Association of Moderate Coronary Artery Disease Burden with Major Adverse Cardiovascular Events following Kidney Transplantation

Abstract

Coronary artery disease (CAD) is the leading cause of mortality in kidney transplant (KT) recipients. While KT candidates with severe CAD often undergo revascularization, the impact of moderate, nonobstructive CAD remains unclear. In this retrospective study of KT recipients at Saint Louis University Hospital (2015–2024), we evaluated patients who underwent pre-transplant invasive coronary angiography but had no stenosis > 70% and did not receive coronary revascularization before transplant. Patients were grouped by the number of coronary vessels with moderate 50–70% stenosis: none (0V), 1–2-vessel (1–2V), and 3-vessel (3V) disease. The primary outcome was post-KT major adverse cardiovascular events (MACE), a composite of cardiovascular death, myocardial infarction, stroke, hospitalization for unstable angina, hospitalization for heart failure, arrhythmia, percutaneous coronary intervention or coronary artery bypass surgery Among 174 KT patients who underwent pre-KT coronary angiography and had moderate CAD, MACE occurred in 9.4%, 14.8%, and 37.5% of the 0V, 1–2V, and 3V groups. After adjustment, 3V disease was associated with a higher risk of MACE (hazard ratio 3.30, 95% CI:1.27–8.56). Left anterior descending artery (LAD) involvement was also independently associated with MACE (p = 0.004).

1. Introduction

Among kidney transplant (KT) recipients, the leading cause of morbidity and mortality is coronary artery disease (CAD).¹ This pattern has persisted as the number of KTs performed each year has risen.² Despite the increased number of KTs performed, demand for available kidneys continues to outpace the available supply. As of 2024, there are up to 90,000 patients on the waiting list for a kidney at any given time.³ This stark difference between supply and demand emphasizes the importance of allocation of transplants. With CAD as the leading cause of death in the KT population, it is crucial to assess pre-transplant risk of major adverse cardiovascular events (MACE) in order to modify the patients’ risk factors prior to transplant or, in cases of prohibitive risk, to exclude them from transplantation.⁴

Invasive coronary angiography (ICA) is commonly performed prior to transplantation. It is frequently used in patients with high risk of CAD, as it can be both diagnostic and therapeutic if a high grade coronary lesion is identified.⁴ Prior studies have shown a significantly higher risk of cardiac events in KT patient with severe (>70%) CAD when compared to moderate (<70%) CAD.⁵ Therefore, these patients are often revascularized prior to KT in an attempt to reduce risk.⁴

While the prognostic value of severe CAD is more uniformly agreed upon, it is less clear what implications a diagnosis of moderate CAD provides. There is a paucity of data regarding the association between MACE and moderate CAD where stenosis was <70%. In this study, we sought to delineate the relationship between the number of vessels affected by moderate coronary artery stenosis and which vessels were affected and their impact on MACE following KT.

2. Materials and Methods

This study was a retrospective analysis conducted at Saint Louis University Hospital, a tertiary care center with an active kidney transplant program. The study period spanned from January 1, 2015 to December 31, 2024. The RedCAP software was utilized to compile all of the patient data into one localized database. The primary objective of this study was to evaluate the association between the number of coronary arteries affected by moderate (50–70%) stenosis, as assessed by pre-transplant ICA, and the incidence of MACE following kidney transplantation.

Eligible participants for this study were adult patients (age ≳ 18 years) who underwent kidney transplantation at our institution during the study period. Per local protocol, non-diabetic patients underwent stress testing; those with positive stress testing as well as all diabetic patients were screened with ICA. All patients with severe coronary artery stenoses (>70%) would undergo coronary artery revascularization by percutaneous coronary intervention (PCI) and/or coronary artery bypass grafting (CABG) prior to KT, and were excluded in this study. Patients were included in this study if they: 1) received a pre-transplant ICA as part of their standard pre-KT evaluation, 2) had complete angiography data and longitudinal follow-up at our hospital, and 3) did not undergo pre-transplant coronary revascularization, therefore without severe (>70%) coronary artery stenosis.

CAD burden was classified based on the number of major coronary vessels - left anterior descending (LAD), right coronary artery (RCA), and left circumflex (LCx) - with 50–70% luminal stenosis on ICA. Patients were stratified into three groups: 0V (no vessel with moderate stenosis), 1–2V (one or two vessels with moderate stenosis), and 3V (three vessels with moderate stenosis). One and two vessel CAD were combined to ensure adequate group size. The degree of stenosis was determined by experienced interventional cardiologists as part of routine clinical care. Involvement of individual coronary arteries (LAD, RCA, and LCx) was recorded.

Demographic and clinical data were obtained from the electronic medical record as additional covariates including age, gender, race, body mass index (BMI), smoking status, hypertension, arrhythmia, obstructive sleep apnea, type 2 diabetes mellitus, dialysis modality (hemodialysis or peritoneal dialysis), duration of dialysis prior to transplantation, and left ventricular ejection fraction (LVEF). The duration of follow-up was calculated from the date of transplantation to the date of the most recent office visit that the patient had at our institution.

The primary outcome of this study was the occurrence of MACE following kidney transplantation, defined as a composite of cardiovascular death, non-fatal myocardial infarction, non-fatal stroke, hospitalization for unstable angina, hospitalization for heart failure, arrhythmia, PCI, or CABG. MACE events were identified through a systematic review of clinical notes and hospital discharge summaries.

Categorical variables including rates of MACE were reported as counts and percentages, and were compared across CAD groups using chi-square tests. Continuous variables including age, follow-up duration, and other baseline clinical characteristics were compared across CAD groups using ANOVA. Cox proportional hazards model was used to assess the independent association between CAD burden and MACE as well as the various subtypes of MACE, while adjusting for confounding variables identified from univariate regression, i.e., age and sex. Adjusted hazard ratios (HRs) with 95% confidence intervals (CIs) were reported. Continuous variables were summarized as mean ± standard deviation (SD). Kaplan-Meier survival curves were generated to illustrate MACE-free survival over time. Additionally, multivariable logistic regression was used to evaluate the association between the involvement of individual coronary arteries and MACE. All analyses were performed using RStudio and JASP statistical software. Statistical significance was defined as a two-tailed p-value < 0.05.

All the data that was extracted from the electronic medical records from Saint Louis University Hospital was approved by the Saint Louis University Hospital Institutional Review Board (Protocol Number: 34091; no separate approval number issued)

3. Results

A total of 174 KT recipients who underwent pre-transplant ICA and did not have severe CAD were included in the statistical analysis. Of these patients, 96 (55.2%) had no moderate coronary artery disease (0V), 54 (31.0%) had one or two-vessel moderate disease (1–2V), and 24 (13.8%) had three-vessel moderate disease (3V).

Baseline characteristics across the three groups are provided in Table 1. Male sex was numerically more prevalent in the 3V (79.2%) group compared to the 1–2V (68.5%) and 0V (47.9%) groups. None of the other baseline demographic characteristics were statistically different. The mean age was similar across all three groups (overall 56.1 ± 12.3 years, p = 0.053). Other baseline characteristics, including race, BMI, smoking status, hypertension, arrhythmia, obstructive sleep apnea, type 2 diabetes mellitus, follow-up length, type of dialysis, dialysis duration, and LVEF were similar across the three groups. The mean duration of follow-up was 52.0 ± 28.2 months from KT with a median duration of 51.3 months. Likewise, the average time from the reported ICA to KT was 22.3 months.

Table 1.

Baseline demographics and clinical characteristics

Variable	Total (n = 174)	0 V (n = 96)	1–2 V (n = 54)	3 V (n = 24)	P value
Male, n (%)	102 (58.6%)	46 (47.9%)	37 (68.5%)	19 (79.2%)	0.004
Age, mean ± SD (years)	56.1 ± 12.3	56.0 ± 12.4	56.1 ± 12.3	56.2 ± 12.3	0.053
Race
White (%)	71 (40.8%)	33 (34.4%)	26 (48.1%)	12 (50.0%)	0.16
Black (%)	97 (55.7%)	60 (62.5%)	25 (46.3%)	12 (50.0%)	0.13
BMI (kg/m2), mean ± SD	29.6 ± 5.7	29.6 ± 5.7	29.6 ± 5.7	29.5 ± 5.7	0.95
Current or former smoker (%)	53 (30.5%)	33 (34.4%)	14 (25.9%)	6 (25.0%)	0.46
Hypertension (%)	162 (93.1%)	87 (90.6%)	52 (96.3%)	23 (95.8%)	0.36
Arrhythmia (%)	169 (97.1%)	95 (99.0%)	51 (94.4%)	23 (95.8%)	0.26
Obstructive sleep apnea (%)	56 (32.2%)	30 (31.3%)	20 (37.0%)	6 (25.0%)	0.55
Type 2 diabetes mellitus (%)	94 (54.0%)	44 (45.8%)	35 (64.8%)	14 (58.3%)	0.07
Follow-up length in months, mean ± SD	52.0 ± 28.2	51.5 ± 27.7	52.0 ± 28.2	54.1 ± 26.9	0.76
Hemodialysis (%)	142 (81.6%)	80 (83.3%)	41 (75.9%)	21 (87.5%)	0.39
Peritoneal Dialysis (%)	32 (18.4%)	16 (16.7%)	13 (24.1%)	3 (12.5%)	0.39
Dialysis duration in months, mean ± SD	51.3 ± 35.9	51.2 ± 35.7	51.3 ± 35.9	50.6 ± 34.9	0.19
LVEF (%)	63%	63%	62%	63%	0.40

The incidence of MACE post-KT increased stepwise with greater moderate CAD burden. MACE occurred in 9.4% of patients in the 0V group, 14.8% in the 1–2 V group, and 37.5% in the 3V group; this difference was statistically significant (p = 0.003).

Post-transplant documentation of a stress test or other equivalent CAD monitoring was identified in 22 of 174 kidney transplant recipients (12.6%). Of the remaining 152 patients, 91 (52.3% of the total cohort) lived outside the St. Louis area, and 90 of these patients specifically had documented follow-up with a physician. The remaining 61 patients were local to St. Louis, and all of these patients had documented follow-up with a physician.

A univariate Cox proportional hazard model was constructed to identify predictors of MACE. In univariate analysis, only the presence of 3V moderate CAD (in comparison with 0V disease) was significantly associated with increased risk of MACE (p = 0.004, Table 2).

Table 2.

Univariate Cox proportional hazard model assessing the association of various variables and MACE following kidney transplantation

Variable	Hazard Ratio (HR)	95% CI	p-value
Sex – Male	2.08	0.87 – 4.94	0.10
Age at Transplant	1.02	0.98 – 1.05	0.34
Race – White	0.79	0.37 – 1.71	0.56
Race – Black	1.18	0.54 – 2.6	0.68
BMI	0.97	0.90 – 1.04	0.39
Current or former smoker	0.54	0.20 – 1.43	0.21
Hypertension	1.90	0.26 – 14.01	0.53
Arrhythmia	0.57	0.09 – 3.77	0.56
Obstructive sleep apnea	0.97	0.42 – 2.23	0.95
Type 2 diabetes mellitus	1.92	0.86 – 4.3	0.11
Hemodialysis	1.05	0.40 – 2.79	0.92
Peritoneal dialysis	0.95	0.36 – 2.52	0.92
Dialysis duration	1.00	1.00 – 1.02	0.09
LVEF	1.02	0.97 – 1.06	0.49
1–2V disease vs. 0V disease	1.55	0.60 – 4.03	0.37
3V disease vs. 0V disease	3.91	1.55 – 9.84	0.004

After adjusting for confounders (including age and sex) in a Cox proportional hazard model, the hazard ratio for MACE was 1.34 (95% CI: 0.51–3.55) for the 1–2V group and 3.30 (95% CI: 1.27–8.56) for the 3V group, using the 0V group as reference (Table 3). Thus, three-vessel CAD was independently associated with a significantly increased risk of MACE following KT. A further multivariable logistic regression analysis was also performed, which showed that involvement of the LAD artery (p = 0.004) was independently associated with MACE while RCA (p = 0.07) and LCx (p = 0.22) artery involvement were not significant predictors.

Table 3.

Multivariable Cox proportional hazard model assessing the association between moderate CAD (1–2V and 3V disease) and MACE following kidney transplantation

Variable	Hazard Ratio (HR)	95% CI	p-value
Sex (male = 1)	1.67	0.68 – 4.10	0.26
Age	1.01	0.98 – 1.04	0.58
1–2V disease vs. 0V disease	1.34	0.51 – 3.55	0.56
3V disease vs. 0V disease	3.30	1.27 – 8.56	0.014

Kaplan-Meier analysis of MACE-free survival was also performed, illustrating the impact of moderate CAD burden on post-transplant outcomes (Figure 1). Patients with moderate 3V disease had significantly lower MACE-free survival compared to those with moderate 0V or 1–2V disease (p = 0.014). The survival curves for the 0V and 1–2 V groups did not differ significantly.

Figure 1.

Kaplan-Meier curve of post-KT MACE-free survival 0V, 1–2V, and 3V Moderate CAD Groups.

Further Cox proportional hazard models that assessed the association between moderate CAD and various subtypes of MACE were created. After adjusting for confounders (including age and sex) in Cox proportional hazards models, three-vessel moderate CAD was independently associated with a significantly increased risk of non-fatal myocardial infarction following KT. The hazard ratio for non-fatal myocardial infarction was 1.74 (95% CI: 0.10–9.28) for the 1–2V group and 3.30 (95% CI: 1.08–19.69) for the 3V group, using the 0V group as reference (p = 0.043, Table 5).

Table 5.

Multivariable Cox proportional hazard model assessing the association between moderate CAD (1–2V and 3V disease) and non-fatal myocardial infarction following kidney transplantation

Variable	Hazard Ratio (HR)	95% CI	p-value
Sex (male = 1)	0.74	0.12 – 4.74	0.75
Age	1.01	0.94 – 1.09	0.74
1–2V disease vs. 0V disease	1.74	0.10 – 9.28	0.70
3V disease vs. 0V disease	11.35	1.08 – 19.69	0.043

Moderate 3V CAD did not show a significant association with other subtypes of MACE including cardiovascular death, non-fatal stroke, hospitalization for unstable angina, revascularization, as well as all-cause mortality compared to the reference group of moderate 0V disease. Specifically, the hazard ratio for cardiovascular death was 0.95 (95% CI: 0.21–4.38) for the 1–2V group and 1.86 (95% CI: 0.41–8.52) for the 3V group, using the 0V group as reference (p = 0.43, Table 4). The hazard ratio for non-fatal stroke was 2.47 (95% CI: 0.40–15.26) for the 1–2V group and 5.11 (95% CI: 0.79–33.10) for the 3V group, using the 0V group as reference (p = 0.09, Table 6). The hazard ratio for hospitalization for unstable angina was 1.12 (95% CI: 0.19–7.56) for the 1–2V group and 1.14 (95% CI: 0.11–11.56) for the 3V group, using the 0V group as reference (p = 0.92, Table 7). The hazard ratio for revascularization following KT was 1.83 × 10^9 for the 1–2V group and 7.98 × 10^9 for the 3V group, using the 0V group as (p = 1.00, Table 8). The hazard ratio for all-cause mortality was 1.59 (95% CI: 0.70–3.61) for the 1–2V group and 1.04 (95% CI: 0.33–3.27) for the 3V group, using the 0V group as reference (p = 0.94, Table 9).

Table 4.

Multivariable Cox proportional hazard model assessing the association between moderate CAD (1–2V and 3V disease) and cardiovascular death following kidney transplantation

Variable	Hazard Ratio (HR)	95% CI	p-value
Sex (male = 1)	6.33	0.78 – 51.71	0.09
Age	0.99	0.95 – 1.04	0.78
1–2V disease vs. 0V disease	0.95	0.21 – 4.38	0.95
3V disease vs. 0V disease	1.86	0.41 – 8.52	0.43

Table 6.

Multivariable Cox proportional hazard model assessing the association between moderate CAD (1–2V and 3V disease) and non-fatal stroke following kidney transplantation

Variable	Hazard Ratio (HR)	95% CI	p-value
Sex (male = 1)	0.80	0.18 – 3.56	0.77
Age	1.05	0.97 – 1.14	0.20
1–2V disease vs. 0V disease	2.47	0.40 – 15.26	0.33
3V disease vs. 0V disease	5.11	0.79 – 33.10	0.09

Table 7.

Multivariable Cox proportional hazard model assessing the association between moderate CAD (1–2V and 3V disease) and hospitalization for unstable angina following kidney transplantation

Variable	Hazard Ratio (HR)	95% CI	p-value
Sex (male = 1)	1.46	0.26 – 8.36	0.67
Age	1.00	0.93 – 1.07	0.96
1–2V disease vs. 0V disease	1.12	0.19 – 7.56	0.86
3V disease vs. 0V disease	1.14	0.11 – 11.56	0.92

Table 8.

Multivariable Cox proportional hazard model assessing the association between moderate CAD (1–2V and 3V disease) and revascularization following kidney transplantation

Variable	Hazard Ratio (HR)	95% CI	p-value
Sex (male = 1)	0.36	0.02 – 8.60	0.53
Age	1.22	0.89 – 1.68	0.22
1–2V disease vs. 0V disease	1.83 × 10^9	-	1.00
3V disease vs. 0V disease	7.98 × 10^9	-	1.00

Table 9.

Multivariable Cox proportional hazard model assessing the association between moderate CAD (1–2V and 3V disease) and all-cause mortality following kidney transplantation

Variable	Hazard Ratio (HR)	95% CI	p-value
Sex (male = 1)	1.39	0.63 – 3.06	0.42
Age	0.99	0.96 – 1.02	0.52
1–2V disease vs. 0V disease	1.59	0.70 – 3.61	0.27
3V disease vs. 0V disease	1.04	0.33 – 3.27	0.94

4. Discussion

In this retrospective study from Saint Louis University Hospital, our main findings were as follows: 1) Patients with 3V moderate CAD had significantly higher odds for MACE following KT, predominantly driven by nonfatal myocardial infarction; 2) Despite higher rates of MACE in the 3V group, overall survival was not significantly different compared to the 0V and 1–2V groups; 3) LAD moderate disease was independently associated with MACE. To our knowledge, this is the first study to specifically evaluate moderate coronary artery disease burden and location in the KT population.

In this study, we only included patients with no more than moderate coronary artery stenosis during pre-KT ICA. Patients who were found to have severe (>70%) CAD during ICA would have received revascularization, either through PCI or CABG, and they were not included in this study. Revascularized patients were excluded because the presumed effect of these procedures is to reduce stenosis thereby reducing cardiac risk, so their inclusion could potentially mask the effects of accelerated atherosclerosis by immunosuppressive medications after KT.^8,9 We sought to better delineate the associations between burden of moderate CAD, location of disease, and long term outcomes post-KT.

Existing data suggest that revascularization of severe lesions leads to reductions in morbidity and mortality following KT.^6,7 Manske et al. showed that revascularization was superior to medical management of hemodynamically significant coronary stenoses in KT candidates, though it should be noted that medical management was limited to a calcium channel blocker and aspirin. Their study was also limited by small sample size (13 receiving revascularization and 13 receiving medical therapy), short duration of follow-up (8.4 months), and sparce use of aspirin.⁶

Current standards for medical management have advanced significantly since that time. More recently, Kumar et al. provided additional data suggesting pre-KT revascularization of severe coronary stenoses was associated with reduced rates of cardiovascular events at 1 and 3 years following transplant.⁷ However, this was a single arm study of an entire cohort of patients receiving ICA, and the comparison was made between patients declining revascularization versus those who received it.

Previous study by Felix et al. provided the clinical context for our study. They evaluated outcomes in KT patients with pre-KT ICA, and found no statistically significant difference in post-KT cardiovascular events between those with CAD with or without revascularization; rather, the presence of CAD, regardless of revascularization status, was associated with worse outcomes compared to those without CAD by ICA.¹⁰ Notably, the Felix study defined CAD by the presence of International Classification of Diseases (ICD-9) codes, therefore it is unclear whether they included only patients with severe CAD, or also those with only mild/moderate CAD in their cohort. In comparison, our study focused exclusively on patients with no more than moderate CAD, and found that there was no significant difference in post-KT MACE between the 0V and 1–2V moderate CAD groups, whereas only 3V moderate disease was associated with increased MACE, which was largely driven by non-fatal myocardial infarction events. The finding that 3V moderate CAD was significantly associated with non-fatal myocardial infarction (HR 11.35, 95% CI: 1.08–19.69, p = 0.043) but showed no significant association with post-transplant revascularization (PCI or CABG, p = 1.00) is noteworthy. A majority of these events were declared by cardiologists to be type II NSTEMIs, resulting from an oxygen supply-demand mismatch, rather than primary type I MIs caused by plaque rupture requiring intervention. Therefore, our study complements the Felix study and adds a layer of nuance in the field.

The Felix study did not analyze the effects of the number of vessels with CAD.¹⁰ Previous studies outside of the KT population have evaluated the effect of increasing disease burden and found a stepwise increase in odds of MACE as the number of affected vessels rose.^11,12 They also found that 3V disease was significantly associated with MACE.^11,12 Our results support the association between 3V disease and MACE, but we did not find the same stepwise increase in risk in the 1–2V population. This discrepancy is likely explained by a smaller effect size, requiring a larger sample size to manifest.

Outside of MACE, we also analyzed for differences in cardiac-related or all-cause mortality and found no significant difference between the 0V, 1–2V, and 3V groups. A prior study of non-KT patients conducted using Veterans Affairs records found that only 3V nonobstructive CAD was associated with increased mortality at 1 year after ICA.¹³ Possible explanations for this difference in findings include a smaller sample size in our study, confounding factors related to our population’s renal disease, and longer follow-up time in our study obscuring a possible increased initial risk in the first year after ICA. While our study found increased rates of MACE in the 3V group, we did not see any difference in mortality. Again, our small sample size may have played a role in this discrepancy.

When looking at the relationship between outcomes and which vessel was diseased, we found that only the LAD was independently associated with increased odds of MACE following KT. Evidence regarding outcomes based on the identity of the diseased vessel outside of the context of an MI is limited. However, prior studies have revealed worse clinical outcomes in ST segment elevation myocardial infarction (STEMI) patients with LAD involvement, likely because it provides blood supply to a large area of the left ventricle.^14,15 However, there is less data about the RCA and LCx. There is a lack of consensus when it comes to RCA or LCx involvement, with some studies suggesting better survival with the RCA compared to the LAD and LCx,¹⁶ and others suggesting that LCx MIs may be worse due to an association with worse prognostic indicators.¹⁷ In our case, both the RCA and LCx were not statistically significantly linked to adverse outcomes.

The finding that 1–2 vessel moderate CAD was not significantly associated with MACE, while being consistent with our observation of non-stepwise risk increase, raises the question regarding the utility of invasive assessment in asymptomatic patients based solely on risk factors. Crucially, ICA is essential for identifying the specific moderate disease subgroups that carry a high post-transplant risk: the 3-vessel (3V) moderate CAD group, which demonstrated a significantly higher MACE risk (HR 3.30, 95% CI: 1.27–8.56) and patients with LAD involvement, which was independently associated with MACE (p = 0.004). This subgroup would likely be missed with risk factor-based screening, or noninvasive functional testing only. Therefore, we posit that ICA remains a necessary stratification tool to exclude occlusive disease and identify extensive moderate CAD that associates poor outcomes.

There are several limitations to our study. First, there were limited cardiac events and a limited number of patients with either 1 or 2 vessel disease alone, so these groups had to be combined for statistical analysis. This limits the granularity of the analysis. Furthermore, as a retrospective study, there is the potential for selection bias in terms of which patients received ICA and certain interventions. This could skew results and affect their ability to be generalized to the greater KT community. However, the decision to proceed with ICA and revascularization, as mentioned, is driven by local protocol. Additionally, we cannot avoid the possibility that our data was affected by incomplete reporting of certain measures or outcomes within patient charts, which could influence the relationships seen and potentially cause underestimation of outcomes. Similarly, we relied on data with the Saint Louis University Hospital network, meaning data collected at other health systems may not have been captured. This could impact our statistical analyses and may have caused underrepresentation in our results. This is partially mitigated by inclusion criteria requiring follow-up within our hospital system.

Strengths of this study include the high degree of detail within the data we collected, allowing for a more granular analysis. Additionally, we captured a longer average follow-up time. Further studies should evaluate the relationship between caliber and location of disease within the coronary vessel and long-term adverse outcomes.

In conclusion, in this retrospective study from a large healthcare system, moderate (50–70%) 3V CAD was associated with increased rates of MACE compared to 0V and 1–2V groups. Furthermore, moderate CAD of the LAD was independently associated with MACE.

List of Abbreviations:

CABG

Coronary artery bypass grafting

CAD

Coronary artery disease

CI

Confidence interval

ICA

Invasive coronary angiography

KT

Kidney transplantation

LAD

Left anterior descending artery

LCx

Left circumflex artery

LHC

Left heart catheterization

LVEF

Left ventricular ejection fraction

MACE

Major adverse cardiovascular events

PCI

Percutaneous coronary intervention

RCA

Right coronary artery

SD

Standard deviation

0V

No vessel with moderate stenosis

1–2V

One to two vessels with moderate stenosis

3V

Three vessels with moderate stenosis