Cardiac magnetic resonance follow-up of myocardial function in patients with chronic total occlusion of the coronary arteries: a retrospective cohort study

Introduction

Chronic total occlusions (CTOs) are identified in 16% to 20% of patients with coronary artery disease undergoing coronary angiography. The procedural volume of percutaneous coronary interventions (PCIs) for CTOs has been steadily increasing, with success rates improving due to enhanced operator experience and advancements in surgical instruments (1). Previous studies have demonstrated conflicting findings about the benefits of CTO artery recanalization, largely because of limitations related to the PCI technique (e.g., it is high risk, is expensive, requires the use of contrast, and can lead to clinical and technical complications). Although there is some evidence that PCI improves cardiac function in CTO by promoting several biologic factors that can reverse cardiac remodeling (2-4), the recent large-scale DECISION-CTO (5), EUROCTO (6), and EXPLORE (7) trials did not demonstrate clear links between PCI and improved global cardiac function indices or reductions in major adverse cardiac events. The REVASC trial showed that PCI did significantly reduce adverse coronary event rates at 12 months, but there were no differences in segmental wall thickening or other indices of left ventricular function between patients who did or did not receive PCI (8).

PCI in CTO may benefit selected high-risk patients, and/or improve left ventricular ejection fraction (LVEF) in some patients with low baseline LVEF (9,10). However, it is not yet clear whether all patients with low baseline LVEF will show improvements in cardiac functions after the procedure.

Cardiomyocytes located within CTO territory can be divided into fully viable, partly viable, and non-viable cells. Viable myocardium can contract normally or abnormally (11). Hibernating myocardium refers to a state of contractile dysfunction within viable myocardium, and occurs in the setting of chronic ischemic heart disease. Previous studies have shown that hibernating myocardium can recover after CTO-PCI (12), but it is still unclear how both baseline cardiac function and myocardial viability can affect patient prognosis following PCI.

It is extremely important to identify patients who will benefit from PCI in CTO. Recent studies in patients with CTO have assessed myocardial viability using late gadolinium enhancement (LGE), aiming to predict prognoses after PCI (13). Klein et al. (14) showed that cardiac magnetic resonance (CMR) can quantitatively assess infarct mass size and that these assessments correlate with positron emission tomography (PET)-scanned infarct size (r=0.81, P<0.0001). Our group has previously demonstrated that CMR imaging-based assessments are consistent with PET imaging assessments and can effectively assess myocardial viability in patients with coronary CTO lesions with a high degree of accuracy (15). CMR imaging is non-invasive, has superior spatial resolution and cardiac structure detection capacities, and can provide integrated information about myocardial viability and cardiac function (16). Quantitative CMR analyses also provide substantial diagnostic and prognostic information that can be used to guide revascularization decisions and to evaluate functional myocardial recovery.

Here, we conducted a retrospective study that used CMR imaging to investigate the effects of CTO artery revascularization on cardiac function. We hope to eventually prospectively identify CTO patients who would benefit most from PCI. We present this article in accordance with the STROBE reporting checklist (available at https://cdt.amegroups.com/article/view/10.21037/cdt-24-492/rc).

Methods

Study population

This retrospective cohort study screened 652 patients who were hospitalized because of angina pectoris and had CTO of a single artery detected on angiography between December 2014 and July 2023. Among these patients, 303 underwent baseline CMR imaging, and 115 underwent follow-up imaging. There were 108 patients met the inclusion criteria and incorporated into the final analysis. Of these patients, 71 underwent PCI and 37 had optimal medical therapy (OMT) (Figure 1). The inclusion criteria were as follows: (I) patients who were ≥18 years old; (II) patients with a single CTO, as confirmed by angiography; and (III) patients with baseline and follow-up CMR data. Exclusion criteria were as follows: (I) patients who had had an acute myocardial infarction within the preceding 3 months; (II) patients with left main coronary artery disease; (III) patients who were unable to complete CMR; (IV) patients with severe renal dysfunction; (V) patients who could not tolerate dual antiplatelet therapy; (VI) patients who were unable to communicate because of cognitive or auditory impairment; (VII) patients with poor CMR image quality at baseline and/or follow-up; and (VIII) patients with life expectancies less than 12 months. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. All patients provided written informed consent, and experimental procedures and study protocol were approved by Beijing Anzhen Hospital’s ethics board (No. 2020050X).

Figure 1 Patient selection flow chart. AMI, acute myocardial infarction; CMR, cardiac magnetic resonance; CTO, chronic total occlusion; LM, left main; OMT, optimal medical therapy; PCI, percutaneous coronary intervention.

Groups

Decisions to recanalize CTO arteries with PCI or to pursue OMT were made using a shared decision-making (SDM) model between both patients and physicians (17). A total of 71 patients were treated with PCI, while 37 patients received OMT only. All patients were discharged on OMT, including a P2Y12 receptor antagonist (clopidogrel or ticagrelor 90 mg twice daily), aspirin (100 mg/day), and a statin (once daily), all of which were administered for 12 months. Other medications, including beta blockers, calcium channel blockers, and nitrates, were prescribed based on each patient’s clinical status, taking into account factors such as heart rate, blood pressure, and overall cardiac function.

SDM definitions

SDM refers to the conversations that patients and clinicians have together to arrive at the final treatment decision of either CTO-PCI or OMT only (17).

Lesion definitions

We defined CTO as a lesion (I) located in the proximal segment of one of the three major epicardial arteries or within the main side branch; (II) with a diameter ≥2.5 mm; that (III) led to thrombolysis in myocardial infarction (TIMI) grade 0 flow lasting >3 months based on patient history. Multi-vessel disease (MVD) was defined as having at least one CTO lesion co-occurring with at least 75% stenosis in one or more of the other arteries described above.

PCI procedure

All patients undergoing PCI were pretreated with a dual-antiplatelet drug at least 24 hours before the procedure. They were also administered intravenous heparin at a dose of 70–100 U/kg-body weight during the procedure. Either an antegrade or retrograde approach was used to recanalize the artery with CTO. A retrograde procedure refers to an attempt to cross the lesion with a collateral vessel. Recanalization failure is defined as a failure of the guidewire or balloon catheter to cross the CTO lesion. Optimal recanalization of the CTO artery was defined as restoration of TIMI grade 3 flow using a drug-eluting stent or balloon angioplasty. Suboptimal recanalization of the CTO artery was defined as the final TIMI grade 2 flow.

CMR detection

CMR was used to assess both cardiac function and myocardial viability. Baseline CMR was measured before PCI and OMT, and post CMR was performed at a median follow-up time of 12 months.

We used a 3-T whole-body scanner (MAGNETOM Verio, A Tim System; Siemens Healthcare, Erlangen, Germany) with a 32-element matrix coil for data collection. Cine cardiac MR with 8 mm sections and no intersecting gaps were acquired in the short-axis (from the base to the apex) and long-axis (two- and four-chamber) planes of the left ventricle (LV) (15,16,18). A two-dimensional phase-sensitive inversion recovery breath-hold sequence was used for LGE imaging, performed 10 minutes after the intravenous administration of gadolinium at a dose of 0.15 mmol/kg body weight (Magnevist, Bayer Healthcare, Berlin, Germany). LGE imaging parameters were as follows: repetition time/echo time =4.10/1.56 ms, flip angle =20°, field-of-view =350×284 mm², and slice thickness =8 mm. LGE images were obtained in two long-axis (two- and four-chamber) views and in multiple short-axis views, covering the full LV from base to apex.

Two experienced radiologists analyzed the CMR LGE images using commercially available software (cvi42; Circle Cardiovascular Imaging, Inc., Calgary, Canada). Two radiologists have 15 and 20 years of working experience, respectively. The radiologists and data analysts were blinded to the patient group allocation throughout the study. LGE was defined as an area of signal enhancement [five standard deviations (SDs) of the signal intensity of non-enhanced myocardium] (18). To measure total myocardial mass—exclusive of papillary muscle mass and the intertrabecular blood pool—endocardial and epicardial LV tracings were manually performed on LGE images. Normal myocardium was defined as myocardial areas without any visually apparent LGE. A region of interest (ROI) in a portion of the normal myocardium (a sample of at least 100 pixels per ROI) on three consecutive midventricular image sections was drawn to determine the mean and SD of the signal intensity for each area. Average mean signal intensity and SD were obtained by averaging the mean signal intensities and SDs of the three midventricular sections. Segmental LGE, expressed as a percentage of segmental myocardial volume, was categorized as 0–50% or >50%, with values between 0 and 50% considered viable myocardium (13,15,16,19,20). Following methods used by Khariton et al. (21) and Samy et al. (22), patients were classified by LVEF (normal ≥50%; decreased <50%). Total LGE was expressed as a percentage of total myocardial volume (18). We deemed an LVEF increase of at least 3.5% to be a significant improvement (23).

Patient and public involvement statement

Patients were not involved in the design or conduct of this study.

Statistical analysis

IBM SPSS 20.0 and Stata software packages were used to conduct statistical and subgroup analyses, respectively. Normally distributed continuous variables and cardiac parameters [LVEF, left ventricular end-diastolic volume (LVEDV), and left ventricular end-systolic volume (LVESV)] were presented as means ± SDs. Student’s t-tests were used to compare independent samples with normally distributed variables. Normally distributed variables that differed between follow-up and baseline time points were analyzed using paired t-tests. Non-normally distributed variables, with the exception of cardiac parameters, were presented as medians with interquartile ranges and were analyzed with non-parametric tests. Categorical variables were presented as frequencies and percentages, and Chi-squared tests were used to examine statistically significant differences. Cox regression was used to test potential predictors of improvement in LVEF function, with the independent variables including age, gender, hypertension, diabetes, hyperlipidemia, PCI and OMI history, CTO location, collateral circulation, major side branch occlusion, CTO-PCI lesion restenosis, use of angiotensin-converting enzyme inhibitors (ACEIs)/angiotensin receptor blockers (ARBs), LVEF, and segmental LGE. A two-sided P value of <0.05 was considered statistically significant. A 95% confidence interval (CI) was used for statistical analysis.

Results

Baseline clinical status

We first compared baseline patient demographics and comorbidities and found no differences between the two patient groups (Table 1). Laboratory measures of clinical characteristics also showed comparable between-group results (Table 1). The only identifiable difference between the PCI and OMT groups was that patients in the OMT group were more likely to be using ACEIs/ARBs than PCI patients (59.5% vs. 38.0%, P=0.03).

To characterize the lesions, we estimated potential between-group differences in CTO artery location and in the number of patients with MVD. We found no statistically significant-between group differences in artery location (P=0.74). A total of 36 patients (50.7%) in the PCI group and 14 patients (37.8%) in the OMT group had MVD, but this difference was not statistically significant (P=0.20). Collateral circulation grading also showed no significant differences between the two groups (P=0.91).

Baseline CMR measurements

We next measured LVEF (successful CTO-PCI vs. OMT: 58.79%±12.16% vs. 60.45%±7.69%, P=0.39), LVEDV (successful CTO-PCI vs. OMT: 121.80±30.40 vs. 126.21±32.98 mL, P=0.49), LVESV [46.69 (36.11, 63.32) vs. 48.48 (35.80, 58.17) mL, P=0.86], total LGE mass [6.15 (1.74, 13.36) vs. 2.96 (1.40, 10.61) g, P=0.16], total LGE volume [successful CTO-PCI vs. OMT: 5.85 (1.66, 12.73) vs. 3.41 (1.42, 11.87) mL, P=0.45], and total LGE volume rate [successful CTO-PCI vs. OMT: 6.95% (2.51%, 15.42%) vs. 4.57% (1.92%, 12.72%), P=0.16] at baseline in both groups (Table 2).

Overall, there were a total of 104 patients with LGE, including 35 (32.4%) patients with LGE >50%. Among the patients with successful CTO-PCI, there were 24 (33.8%) patients with LGE >50%, and among the patients with OMT, there were 11 (29.7%) patients with LGE >50%. There were not statistically significant between the two groups (Table 2).

Effects of PCI on cardiac function and myocardial viability

Next, we evaluated the impact of PCI on cardiac function and myocardial viability. Due to poor image quality, LGE could not be measured at the follow-up timepoint in three PCI patients. LGE and cardiac function were not measured at the follow-up timpoint in two patients in the OMT group. Therefore, LGE and cardiac function at follow-up time points in these patients were not included in the statistical analyses

We found that, for patients with successful CTO-PCI, LVEF (post-PCI vs. pre-PCI: 61.00%±9.40% vs. 58.79%±12.16%, P=0.07), LVEDV (post-PCI vs. pre-PCI: 126.53±31.41 vs. 121.80±30.40 mL, P=0.10), and LVESV [post-PCI vs. pre-PCI: 47.09 (35.22, 61.11) vs. 46.69 (36.11, 63.32) mL, P=0.96] did not differ at follow-up compared to baseline (P>0.05). For patients with OMT, LVEF (post-OMT vs. pre-OMT: 59.68%±9.33% vs. 60.29%±7.85%, P=0.60), LVEDV (post-OMT vs. pre-OMT: 125.93±29.26 vs. 128.76±32.04 mL, P=0.47), and LVESV [post-OMT vs. pre-OMT: 51.41 (36.73, 62.07) vs. 48.48 (35.80, 58.17) mL, P=0.74] also did not differ from baseline measurements (Figure 2).

Figure 2 Effects of CTO-PCI on cardiac function, assessed by CMR. In the PCI group, (A) LVEF; (B) LVEDV; (C) LVESV. The paired-sample t-test was used to compare LVEF and LVEDV between baseline and follow-up, while an independent t-test was used for comparisons between groups. Non-parametric tests were applied for comparisons of LVEDV between baseline and follow-up, as well as for intergroup comparisons. CMR, cardiac magnetic resonance; CTO, chronic total occlusion; LVEDV, left ventricular end-diastolic volume; LVEF, left ventricular ejection fraction; LVESV, left ventricular end-systolic volume; OMT, optimal medical therapy; PCI, percutaneous coronary intervention.

LVEF in the PCI group did not significantly differ from OMT group LVEF after a median of 12 months of follow-up (PCI vs. OMT: 61.00%±9.40% vs. 59.68%±9.33%, P=0.50). Likewise, there were no between-group differences in LVEDV (PCI vs. OMT: 126.53±31.41 vs. 125.93±29.26 mL, P=0.93) and LVESV [PCI vs. OMT: 47.09 (35.22, 61.11) vs. 51.41 (36.73, 62.07) mL, P=0.68] measures at the time of follow-up (Figure 2).

We next evaluated myocardial viability by measuring total LGE volume, total LGE mass, and total LGE. We found no significant between-group differences in these metrics at the follow-up timepoint (P>0.05, Table 3). In the PCI group, total LGE mass [pre-PCI vs. post-PCI: 6.15 (1.74, 13.26) vs. 6.84 (2.29, 15.66) g, P=0.60], total LGE volume [pre-PCI vs. post-PCI: 5.85 (1.66, 12.73) vs. 6.52 (2.19, 14.92) mL, P=0.54] and total LGE [pre-PCI vs. post-PCI: 6.95% (1.51%, 15.42%) vs. 9.06% (3.38%, 16.46%), P=0.32] at follow-up did not significantly differ from baseline values (P>0.05, Table 3). The OMT group also showed no significant differences in total LGE mass [pre-OMT vs. post-OMT: 2.96 (1.40, 10.61) vs. 4.16 (1.98, 14.59) g, P=0.27], total LGE volume [pre-OMT vs. post-OMT: 3.41 (1.42, 11.87) vs. 3.96 (1.88, 13.90) mL, P=0.74] or total LGE [pre-OMT vs. post-OMT: 4.57% (1.92%, 12.72%) vs. 4.87% (2.63%, 15.27%), P=0.32] between the baseline and follow-up time points (Table 3).

Multifactorial analysis of LVEF recovery after successful CTO-artery recanalization

Our Cox regression analysis included age, gender, hypertension, diabetes, hyperlipidemia, PCI and OMI history, CTO location, collateral circulation, major side branch occlusion, restenosis of the CTO-PCI lesion, use of ACEIs/ARBs, and LVEF and segmental LGE as covariates. LVEF <50% combined with segmental LGE ≤50% were predictive for LVEF recovery following PCI [hazard ratio (HR) =6.53; 95% CI: 1.14–37.39; P=0.04] (Table 4).

Cardiac function changes in subgroups treated successfully with CTO-PCI

Patients were categorized into different subgroups based on their baseline LVEF and segmental LGE measurements. Age, gender, smoking, medical comorbidities (hypertension, diabetes, hyperlipidemia), PCI history, ACEI and beta-blocker use, CTO artery, MVD, and collateral circulation did not differ between these two subgroups. However, OMI history and HDL levels did differ between the subgroups (Table S1).

Among patients with baseline LVEF <50%, LVEF increased from 43.46% (40.18%, 47.28%) to 55.06% (43.72%, 61.13%) following PCI (P=0.002, Figure 3). LVEDV and LVESV did not significantly change among patients with decreased LVEF at baseline. Further analysis revealed that, among patients with LVEF <50% and segmental LGE ≤50%, LVEF increased [46.93% (40.14%, 47.49%) vs. 61.13% (47.48%, 64.54%), P=0.01] and LVESV decreased [73.60 (55.87, 96.45) vs. 55.90 (41.13, 75.82) mL, P=0.04] following PCI, but LVEDV did not change (P>0.05). In patients with LVEF <50% and segmental LGE >50%, neither LVEF [pre-PCI vs. post-PCI: 43.22% (40.23%, 45.54%) vs. 46.03% (40.75%, 59.06%), P=0.11], LVEDV [pre-PCI vs. post-PCI: 132.26 (116.81, 161.61) vs. 135.01 (120.52, 190.40) mL, P=0.07] nor LVESV [pre-PCI vs. post-PCI: 74.07 (60.68, 91.97) vs. 71.23 (59.55, 93.82) mL, P=0.80] changed following PCI (Figure 3).

Figure 3 Effects of CTO-PCI on cardiac function among patients in LVEF and LGE-based subgroups. (A) Patients with LVEF ≥50%; (B) patients with LVEF <50%. Patients with baseline LVEF <50% and segmental LGE ≤50% showed improved LVEF but decreased LVESV after PCI. LVEF, LVEDV, and LVESV values are presented as medians with interquartile ranges and were analyzed using non-parametric tests. *, P<0.05. CTO, chronic total occlusion; LGE, late gadolinium enhancement; LVEDV, left ventricular end-diastolic volume; LVEF, left ventricular ejection fraction; LVESV, left ventricular end-systolic volume; PCI, percutaneous coronary intervention.

Of patients with baseline LVEF ≥50%, LVEF [pre-PCI vs. post-PCI: 65.37% (57.16%, 69.93%) vs. 64.10% (60.00%, 68.56%), P=0.81], LVEDV [pre-PCI vs. post-PCI: 114.66 (95.14, 132.17) vs. 118.47 (95.61, 136.93) mL, P=0.30], and LVESV [pre-PCI vs. post-PCI: 40.02 (31.29, 51.63) vs. 40.32 (31.42, 56.27) mL, P=0.41] did not change after PCI. For patients with either segmental LGE >50% or ≤50%, LVEF, LVEDV, and LVESV also remained unchanged following PCI (Figure 3).

Discussion

Here, we determined that global myocardial function was not improved following successful PCI (as defined by no statistically significant changes in LVEF, LVEDV, or LVESV at a median follow-up time of 12.00 months) among a combined group of patients with CTO. However, a subgroup of CTO patients with baseline LVEF <50% and segmental LGE ≤50% did appear to benefit from PCI. Our findings emphasize the importance of quantitatively assessing cardiac function and myocardial viability before performing PCI.

Using PET imaging as a baseline comparison measure, we have previously shown that CMR has a high sensitivity and specificity for differentiating viable and non-viable myocardium at a segmental LGE cut-off value of 50% (15), largely because its spatial resolution is very high at this value. Thus, we employed a cut-off value of 50% for quantitative segmental LGE estimation in the present study.

Here, we assessed myocardial function at a median follow-up time of 12 months after revascularization. It is important to note that non-CTO lesions can also induce myocardial necrosis, suggesting that the value of CTO-PCI in patients with concurrent non-CTO lesion arteries also needs to be evaluated. We addressed this possibility in our study by quantitatively investigating global myocardial function changes with both total LGE and LGE in individual cardiac segments.

Cardiac function outcomes vary among patients

Our findings suggested that functional myocardial recovery could be stratified into three categories: significantly improved, preserved, and impaired. Using these distinctions, we determined that cardiac function deteriorated in 25.4% of the patients after PCI treatment (defined as LVEF reductions of at least 3.5%) but improved in 40.8% of patients (defined as LVEF increases of at least 3.5%).

Previous studies have not clearly characterized changes in myocardial function after CTO artery revascularization and neither have not fully explored potential underlying clinical mechanisms. Many factors may contribute to functional myocardial changes after CTO-revascularization, including myocardial injury during the PCI procedure, especially when “retrograde” approaches are used and/or in the case of a side branch occlusion (24), CTO-PCI lesion restenosis, progress or new development in non-CTO lesions, and microvascular dysfunction (25) following the procedure. Thus, many iatrogenic, physiologic, and pathophysiologic factors could underlie myocardial function changes and could have contributed to the negative results seen in several previous studies. Perhaps due to our relatively small sample size, we did not find that CTO-PCI lesion restenosis or side branch occlusion affected myocardial function recovery in the successful CTO-PCI group. After adjusting for confounding factors, we found that both baseline LVEF <50% and segmental LGE ≤50% were strong predictors of LVEF recovery after successful CTO-PCI.

Our findings suggest that clinicians could identify patients who would most benefit from PCI ahead of time by quantitatively measuring baseline LVEF and myocardial viability.

Patients with decreased baseline LVEF and segmental LGE less than 50% benefit most from PCI

We found that only 26.8% of patients with decreased LVEF (<50%) at baseline underwent PCI, but LVEF was increased among these patients at 12-month follow-up. In a previous study by Galassi et al. (9), 34.2% of patients had LVEF <50%. This discrepancy may be due to the fact that the number of segments with transmural myocardial scarring is limited within CTO territory because of myocardial protection mechanisms that are engaged during gradually developing occlusion, which allows for the development of collateral circulation (26,27). Werner et al. also showed that collateral function in cardiac artery CTO is related to regional myocardial function, meaning that the 64.8% of our patients with grade 3 TIMI collateral circulation could have contributed to the limited number of patients with LVEF <50% (28).

Subgroup analyses also showed that patients with LVEF <50% at baseline benefited the most from successful PCI. Galassi et al. (9) subdivided patients into three groups: group one had LVEF ≥50%, group two had LVEF 35% to 50%, and group three had LVEF ≤35%. Their results revealed that patients with low baseline LVEF (≤35%) had LVEF improvement (from 29.1%±3.4% to 41.6%±7.9%) 6 months after PCI. Likewise, Cardona et al. reported that PCI improved LVEF and LVEDV among patients with low baseline LVEF (≤40%) and evidence of viable myocardium (10). A study conducted by Samy et al. (22), which included 76 patients, showed that CTO-PCI improved echocardiography-assessed LVEF among patients with baseline LVEF <50% at 6 months of follow-up. Current studies suggest that (9,29) having a baseline LVEF <50% increases the difficulty and chance of procedural complications during CTO-PCI, underlining the importance of selecting patients who would most benefit from successful procedures. However, these studies did not provide information about myocardial viability, so it remained unclear if all patients with decreased baseline LVEF (LVEF <50%) could benefit from CTO-PCI.

Previous studies have suggested that viable myocardium tends to recover after CTO-PCI, but that the procedure is unlikely to benefit non-viable myocardium. Nakachi et al. (20) showed that segmental LGEs of 50% were related to cardiac function recovery using a semi-quantitative approach. Additionally, Schumacher et al. showed that viable CTO segments (i.e., LGEs ≤50%) were associated with greater segmental wall thickening than both segments with preserved function and segments with >50% LGE (30). However, it remains unclear if all patients with viable myocardium would demonstrate functional improvement following CTO-artery recanalization.

Evaluations of baseline myocardial viability and function could help identify the patients who would most benefit from CTO-PCI treatment. Interestingly, for patients with both baseline LVEF <50% and segmental LGE ≤50%, we found that LVEF significantly improved after PCI (Figures 3,4). However, there were no beneficial effects of PCI for patients with segmental LGE of >50% and baseline LVEF <50%. This discrepancy could be caused by CTO arteries restoring the contractile function of hibernating myocardium in patients with segmental LGE <50% (12).

Figure 4 A case with RCA-CTO after successful PCI. Here, all segmental LGE sizes were <50% at baseline. LVEF increased from 47.62% to 63.62% PCI. (A,B) LGE imaging of the short-axis (at baseline); (C) segmental infarct extent visible in the 16-segment mode (Bull’s eye plot) (at baseline); (D) angiography at the time of RCA-CTO; (E,F) LGE imaging of the short-axis (at follow-up), the blue arrows (E,F) and the yellow area (F) are LGE; (G) segmental infarct extent, displayed in the 16-segment mode (Bull’s eye plot) (at follow-up); (H) angiography at the follow-up timepoint. The green contour delineates the epicardial border, the red contour delineates the endocardial border, the purple contour indicates the right ventricular insertion point, and the blue-shaded region indicates the reference area of normal myocardium. CTO, chronic total occlusion; LGE, late gadolinium enhancement; LVEF, left ventricular ejection fraction; PCI, percutaneous coronary intervention; RCA, right coronary artery.

Our findings also suggested that, for patients with LVEF <50% but non-viable myocardium, myocardial function did not recover after CTO-PCI. Myocardial function improvement was also limited for patients with preserved or normal baseline LVEF. For patients with LVEF ≥50% and viable myocardium, OMT can be used instead of PCI before decreases in LVEF occur. Thus, a dynamic observation of both baseline LVEF and myocardial viability is needed when assessing candidates for PCI.

Study limitations

There are several limitations in this study: (I) we had a relatively small sample size, meaning that not all potential clinical factors were accounted for, and subgroup analyses were conducted with even smaller sample sizes. Despite this, the pathophysiological rationale of our findings remains convincing. (II) Treatment with either CTO-PCI or OMT was not randomly divided between the two patient groups, meaning that OMT patients may have had more complex lesions at baseline, confounding the analysis. However, we found minimal differences in comorbidities, lesion characteristics, and cardiac function between the two patient groups. An SDM model was used to determine drug treatment optimization or CTO lesion opening, which mirrored real-world scenarios. Moreover, we compared cardiac function before and after successful CTO-PCI, and analyzed the factors that could have influenced functional changes in a patient subgroup with successfully opened CTO arteries. This limitation, therefore did not affect our analysis of factors that impact cardiac function recovery after successful recanalization. (III) Future studies with longer follow-up periods will provide more comprehensive evidence about specific patient groups that could benefit from PCI.

Conclusions

For patients with CTO, early assessment of myocardial function and viability using CMR and LGE may assist in identifying those who are most likely to have improved cardiac function following PCI treatment. Our study suggested that patients with baseline LVEF <50% and segmental LGE ≤50% can experience successful cardiac recovery after CTO-PCI.

Acknowledgments

The authors appreciate Yi He and Lili Zhu’s assistance with MRI and echocardiography, respectively. We also thank MedEditing for their help in polishing our paper.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://cdt.amegroups.com/article/view/10.21037/cdt-24-492/rc

Data Sharing Statement: Available at https://cdt.amegroups.com/article/view/10.21037/cdt-24-492/dss

Peer Review File: Available at https://cdt.amegroups.com/article/view/10.21037/cdt-24-492/prf

Funding: This study was supported by the Capital Funds for Health Improvement and Research (No. 2022-1-2061), the Beijing Nova Program (No. 20220484222), the Beijing Hospitals Authority Youth Program (No. QML20210603), the Beijing Hospitals Authority’s Ascent Plan (No. DFL20220603), the High-Level Public Health Technical Talents from Beijing Municipal Ministry of Health (No. Leading Talents-02-01), and the Talents Promoted by the Beijing Association for Science and Technology.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://cdt.amegroups.com/article/view/10.21037/cdt-24-492/coif). The authors have no conflicts of interest to declare.

Etbical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. All patients provided written informed consent, and experimental procedures and study protocol were approved by Beijing Anzhen Hospital’s ethics board (No. 2020050X).

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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