main or proximal LAD, are associated with a greater risk of long-term major adverse cardiac events than lesions in the left circumflex artery (LCX) or right coronary artery (RCA)5,6,7. IThe worse outcome in patients with LAD-related infarction is correlated to a larger area subtended by this vessel, because the LAD supplies 40–50% of the left ventricular myocardium8. However, in most studies of LAD-related infarction, the features of myocardial infarction or microcirculation function at different narrowing distances from the LAD ostium are rarely mentioned or objectively displayed.

Cardiac magnetic resonance (CMR) imaging can be used to evaluate the degree of myocardial injury early in the postreperfusion period in STEMI patients9,10,11. Gadolinium-enhanced CMR can accurately visualize infarct size, infarct extent and microvascular obstruction (MVO). Left ventricular (LV) volumes and the LV ejection fraction (LVEF) can also be obtained by CMR. Changes in the LV end-diastolic volume (LVEDV) and LV end-systolic volume (LVESV) can be used to evaluate LV remodeling. Adverse LV remodeling still occurs in a significant proportion of STEMI patients, and its presence is always predisposed to heart failure and worse clinical outcomes. As a result, CMR is increasingly being used to predict adverse LV remodeling and clinical end points after STEMI12,13,14.

Total occlusion of the culprit lesion shown by angiography is also a known risk factor for death and morbidity in patients with acute myocardial infarction (AMI)15,16. Currently, few studies have focused on the relationship between culprit lesion features [distance from the LAD ostium and thrombolysis in myocardial infarction (TIMI) flow] and CMR findings in LAD-related myocardial infarction, or the predictive value of culprit lesion features for adverse LV remodeling. Therefore, in this study, we evaluated the effects of culprit lesion location and complete LAD occlusion on STEMI outcomes using CMR.

Materials and methods

Study population

The study protocol was approved by the Ethics Committee of the Affiliated Hospital of Xuzhou Medical University (NO. XYFY2023-KL413-01). This retrospective study protocol complied with the Declaration of Helsinki and owing to the retrospective nature of the study, the Ethics Committee of the Affiliated Hospital of Xuzhou Medical University waived the need to obtain informed consent.

The inclusion criteria were as follows: (a) Patients with confirmed STEMI in our hospital between September 2019 and September 2021. (b) Patients who underwent PCI within 12 h from the first onset of STEMI, and coronary angiography revealed that the responsible vessel was the LAD In addition, there was no significant stenosis of the right coronary artery/left circumflex artery. (c) Patients who underwent two CMR examinations within 7 days (baseline) and 4 months (convalescent phase) after PCI. (d)The time from first medical contact to wire balloon (FMC2B) and door-to-balloon (D2B) time, expressed in minutes, was recorded. Patients with multiple vessel diseases, prior myocardial infarction, left main (LM) artery infarction or CMR image quality that did not meet the diagnostic requirements were excluded from the analysis.

Angiogram analysis

The lesion responsible for STEMI was defined as the culprit lesion at the first angiogram. Angiograms were analyzed by two investigators on a workstation (General Electric Company, USA, version aw4.7). DSA images were digitized and input into the computer system, enabling the vascular outline and spatial position to be accurately analyzed by the software. The core of the quantitative coronary angiography software was to automatically or semi-automatically identify the vascular edge and generate a virtual centerline at the center of the lumen, representing the spatial path of the vessel. The software continuously traced along this central line, decomposes the central line into countless tiny segments, and accumulates the lengths of these tiny segments to calculate the total path length of the central line. The TIMI score of responsible coronary angiography was recorded during the primary PCI operations17. TIMI 0 was defined as total occlusion (TO), TIMI 1–3 was defined as non-total occlusion (non-TO). In addition, rthe presence of collateral vessels/diagonal vessels before occlusion of the LAD artery was recorded.

CMR protocol and CMR data analysis

CMR scans were performed on a 3.0T MR scanner (Ingenia, Philips Healthcare, Best, The Netherlands), using the surface cardiac coil and the posterior spinal coil. All images were acquired with electrocardiographic gating and breath holding. The CMR protocol included cine imaging, T2 weighted imaging (T2WI), and late gadolinium enhancement (LGE). The LGE sequence was obtained 10–15 min after the administration of gadolinium-based contrast agent (intravenous infusion of 0.15 mmol/kg contrast agents, at an injection rate of 3 mL/s, followed by a 30 mL saline flush). Two cardiac radiologists with 9 and 11 years of experience, respectively, performed CMR analysis of myocardial function and infarct characteristics using a commercially available workstation (Circle Cardiovascular Imaging, cvi42®; v5.12.4, Calgary, Alberta, Canada). The LVEDV, LVESV and LVEF were obtained from the short-axis cine-CMR sequence. Infarct size (IS), infarct extent and microvascular obstruction (MVO) were evaluated by the LGE images. The delayed enhancement region was defined as the region with signal intensity greater than five standard deviations of the signal intensity of the distal normal myocardium at the same level on the LGE images, and the MVO region was defined as the low signal region within the high signal region on the LGE images, MVO (+) means MVO is present, whereas MVO (-) indicates that MVO is absent. The infarct size is expressed as a percentage of the LV myocardium for statistical analysis12.

Observation indicators and evaluation criteria

  1. (i)

    Basic clinical data of the selected patients, including sex, age, body mass index (BMI), Killip cardiac function classification, smoking history, and history of hypertension, hyperlipidemia, and diabetes were collected.

  2. (ii)

    The peak values of the serological myocardial enzyme indices included high-sensitivity cardiac troponin-T (hs-cTnT), creatine kinase-myocardial band (CK-MB), and N-terminal pro-brain natriuretic peptide (NT-proBNP) within 48 h after admission.

  3. (iii)

    The LVEDV and LVESV parameters obtained by two CMR examinations were used to define adverse LV remodeling: an LVEDV increase ≥ 20%18.

Statistical analysis

All the statistical analyses were performed with SPSS (version 23.0, Statistical Package for the Social Sciences, IBM Corporation, Armonk, NY, USA), and two-tailed p < 0.05 was considered to indicate statistical significance. Continuous variables are expressed as mean and standard deviations (SDs) or medians and interquartile ranges (IQRs), whereas categorical variables are expressed as counts and percentages. Continuous variables were compared by using the t-test or the Mann–Whitney U test and categorical variables were compared by using the χ2 test. The correlations between LAD narrowing distance and CMR characteristics were evaluated by using the Spearman’s rank correlation test. Univariate and stepwise multivariate logistic regression analyses were used to identify predictors of adverse LV remodeling. Only variables with p < 0.05 in univariate regression analyses were used for multivariate regression. The collinearity of the parameters is verified by variance inflation factor (VIF), and VIF < 5 indicates that there is no collinearity. Receiver operating characteristic (ROC) curve analysis was used to evaluate the diagnostic accuracy of the model for predicting adverse LV remodeling at the clinical follow-up.

Results

Patient characteristics and conventional CMR findings

The clinical characteristics of the 82 patients included in the final study are shown in Table 1. Most(80.2%) of the culprit lesions causing AMI occurred between 20 and 40 mm from the LAD ostium, and the mean (± SD) distance from the LAD ostium was 27.0 ± 8.4 mm. The TIMI = 0 subgroup accounted for 46.3%, and the ratio of collateral vessels/diagonal vessels before occlusion was present in approximately 78% (64/82) of patients.

Table 1 Baseline characteristics of study population.
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The mean(± SD) distance from the LAD ostium to the LAD culprit lesion was 21.6 ± 5.9 mm in patients with adverse LV remodeling and 30.6 ± 7.9 mm in patients without adverse LV remodeling (p < 0.05). Compared with patients without adverse LV remodeling, patients with adverse LV remodeling had higher hs-cTnT and CK-MB levels, larger infarct sizes, and lower LV ejection fractions. Compared with patients without adverse LV remodeling, patients with adverse LV remodeling also had greater ratios of adverse LV remodeling, and the ratio of collateral vessels/diagonal vessels before occlusion was lower in the adverse LV remodeling group (all p < 0.05). There was no significant difference in the TIMI = 0 between the two groups.

Associations between culprit lesion features and CMR measurements

LAD culprit lesion location (CLL) was negatively correlated with infarct size (r = −0.41, p < 0.05), but weakly correlated with the LV ejection fraction (r = 0.31, p = 0.005) (Fig. 1A-B). The LAD-CLL was significantly longer in patients without MVO than in patients with MVO (30.8 ± 9.6 mm vs. 25.6 ± 7.5 mm, p = 0.008) (Fig. 1C). Compared with those of nontransmural MI patients, the LAD-CLLs of transmural MI patients were shorter (30.6 ± 8.4 mm vs. 25.0 ± 7.8 mm, p = 0.001) (Fig. 1D).

Fig. 1
Fig. 1The alternative text for this image may have been generated using AI.
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Correlations of the LAD culprit lesion location with infarct size (A) and left ventricular ejection fraction (B) on the basis of CMR. LAD culprit lesion location in patients with or without MVO (C), and in patients with transmural or nontransmural MI (D).

Total occluded culprit lesions (TIMI = 0, n = 38) had a mean distance of 27.0 ± 8.0 mm from the ostium of the LAD, whereas non-total occluded culprit lesions (TIMI ≧ 1, n = 44) had a mean distance of 27.1 ± 8.8 mm from the ostium of the LAD (p = 0.955). We also evaluated the influence of TIMI = 0 on CMR measurements, and found that there were no significant differences in infarct size (TIMI = 0 vs. TIMI ≧ 1, 18.2 ± 6.6% vs. 18.0 ± 5.6%, p = 0.741), or the LV ejection fraction (TIMI = 0 vs. TIMI ≧ 1, 46.7 ± 8.2% vs. 49.4 ± 9.3%, p = 0.193) (Fig. 2A-B). Moreover, there were no significant differences in proportions of MVO (+) and transmural myocardial infarction between the TIMI = 0 group and the TIMI ≧ 1 group (Fig. 2C-D).

Fig. 2
Fig. 2The alternative text for this image may have been generated using AI.
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Myocardial infarct size (A) and LVEF (B) were compared according to the TIMI. The proportions of MVO (C) and transmural MI (D) patients were compared according to the TIMI.

Culprit lesion features to predict adverse left ventricular remodeling

Thirty-two (39.0%) patients exhibited adverse LV remodeling at the 4-month follow-up. Backward stepwise logistic regression analyses for predicting adverse LV remodeling were performed. Clinical indicators and culprit lesion features were included in the analysis. According to the univariable logistic regression analysis, BMI, collateral vessel/diagonal vessel, LAD-CLL, hs-cTnT and CK-MB were associated with adverse LV remodeling (all p < 0.05). Multivariate logistic regression analysis demonstrated that LAD-CLL [odds ratio (OR) = 0.837, 95% confidence interval (CI) = 0.754–0.929, p = 0.001] and BMI (OR = 1.286, 95% CI = 1.065–1.554, p = 0.006) were independent predictors of adverse LV remodeling (Table 2). VIF of BMI, LAD-CLL, hs-cTnT and CK-MB were 1.013, 1.170, 1.769 and 1.749 respectively, indicating that the model we constructed did not be affected by collinearity. According to the ROC curve analysis, LAD-CLL had a moderate discriminating ability to predict adverse LV remodeling (AUC = 0.805, 95% CI = 0.710–0.901, p < 0.05). A cutoff value of LAD-CLL < 23.2 mm was identified as the optimal threshold for predicting LV remodeling with a sensitivity of 68.8% (95% CI = 51.43% − 82.05%) and a specificity of 82.0% (95% CI = 69.20% − 90.23%). The AUC of BMI was 0.691(95%CI = 0.565–0.816). Angiography and cardiac magnetic resonance images of two typical acute myocardial infarction samples are shown in Fig. 3.

Table 2 Logistic regression analysis for the prediction of short-term adverse.
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Fig. 3
Fig. 3The alternative text for this image may have been generated using AI.
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Angiography and cardiac magnetic resonance images of two typical acute myocardial infarctions examples. Patient one (A-D): A 65-year-old male STEMI patient, with a total occluded proximal segment of the LAD (A, arrow), post-PCI TIMI = 3(B). C: CMR examination 4 days after PCI, revealed nontransmural MI without MVO of the anterior wall from the intermediate to apex level. D: CMR examination 4 months after PCI revealed a myocardial scar after MI. Patient two (E-H): A 62-year-old female STEMI patient was diagnosed with incomplete occlusion in the middle section of the LAD (E, arrow), post-PCI TIMI = 3 (F). G: CMR examination 3 days after PCI revealed transmural MI with MVO of the anterior wall from the intermediate to apex level. H: CMR examination 4 months after PCI, MVO was absent.

Discussion

In this study, we investigated the correlation between angiographic and CMR characteristics, and assessed the predictive value of culprit lesion features in adverse LV remodeling in LAD-related STEMI. The angiographic characteristics included the distance of the culprit lesion from the ostium of the LAD artery, the TIMI flow grade and the presence of collateral vessels/diagonal vessels before occlusion. The main findings can be summarized as follows: (1) The distance of the culprit lesion from the ostium of the LAD was negatively mild correlated with infarct size. (2) The distance of the culprit lesion was relatively shorter in the MVO (+) and transmural MI group than in the MVO absent and nontransmural MI groups. (3) Patients with proximal occlusion are at a greater risk of adverse LV remodeling after PCI in myocardial infarction.

PCI has gradually become a mainstream therapy for STEMI, and greatly reduces STEMI mortality through early invasive revascularization3,4. LAD-CLL, TIMI and the presence of collateral vessels/diagonal vessels before occlusion are displayed during angiography immediately after reperfusion in the acute phase of myocardial infarction. The location of the culprit lesions is an important clinical predictor of outcomes in patients with AMI. Previous studies revealed that culprit lesion located in the left main or proximal LAD were associated with a greater risk for long-term major adverse cardiac events5,6,7. To confirm these findings, we evaluated the relationship between LAD-CLL and myocardial injury objectively via CMR. In our study, the proximal location of the culprit lesion resulted in a larger infarct size, a lower LV ejection fraction, and higher ratios of MVO and transmural MI, which could lead to further fatal complications. Together, these findings could be explained by the fact that in the case of proximal occlusion, the extent of myocardial injury is significantly greater than that in distal occlusion.

The TIMI flow grade was visible and easy to use. The pre-PCI TIMI flow grade has been shown to be an important predictor of clinical outcomes, including mortality, in patients with STEMI17,19,20. Karwowski et al.17 revealed that a TIMI = 0 was associated with greater impairment of the baseline LV ejection fraction and was an independent predictor of 1- and 36-month mortality in LAD-related STEMI patients. However, Bauer et al.20 reported that the TIMI flow grade was not independently associated with a higher rate of other adverse ischemic events. Our results revealed no statistically significant differences in infarct size or LV ejection fraction, or in the ratios of MVO to transmural MI, between the total occlusion group and the nontotal occlusion group. Most enrolled patients in our study underwent interventional stent placement, which means that the ratio of patients with TIMI = 0 and TIMI = 1 is relatively high, this bias may affect the ability of TIMI grading to assess left ventricular remodeling. Notably, the presence of collateral vessels/diagonal vessels before occlusion may affect the perfusion of the myocardium21.The formation of collateral circulation can be observed in most patients with chronic complete occlusion, whereas in patients with acute myocardial infarction, approximately 69% of patients can form collateral circulation at the acute infarction stage, and this proportion increases to 75% within 3–6 h after symptom onset22,23. Waldecker et al.22 showed that on angiography, collateral circulation formed near the distal myocardium of acute coronary occlusion in 334 (69%) of 626 acute myocardial infarction patients in the acute stage. The ratio of collateral circulation in our study was relatively high, approximately 78% (64/82). The formation of coronary collateral circulation plays an important role in acute myocardial infarction. The formation of collateral circulation often indicates that the residual left ventricular ejection fraction can be improved, and it is also one of the bases for the recovery and remodeling of ventricular function after myocardial infarction24. Therefore, it is important for evaluating the prognosis of myocardial infarction. However, owing to the numerous factors affecting the formation of coronary collateral circulation in patients with acute myocardial infarction, such as the time of symptom onset to wire, the FMC2B time, the method of revascularization (thrombolysis and percutaneous coronary intervention, etc.), and the method of evaluating collateral circulation, few studies have been conducted in this field due to various factors. In subsequent studies, more attention should be given to the effects of collateral circulation on myocardial injury and prognosis.

Adverse LV remodeling occurs in a significant proportion of patients with acute myocardial infarction, especially LAD-related myocardial infarction, despite reperfusion of the infarct-associated arteries by percutaneous coronary intervention25. The left ventricular wall remodeling process significantly increases the risk of major adverse cardiovascular events, including death18. CMR is increasingly used to evaluate surrogate clinical end points and long-term prognoses following acute myocardial infarction26,27,28,29. Previous CMR studies on left ventricular remodeling after myocardial infarction have focused mostly on serological indicators and CMR parameters after acute infarction, there is no doubt that myocardial infarction size and MVO are important indicators affecting the prognosis of STEMI patients. However, CMR examination cannot be performed immediately after PCI. In comparison, predicting left ventricular remodeling after myocardial infarction through coronary angiography can identify high-risk patients earlier. therefore, more attention should be given to the features of angiography, especially for some patients with contraindications for MRI examination.

Limitations

First, the time from symptom onset (symptom onset) to seeking medical assistance (S2FMC time) was part of the total ischemic time, but was not included in this study. Although the initial symptoms are not typical, which may cause bias in time recall, the total duration of myocardial ischemia is a very important indicator and should be supplemented in subsequent studies. Second, in the present analysis, we did not analyze the lesion length since the length of the total occlusion lesions is difficult to measure accurately. Third, preventing, slowing or reversing left ventricular remodeling to reduce the risk of left heart failure and death is the main therapeutic goal of left ventricular remodeling after myocardial infarction, in which drug therapy plays a crucial role. However, the role of drug therapy after myocardial infarction was not considered in the present study. Finally the sample size in this single-center study was relatively small, and multicenter studies with larger sample size are needed to confirm our results.

In conclusion, in patients with LAD-related acute myocardial infarction undergoing primary PCI, LAD-CLL may be an independent predictor of short-term adverse LV remodeling.