Impact of Calcification Location in the Left Main Coronary Artery Bifurcation on Short-Term Prognosis After Left Main Stenting

Abstract

Background: The effect of the location of calcification in the left main coronary artery (LMCA) bifurcation on cardiovascular events remains unclear.

Methods and Results: This retrospective study included 498 patients who underwent LMCA stenting at a single center between 2014 and 2018. Moderate or severe calcification was visually assessed by coronary angiography. The primary endpoint was 3-year target lesion failure (TLF), defined as cardiac death, target vessel myocardial infarction, or clinically driven target lesion revascularization. Most patients (n=314; 63.1%) had no calcification in the LMCA bifurcation. One-segment calcification was observed in 45 (9.0%) patients, primarily in the left anterior descending artery (LAD; n=43 [8.6%]). Two-segment calcification was observed in 81 (16.3%) patients, most commonly involving the LMCA and LAD (n=70; 14.1%). Three-segment calcification was observed in 58 (11.6%) patients. Overall, 58 (11.6%) patients developed TLF within 3 years. Multivariable Cox regression analysis revealed a significant association between calcification in the left circumflex artery (LCX) and 3-year TLF (adjusted hazard ratio [aHR] 4.46; 95% confidence interval [CI] 1.81–10.99; P=0.001). In contrast, there was no significant association between calcification at the LMCA (aHR 1.29; 95% CI 0.47–3.55; P=0.623) or LAD (aHR 0.49; 95% CI 0.17–1.45; P=0.199) and the primary endpoint.

Conclusions: Moderate or severe calcification in the LCX is significantly associated with 3-year TLF in patients who have undergone LMCA stenting.

The left main coronary artery (LMCA) supplies a large amount of the myocardium. Therefore, coronary artery disease affecting the LMCA is the most high-risk lesion subset and is associated with a substantial risk of cardiovascular morbidity and mortality.¹ Percutaneous coronary intervention (PCI) has become a well-established procedure in recent years. Technological advances have facilitated the optimization of procedural techniques and treatment strategies. This has improved the prognosis for bifurcation lesions after PCI.² Nevertheless, PCIs for bifurcation lesions in the LMCA remain technically complex, and the most appropriate treatment for such lesions is yet to be determined. The Medina classification is a widely accepted method for the categorization of coronary bifurcation lesions. This system assigns a binary value (0 or 1) to the proximal and distal main vessels and side branches in a specific sequence based on the presence of significant stenosis observed in coronary angiography.³ The particular distribution of stenosis in the LMCA bifurcation (e.g., true bifurcation lesions [TBL]) is known to be associated with the risk of cardiovascular events after PCI.^4,5

Coronary artery calcification (CAC) is a challenge in PCI because of its association with stent malapposition, underexpansion,⁶ stent fracture,⁷ and delayed endothelialization after stent implantation.⁸ Accordingly, even with the development of improved PCI techniques and devices, patients with moderate or severe coronary calcification still have poorer outcomes than patients without calcification. Notably, most of these previous studies excluded patients with severely calcified LMCA bifurcation lesions.^9,10 In patients undergoing LMCA PCI, severe calcification in the LMCA bifurcation is anecdotally known to lead to poor outcomes. However, there is no evidence available regarding the impact of the location of the calcification in the LMCA bifurcation on prognosis after PCI. Therefore, the aim of the present study was to evaluate the association between cardiovascular events and the location of the calcification in the LMCA bifurcation in patients who underwent PCI for LMCA bifurcation lesions.

Methods

Study Population

This retrospective study included consecutive patients who underwent a first implantation of a second-generation or later drug-eluting stent in the LMCA between January 2014 and December 2018 at Kurashiki Central Hospital. There were no restrictions on clinical indications. We excluded patients with protected LMCAs and those with LMCA obstructions. A flow diagram of the participant selection and recruitment process is provided in Figure 1.

Figure 1.

Study flowchart. LMCA, left main coronary artery; PCI, percutaneous coronary intervention; TLF, target lesion failure.

The study was conducted in accordance with the principles of the 2013 revision of the Declaration of Helsinki. Because of the retrospective nature of the study, the Medical Ethics Committee of Kurashiki Central Hospital waived the requirement for informed consent; instead, patients were able to opt-out. The study was approved by the Institutional Review Board of Kurashiki Central Hospital (Reference no. 4396).

Calcification Severity and Distribution

In all patients, the severity and distribution of coronary calcification were evaluated by several physicians (K. Sasaki and Y. Sawayama) by visual assessment of coronary angiography images. Moderate calcification was defined as radiopaque densities observed during the cardiac cycle affecting only one side of the vascular wall. Severe calcification was defined as radiopaque densities without cardiac motion that were visible before contrast injection, typically involving both sides of the arterial wall.¹¹ Moderate or severe calcification on coronary angiography within 5 mm of the distal bifurcation of the LMCA was determined regardless of the presence or absence of stenosis. Figure 2 shows images of calcification in 4 representative patients.

Figure 2.

Coronary angiography images from 4 representative patients with different calcification distribution patterns at the left main coronary artery (LMCA) bifurcation. (A–D) Fluoroscopic images before contrast injection, with calcifications visible in the non-contrast images (arrows). (E–H) Fluoroscopic images after contrast injection. In Patient 1, no severe calcification is observed at the LMCA bifurcation. In Patient 2, severe calcification is observed in the left anterior descending artery (LAD). In Patient 3, severe calcification is observed in both the LMCA and LAD. In Patient 4, severe calcification is observed in the LMCA, LAD, and left circumflex artery.

PCI Procedures

PCI was performed using a 6- to 8-Fr guiding catheter. The choice of PCI device was left to the discretion of the PCI operator. Debulking devices were also used at the operator’s discretion. A provisional stenting strategy was used to treat the bifurcation lesions. Intravascular imaging (either intravascular ultrasound or optical coherence tomography) was routinely used with almost all lesions. The decision to use intravascular imaging for side branches was left to the discretion of the operator.

Definitions and Outcome Measurements

The primary outcome measure was target lesion failure (TLF), defined as cardiac death, target vessel myocardial infarction, or clinically driven target lesion revascularization (TLR), with analysis based on the time to the first event. Secondary outcomes included each of the TLF components, all-cause mortality, and definite stent thrombosis. Cardiac death was defined as any death due to a proximate cardiac cause (e.g., myocardial infarction, heart failure, fatal arrhythmia), unwitnessed deaths and deaths of unknown cause, and any procedure-related deaths, including those related to concomitant treatments.¹² The target vessel was defined as the entire major coronary vessel, including side branches.¹³ Myocardial infarction was defined according to the universal definition¹⁴ as an elevation in cardiac troponin >10 times of 99th percentile upper reference limit in patients with normal baseline values with at least one of the following elements: new pathological Q waves; imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischemic etiology; and/or angiographically documented native coronary artery occlusion. TLR was defined as the repeated revascularization of lesions within 5 mm of the previous stenting or ballooning site.¹³ Definite stent thrombosis was defined as angiographic confirmation of a thrombus originating at the stent or within 5 mm of either end of the stent and at least one of the following criteria within 48 h: acute onset of ischemia symptoms at rest; electrocardiogram changes suggestive of acute ischemia; and a typical rise and fall in levels of myocardial markers.¹² TBL were defined as lesions significantly involved in both the main vessel and the ostium of the side branch.¹⁵

Statistical Analysis

The study population was divided into 2 groups according to the occurrence of 3-year TLF. Patient characteristics and the location of calcification within the LMCA bifurcation were compared between the 2 groups. Normally distributed continuous variables are presented as the mean±SD and were compared using Student’s t-tests. Continuous variables with a skewed distribution are presented as the median with interquartile range and were compared using the Mann-Whitney U test. Categorical variables were compared using Chi-squared or Fisher’s exact tests.

To assess the impact of calcification location (i.e., LMCA, left anterior descending artery [LAD], or left circumflex artery [LCX]) on the primary and secondary outcomes, we calculated adjusted hazard ratios (aHRs) and 95% confidence intervals (CIs) using a Cox proportional hazard regression model. Based on previous reports,^16,17 clinical and procedural covariates were included in the model for mulitivariable analysis. To avoid overfitting due to the limited number of events, we restricted the covariates to age, sex, left ventricular dysfunction (left ventricular ejection fraction <40%), clinical presentation (acute coronary syndrome [ACS] or not), TBL, the use of intravascular imaging for LCX, the use of a rotablator, and the location of moderate or severe calcification in the LMCA bifurcation. In addition, we performed interaction tests of the clinically relevant subgroups: age ≥75 or <75 years; sex; the presence or absence of left ventricular dysfunction; the presence or absence of TBL; clinical presentation; and whether intravascular imaging was performed for LCX. The multivariable Cox proportional hazard regression model was the same as that used in the main analysis.

All P values reported are 2-sided, and P<0.05 was considered statistically significant. SAS v. 9.4 (SAS Institute, Cary, NC, USA) was used for all statistical analyses.

Results

Patient Characteristics

Of the 498 patients included in the study, 58 (11.6%) developed TLF within 3 years. The median follow-up period was 1,095 days. Table 1 presents baseline patient characteristics, lesion characteristics, and the PCI procedures used. The mean patient age was 73.4 years, and 78.1% were male. In this cohort, 44.8% of patients had diabetes, 74.9% had hypertension, 64.7% had dyslipidemia, and 11.0% were current smokers. PCI for ACS accounted for 30.7% of the PCIs performed. Compared with patients who did not experience TLF, those who did had a higher incidence of previous myocardial infarction (15.5% vs. 3.6%; P=0.001) and a higher incidence of ACS (60.3% vs. 26.8%; P<0.001). The TLF group had a lower mean left ventricular ejection fraction (52.5% vs. 56.5%; P<0.001) and a higher mean serum creatinine level (1.02 vs. 0.85 mg/dL; P<0.001). The group with TLF had a significantly higher rate of TBL according to the Medina classification (56.9% vs. 40.0%; P=0.014). Other baseline patient characteristics were comparable between the 2 groups.

Table 1.

Baseline Patient Characteristics

	All patients (n=498)	No TLF (n=440)	TLF (n=58)	P value
Age (years)	73.4±10.0	73.4±9.7	72.9±11.5	0.709
Male sex	389 (78.1)	346 (78.6)	43 (74.1)	0.436
BMI (kg/m2)	23.2 [21.3–25.4]	23.4 [21.3–25.4]	23.2 [21.4–25.9]	0.946
Risk factors and history
Diabetes	223 (44.8)	193 (43.9)	30 (51.7)	0.258
Hypertension	373 (74.9)	333 (75.7)	40 (69.0)	0.268
Dyslipidemia	322 (64.7)	291 (66.1)	31 (53.5)	0.057
Current smoker	55 (11.0)	48 (10.9)	7 (12.1)	0.791
Hemodialysis	25 (5.0)	16 (3.6)	9 (15.5)	0.001
Previous MI	176 (35.3)	156 (35.5)	20 (34.5)	0.884
Previous PCI	219 (44.0)	197 (44.8)	22 (37.9)	0.324
Physiological examinations and laboratory tests
LVEF (%)	56.0 [47.0–60.0]	56.5 [48.0–60.0]	52.5 [30.0–56.0]	<0.001
Creatinine (mg/dL)	0.86 [0.72–1.06]	0.85 [0.72–1.03]	1.02 [0.83–1.51]	<0.001
eGFR (mL/min/1.73 m2)	63.2 [46.3–78.0]	65.4 [48.3–79.5]	48.9 [29.2–64.1]	<0.001
Clinical presentation
ACS	153 (30.7)	118 (26.8)	35 (60.3)	<0.001
Lesion characteristics
Syntax score ≥33	143 (28.7)	122 (27.7)	21 (36.2)	0.180
TBL	209 (42.0)	176 (40.0)	33 (56.9)	0.014
PCI procedures
Intravascular imaging	462 (92.8)	412 (93.6)	50 (86.2)	0.055
Intravascular imaging for LCX	277 (55.6)	251 (57.1)	26 (44.8)	0.078
Use of rotablator	23 (4.6)	20 (4.6)	3 (5.2)	0.742
Use of rotablator
From LMCA to LAD	20 (4.0)	18 (4.1)	2 (3.5)	1.000
From LMCA to LCX	5 (1.0)	3 (0.7)	2 (3.5)	0.106
Two-stent implantation	77 (15.5)	59 (13.4)	18 (31.0)	<0.001
LMCA-LAD stenting
With KBT	371 (74.5)	339 (77.1)	32 (55.2)	<0.001
Without KBT	25 (5.0)	21 (4.8)	4 (6.9)	0.517
LMCA-LCX stenting	25 (5.0)	21 (4.8)	4 (6.9)	0.517

Unless indicated otherwise, data are presented as the mean±SD, median [interquartile range], or n (%). P values were calculated between patients with and without 3-year target lesion failure (TLF). ACS, acute coronary syndrome; BMI, body mass index; eGFR, estimated glomerular filtration rate; KBT, kissing balloon technique; LAD, left anterior descending artery; LCX, left circumflex artery; LMCA, left main coronary artery; LVEF, left ventricular ejection fraction; MI, myocardial infarction; PCI, percutaneous coronary intervention; TBL, true bifurcation lesion.

Intravascular imaging was used during the index PCI in most patients (92.8%), and 55.6% of patients underwent intravascular imaging for the LCX direction. Patients treated with a rotablator accounted for 4.6% of the total. Overall, the most common stenting strategy was crossover stenting for LMCA-LAD. This was combined with the kissing balloon technique for the LCX (74.5%). This strategy was significantly less common in the group with than without TLF (55.2% vs. 77.1%; P<0.001). Two-stent implantation was implemented in 15.5% of all patients. It was more frequently required in the group with than without TLF (31.0% vs. 13.4%; P<0.001). Supplementary Table 1 presents baseline patient characteristics according to the presence or absence of moderate or severe calcification in the LCX.

Location and Distribution of Calcification in the LMCA Bifurcation

Figure 3 shows the distribution of moderate or severe calcification in the LMCA bifurcation. In the present study cohort, most patients did not have any calcification in any segment (314/498; 63.1%). Of those with calcification in just 1 segment (45/498; 9.0%), most had calcification in the LAD (43/498; 8.6%). Among patients with calcification in 2 segments (81/498; 16.3%), the most common segments were the LMCA and LAD (70/498; 14.1%). Moderate or severe calcification in all 3 segments was seen in 58 of 498 (11.6%) patients. There were no instances of 2-segment calcification in the LMCA and LCX and no instances of 1-segment calcification in the LMCA.

Figure 3.

Distribution of moderate or severe calcification at the left main coronary artery (LMCA) bifurcation. In the table below the graph, “+” indicates moderate or severe calcification, whereas “–” indicates no moderate or severe calcification. The schematic diagrams above the bar graph show the most common distribution of calcification based on the number of segments affected. In the schematic diagram, moderate or severe calcification is represented by gray circles. LAD, left anterior descending artery; LCX, left circumflex artery.

Table 2 presents 3-year TLF rates according to the location and distribution of calcification. TLF occurred in 20 of 128 (15.6%; P=0.104) patients with LCMA calcification and in 25 of 182 (13.7%; P=0.270) patients with LAD calcification. In contrast, LCX calcification was significantly correlated with TLF, which occurred in 19 of 71 (26.8%; P<0.001) patients with LCX calcification. The incidence of TLF varied depending on calcification distribution, with a significant relationship between the pattern of calcification distribution and the incidence of TLF (P<0.001). Figure 4 shows Kaplan-Meier curves for the cumulative incidence of TLF over 3 years according to the presence of moderate or severe calcification in the LCX. TLF occurred significantly more frequently in those with moderate or greater calcification in the LCX than in those with mild or no calcification (log-rank P<0.001).

Table 2.

Frequency of 3-Year TLF Occurrence According to the Location and Distribution of Calcification in LMCA Bifurcation

	TLF	P value
Location of moderate or severe calcification
LMCA	20/128 (15.6)	0.104
LAD	25/182 (13.7)	0.270
LCX	19/71 (26.8)	<0.001
Distribution of moderate or severe calcification		<0.001
None	32/314 (10.2)
LCX alone	1/2 (50)
LAD alone	2/43 (4.7)
LMCA alone	0/0 (0)
LAD, LCX	3/11 (27.3)
LMCA, LCX	0/0 (0)
LMCA, LAD	5/70 (7.1)
LMCA, LAD, LCX	15/58 (25.9)

Unless indicated otherwise, data are presented as the number of patients who experienced TLF/the total number of patients in that group (%). P values were calculated for comparisons between patients with and without 3-year TLF. Abbreviations as in Table 1.

Figure 4.

Kaplan-Meier curves for the cumulative incidence of target lesion failure (TLF) over 3 years according to the presence (blue) or absence (red) of moderate or severe calcification at the left circumflex artery (LCX). TLF occurred significantly more frequently in the group with moderate or severe calcification at the LCX (log-rank P<0.001).

The rates of secondary outcome events according to calcification location are presented in Supplementary Table 2. Patients with LCX calcification had higher rates of all secondary outcome events than those with LMCA or LAD calcification. The frequency of 3-year clinical endpoint occurrence according to the use of intravascular imaging for the LCX is presented in Supplementary Table 3. There was no significant difference in any of the clinical endpoints according to the use or not of intravascular imaging for the LCX.

Multivariable Analysis of TLF

The results of multivariable Cox regression analysis are presented in Table 3. Moderate or severe calcification in the LCX was significantly associated with 3-year TLF (aHR 4.46; 95% CI 1.81–10.99; P=0.001), even after adjustment for TBL using the Medina classification. Conversely, neither LMCA (aHR 1.29; 95% CI 0.47–3.55; P=0.623) nor LAD (aHR 0.49; 95% CI 0.17–1.45; P=0.199) calcification was significantly correlated with 3-year TLF. Supplementary Tables 4–8 present secondary outcomes for patients with different calcification locations. LCX calcification was an independent risk factor for 3-year cardiac death (aHR 6.08; 95% CI 1.86–19.87; P=0.003). A higher risk of 3-year TLF in patients with moderate or severe calcification in the LCX was consistently found across subgroups (Figure 5).

Table 3.

Multivariable Cox Regression Analysis on the Primary Outcome (3-Year TLF)

	Univariable analysis		Multivariable analysis
	HR (95% CI)	P value	HR (95% CI)	P value
Age ≥75 years	1.14 (0.68–1.91)	0.611	0.88 (0.51–1.51)	0.639
Male sex	0.78 (0.43–1.41)	0.408	0.75 (0.40–1.40)	0.359
Left ventricular dysfunctionA	4.65 (2.70–8.00)	<0.001	4.98 (2.84–8.74)	<0.001
ACS	3.73 (2.21–6.32)	<0.001	3.21 (1.88–5.49)	<0.001
True bifurcation lesion	1.96 (1.17–3.30)	0.011	1.65 (0.96–2.84)	0.070
Intravascular imaging for LCX	0.62 (0.37–1.03)	0.067	0.61 (0.36–1.04)	0.071
Use of rotablator	1.28 (0.40–4.09)	0.678	0.94 (0.27–3.24)	0.925
LMCA calcification	1.61 (0.94–2.77)	0.084	1.29 (0.47–3.55)	0.623
LAD calcification	1.39 (0.83–2.34)	0.216	0.49 (0.17–1.45)	0.199
LCX calcification	3.38 (1.95–5.85)	<0.001	4.46 (1.81–10.99)	0.001

^ADefined as ejection fraction <40%. CI, confidence interval; HR, hazard ratio. Other abbreviations as in Table 1.

Figure 5.

Comparison of 3-year target lesion failure (TLF) rates in different subgroups. Subgroup analysis showed a consistent positive association between TLF and left circumflex artery (LCX) calcification across all subgroups. ACS, acute coronary syndrome; CI, confidence interval; HR, hazard ratio; IV, intravascular; LV, left ventricular; TBL, true bifurcation lesion; TLF, target lesion failure.

Discussion

This study assessed the effects of the location and distribution of calcification in the LMCA bifurcation on clinical outcomes after PCI. The main findings of this study are as follows:

1. A unique distribution of moderate or severe calcification in the LMCA bifurcation was identified in patients undergoing PCI for LMCA.

2. The incidence of 3-year TLF differed according to the location and distribution of calcification in the LMCA bifurcation, with a higher incidence in patients with calcification in the LCX.

3. Even after adjusting for the presence of TBL using the Medina classification, moderate or severe calcification in the LCX was significantly associated with the occurrence of 3-year TLF.

The specific distribution of stenosis (e.g., TBL) in LMCA bifurcation lesions is known to contribute to the risk of cardiovascular events after PCI.^4,5 However, there has been insufficient research into the effects of calcification distribution on patient outcomes after LMCA PCI. The novel finding of the present study is that the specific location of calcification may be associated with the risk of TLF after PCI. Importantly, this result was independent of the presence of TBL, which is a risk factor for cardiovascular events after PCI.⁵ Furthermore, the positive association between TLF and LCX calcification was consistently observed across all subgroups. Identifying those patients with poorer predicted prognoses would be beneficial when monitoring the clinical course after PCI, especially in patients who already have a high risk of cardiovascular events, such as those who undergo LMCA PCI. In clinical practice, coronary artery bypass grafting as a revascularization procedure may need to be considered as a viable alternative for patients with complex LCX calcification.

We could not determine the mechanism by which LCX calcification, but not LMCA or LAD calcification, is independently associated with TLF because of the retrospective nature of the present study. However, some possible explanations can be posited. We found that when patients had moderate or severe calcification in only 1 segment, it was predominantly in the LAD. In those with calcification in 2 segments, these segments were usually the LMCA and LAD. When calcification was present in the LCX, it was generally additional to calcification in both the LMCA and the LAD. These findings suggest that patients with LCX calcification represent a subset with advanced atherosclerosis at high risk of cardiovascular events. This speculation is supported by the fact that, in our cohort, LCX calcification showed a robust association with hard outcomes (i.e., cardiac death), but not with clinically driven TLR, which is primarily affected by lesion characteristics.

CAC is a hallmark of advanced atherosclerosis and is associated with an overall increase in the amount of plaque, a higher risk of future adverse events, and worse outcomes after surgery or PCI.^9,18 In asymptomatic patients with a CAC score ≥1,000, as identified by computed tomography (CT), severe CAC in the LMCA is associated with high mortality risks.¹⁹ However, in the present study, we found no significant relationship between TLF or cardiac death and calcification in the LMCA. This may be because the study cohort consisted of patients undergoing PCI and calcification was assessed using fluoroscopy rather than CT.

Study Limitations

This study has several limitations. First, the data were collected retrospectively in a single center, and there was patient selection bias. Second, we found no correlation between TLF and calcification in the LMCA or LAD. Generally, the presence of calcification predicts a poor prognosis after PCI. However, because this study was limited to patients who underwent PCI in the LMCA, the results may not be applicable to the general population. Third, we used qualitative definitions of CAC on fluoroscopy. Fluoroscopic detection of calcium depends on the overall amount of calcium (measured by arc, length, or thickness). In addition, the severity of CAC was assessed visually using coronary angiography, which is inferior to intravascular imaging in sensitivity and specificity.²⁰ Although intravascular imaging was primarily used in the main vessel, the imaging data for side branches was limited. In addition, findings such as calcified nodules and eccentric calcification, which are confirmed by intravascular imaging, have been shown to be associated with poor prognosis after PCI.²¹ Because of the lack of imaging data, we could not analyze the effects of lesion characteristics on clinical outcomes. CT is also excellent for detecting calcification, and CAC scoring with CT has been demonstrated to predict long-term atherosclerotic cardiovascular disease in both patients with and without coronary artery disease.^22,23 However, not all patients undergoing PCI undergo intravascular imaging of the side branches or cardiac CT scans to evaluate the CAC. In this regard, our study highlights the clinical significance of visual assessment of CAC by coronary angiography. It also builds on the findings of previous studies that have identified an association between fluoroscopically detected calcification and cardiovascular events, providing deeper insights into their relationship.^11,16 Fourth, the decision to use a debulking device and intravascular imaging for side branches during PCI was at left to the discretion of the operator. The study period was from 2014 to 2018, which may have influenced the use of debulking devices and intravascular imagings, because debulking devices and intravascular imaging for side branches were not as actively used for more advanced calcified lesions as they are now. Therefore, it may not be possible to directly apply our findings to outcomes with current treatments. Improving treatment outcomes may be possible by developing PCI strategies that incorporate both debulking and imaging for calcification, recognizing that patients with LCX calcification represent a high-risk group for cardiovascular events. Finally, physiological assessments are useful for evaluating PCI indications and strategies, as well as for predicting outcomes after PCI.²⁴ However, physiological data were lacking in the present study.

Conclusions

In patients who underwent stenting for LMCA, the incidence of TLF within 3 years of PCI differed according to the location of moderate or severe calcification in the LMCA bifurcation. In particular, the presence of calcification in the LCX was strongly associated with the TLF within 3 years of PCI. This correlation was independent of the effects of stenosis distribution.

Acknowledgment

The authors thank Enago (www.enago.jp) for English language review of a draft of this manuscript.

Sources of Funding

This study did not receive any specific funding.

Disclosures

The authors declare no conflicts of interest associated with this manuscript.

IRB Information

This study was approved by the Institutional Review Board of Kurashiki Central Hospital (Reference no. 4396).

Data Availability

The deidentified participant data will not be shared.

Supplementary Files

Please find supplementary file(s);

https://doi.org/10.1253/circj.CJ-25-0028

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