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Table of Contents
ORIGINAL ARTICLE
Year : 2019  |  Volume : 9  |  Issue : 3  |  Page : 123-130

Predictors for coronary artery ectasia


Department of Cardiology, Faculty of Medicine, Zagazig University, Zagazig, Egypt

Date of Web Publication3-Dec-2019

Correspondence Address:
Prof. Ahmed Shawky Shereef
Department of Cardiology, Faculty of Medicine, Zagazig University, Zagazig
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/JICC.JICC_30_19

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  Abstract 


Background: Coronary artery ectasia (CAE) is characterized by dilation of an arterial segment to a diameter ≥1.5 times that of the adjacent normal coronary artery, 10%–20% of CAE have been described in association with inflammatory or connective tissue diseases. The underlying mechanisms of ectasia formation are not yet entirely known, so the aim is to assess the validity of the high-sensitivity C-reactive proteins (Hs-CRP) and the hematological parameters (platelet to lymphocyte ratio [PLR], mean platelet volume [MPV], and neutrophil-to-lymphocyte ratio [NLR]) to predict CAE. Patients and Methods: 60 patients with chronic stable angina were classified into three groups as follows: Group 1: CAE without coexisting atherosclerotic coronary arteries (20 patients), Group 2: CAE with coexisting atherosclerotic coronary arteries (20 patients), and Group 3: Normal coronary angiography (20 patients) as control group. Our patients were submitted to: (1) complete history taking, (2) thorough clinical examination, (3) electrocardiography, (4) laboratory investigation with special interest in complete blood picture and Hs-CRP, (5) transthoracic echocardiography, and (6) coronary angiography. Markis classification was used for classification of CAE. Results:(1) NLR ≥2.65 can predict CAE with sensitivity 52.5% and specificity 100% (P < 0.001). (2) PLR ≥110.5 can predict CAE with sensitivity 82.5% and specificity 60% (P = 0.001). (3) MPV ≥8.25 can predict CAE with sensitivity 72.5% and specificity 55% (P = 0.007). (4) Hs-CRP ≥2.35 mg/dl can predict CAE with sensitivity 95% and specificity 85% (P < 0.001). Conclusion: NLR, MPV, PLR, and Hs-CRP can predict CAE. They are available, cheap, and easily calculated.

Keywords: Coronary ectasia, high sensitivity C-reactive protein, complete blood picture


How to cite this article:
Shereef AS, Kandeel NT. Predictors for coronary artery ectasia. J Indian coll cardiol 2019;9:123-30

How to cite this URL:
Shereef AS, Kandeel NT. Predictors for coronary artery ectasia. J Indian coll cardiol [serial online] 2019 [cited 2019 Dec 7];9:123-30. Available from: http://www.joicc.org/text.asp?2019/9/3/123/272169




  Introduction Top


Coronary artery ectasia (CAE) is an aberration of the coronary arteries that have been characterized by diffuse or localized dilatation of the epicardial coronary arteries without obstruction to a diameter ≥1.5 times that of the adjacent normal coronary artery.[1] About 10%–20% of CAE have been described in association with inflammatory or connective tissue diseases. Moreover, previous studies demonstrated that the neurohormonal process, inflammation, and cardiovascular risk factors are related to CAE.[2]

In short, CAE may be a form of atherosclerosis with more active inflammatory properties than normal vessels.[3]

Hence, we aimed to assess the validity of the inflammatory markers (high-sensitivity C-reactive proteins [Hs-CRP]) and the hematological parameters (platelet-to-lymphocyte ratio [PLR], mean platelet volume [MPV], and neutrophil-to-lymphocyte ratio [NLR]) to predict CAE.


  Patients and Methods Top


The study included 60 patients with chronic stable angina, and it was conducted in Zagazig University Hospitals in the period from May 2016 to January 2017. All patients gave informed consent to participate in the study and ethical committee approval was done.

The study included 37 male patients and 23 female patients. They were classified into three groups:

  • Group 1: Patients with CAE without coexisting atherosclerotic coronary arteries (20 patients)
  • Group 2): Patients with CAE with coexisting atherosclerotic coronary arteries (20 patients)
  • Group 3: Patients with normal coronary angiography (control group, 20 patients).


Inclusion criteria

Patients with chronic stable angina were included in the study.[4]

Exclusion criteria

Patients with ≥1 of the following criteria were excluded from the study.

  • Significant valvular heart disease and congenital heart disease
  • Left ventricular dysfunction (ejection fraction <40%) and cardiomyopathy
  • Hypothyroidism or hyperthyroidism
  • Acute or chronic hepatic, renal, and pulmonary disease
  • Acute or chronic infectious disease, malignancies, or autoimmune diseases
  • Patients who had undergone surgical or percutaneous revascularization.


Methods of the study

All our patients were submitted to:

  • Complete history taking
  • Clinical examination
  • Electrocardiography


Laboratory investigation – laboratory parameters were collected from the patients after a 12 h overnight fasting and done at clinical pathology laboratories in Zagazig university hospital with special interest in: complete blood picture including mean platelet count, mean platelets volume, platelets distribution width, total, and differential leukocytic count to calculate both PLR and NLR.

  • Transthoracic echocardiography
  • Coronary angiography


Angiograms were analyzed by two blinded interventional cardiologists without knowledge of the clinical status or laboratory measurements.

Coronary diameter was measured as the maximum diameter of the ectatic segment using a computerized quantitative coronary angiographic analysis system. CAE without coexisting atherosclerotic coronary arteries was defined as a coronary artery segment with a diameter of ≥1.5 times the adjacent normal coronary segment without any lesions.[5] Markis classification was used for classification of CAE,[6] this classification based on the extent of ectatic involvement in decreasing order of severity:

  1. Type I: diffuse ectasia of two or three vessels.
  2. Type II: diffuse disease in one vessel and localized disease in another vessel
  3. Type III: diffuse ectasia of one vessel only.
  4. Type IV: localized or segmental ectasia.


CAE with coexisting atherosclerotic coronary arteries disease patients were selected in a consecutive manner from the catheterized patients during the same study period and who had 50% or more stenosis at coronary angiograms associated with CAE. The control group was selected in a consecutive manner from the catheterized patients during the same study period and who proved to have normal coronary angiograms.


  Results Top


[Table 1] shows the comparison between the three groups regarding the hematological parameters.
Table 1: Comparison between three groups regarding to the hematological parameters

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Regarding to NLR, there is high statistical difference (P< 0.001) between the three groups, Group 1 is 2.94 ± 0.75 compared to Group 2 which is 2.64 ± 0.62 and control group is 2.11 ± 0.46.

Regarding to PLR, it was high in Group 1 (125.80 ± 17.60) and Group 2 (125.45 ± 12.93) when compared with control group (109.70 ± 17.28) with high statistical significant difference (P = 0.003).

Regarding to MPV, it was high in Group 1 (8.58 ± 0.40) and Group 2 (8.57 ± 0.27) when compared to control group (8.26 ± 0.37) with high statistical significant difference (P = 0.008).

Regarding to platelet distribution width (PDW), there is no high statistical significant difference between the groups (P = 0.540).

Regarding to Hs-CRP, it was high in Group 1 (3.27 ± 0.48) and Group 2 (3.16 ± 0.55) when compared with Group 3 (1.92 ± 0.44) with high statistical significant difference (P< 0.001).

[Table 2] shows the comparison between the three groups regarding the significant hematological parameters.

  • NLR – Regarding to NLR, we found that there is significant difference when we compared between both types of ectasia (Group 1, 2) and the control group (Group 3) P < 0.001 and P = 0.027 respectively, but there is no significant difference when we compared between the both types of ectasia (P = 0.413)
  • PLR – Regarding to PLR, we found that there was significant difference when we compared between both types of ectasia (Group 1, 2) and the control group (Group 3) P = 0.007 and P = 0.009 respectively, and there also significant difference when we compared between both types of ectasia (P< 0.001)
  • MPV – Regarding to MPV, we found that there was significant difference when we compared between both types of ectasia (Group 1, 2) and the control group (Group 3) P = 0.017 and P = 0.022 respectively. However, there is no significant difference when we compared between both types of ectasia (P = 1.00)
  • Hs-CRP – Regarding to Hs-CRP, we found that there was significant difference when we compared between both types of ectasia (group 1,2) and the control group (Group 3) P < 0.001 P < 0.001 respectively, but there was no significant difference when we compared between both types of ectasia (P = 1.00).


[Table 3] and [Figure 1] show that NLR with value ≥2.65 can detect CAE with sensitivity of 52.5% and specificity of 100% (95% confidence interval [CI], area under the curve [AUC] =0.778, P < 0.001).
Table 2: P value for pair-wise comparison between the three groups regarding to the significant hematological parameters

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Table 3: Receiver operating characteristic analysis for detecting of coronary artery ectasia

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Figure 1: Receiver operating characteristic curve of neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, mean platelet volume, and high-sensitivity C-reactive protein to detect coronary artery ectasia

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PLR with value ≥110.5 can detect CAE with sensitivity of 82.5% and specificity of 60% (95% CI, AUC = 0.756, P < 001).

MPV with value ≥8.25 can detect CAE with sensitivity of 72.5% and specificity of 55% (95% CI, AUC = 0.575, P = 0.007).

Hs-CRP with value ≥2.35 can detect CAE with sensitivity of 95% and specificity of 85% (95% CI, AUC = 0.944, P < 0.001).

[Table 4] and [Figure 2] show that the combination between NLR and PLR can detect CAE with sensitivity 82.5% and specificity 60% (95% CI, AUC = 0.759, P = 0.001).
Table 4: Receiver operating characteristic analysis of combination factors for detecting of coronary artery ectasia

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Figure 2: Receiver operating characteristic curve show combination factors between significant factors to detect coronary artery ectasia

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Combination between NLR and MPV can detect CAE with sensitivity 57.5% and specificity 85% (95% CI, AUC = 0.771, 0.759, P = 0.001).

Combination between NLR and Hs-CRP can CAE with sensitivity 77.5% and specificity 90% (95% CI, AUC = 0.908, P < 0.001).

Combination between MPV and PLR can CAE with sensitivity 82.5% and specificity 60% (95% CI, AUC = 0.757, P = 0.001).

Combination between Hs-CRP and PLR can detect CAE with sensitivity 87.5% and specificity 60% (95% CI, AUC = 0.765, P = 0.001).

Combination between Hs-CRP and MPV can CAE with sensitivity 90% and specificity 80% (95% CI, AUC = 0.924, P < 0.001).

[Table 5] shows the significant difference between the four types of CAE regarding NLR, PLR, MPV, and PDW.
Table 5: Comparison between different types of ectasia regarding to the hematological parameters

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[Table 6] shows significant negative correlation between hematological parameters (NLR, MPV, PDW, PLR, and Hs-CRP) with types of CAE to Markis classification that means positive correlation with severity of CAE.
Table 6: Univariate correlation between coronary artery ectasia types and hematological factors

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In [Table 7] by entering NLR, PLR, Hs-CRP, and MPV in multivariate regression model, we found that the only significant predictor of CAE in a stable model is Hs-CRP that can be used as an independent predictor of CAE (P< 0.001, odds ratio = 1.509, 95% CI between 1.218 and 1.869).
Table 7: Multivariate logistic regression to detect independent predictors of coronary artery ectasia

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  Discussion Top


CAE can be found in up to 5% of angiographic and in 0.22%–1.4% of postmortem examinations.

[7] In majority of cases, the disease coexists with coronary artery disease (CAD). As a consequence of the presence of immobile or turbulent blood flow in the aneurysmal segment, the repeated dissemination of microemboli to distal segments of the ectasia or a thrombotic occlusion (angina pectoris and myocardial infarction) has been seen in such patients.[8]

Hematological parameters

Neutrophil-to-lymphocyte ratio

Regarding to NLR in our study, we found that there was a significant difference when we compared between both types of CAE (isolated CAE and atherosclerotic CAE) and the control group (normal coronary arteries), but there is no significant difference when we compared between isolated CAE and atherosclerotic CAE, also we found by the receiver operating characteristic (ROC) curve that a NLR at a level 2.65 measured on admission had 52.5 sensitivity and 95% specificity in predicting CAE, and the combination between NLR and PLR can predict CAE with sensitivity 82.5% and specificity 60% (95% CI, AUC = 0.759, P = 0.001) and the combination between NLR and MPV can predict CAE with sensitivity 57.5% and specificity 85% (95% CI, AUC = 0.771, P = 0.001) and the combination between NLR and Hs-CRP can predict CAE with sensitivity 77.5% and specificity 90% (95% CI, AUC = 0.908, P < 0.001), we also investigated the presence of associations between NLR and severity of ectasia (according to Markis classification), the present study shows significant association between NLR and types of CAE, as there is significant negative correlation between NLR and types of CAE (R = −0.618, P ≤ 0.001).

This was in agreement with Yalcin et al. in 2014 who studied 198 patients who had undergone coronary angiography for suspected coronary artery disease and founded that there is a significant correlation between CAE and NLR.[9]

Inflammation has been shown to be an important pathogenic insulting factor for various cardiovascular diseases including coronary heart disease. In this regard, NLR has been shown to be closely related to numerous inflammatory diseases including some cardiovascular diseases. For example, Kaya et al. in 2014 found that NLR was closely related to the severity of atherosclerosis. Severe atherosclerosis was accompanying with higher levels of NLR.[10]

Increased WBC count is a simple and useful parameter which was found to be an independent risk factor for major cardiovascular diseases. It was also reported to be associated with the severity of coronary artery lesions.[11]

Recently, there has been a focus on white blood cell subtypes such as neutrophil, lymphocyte, and NLR as the predictors of cardiovascular risk. NLR may be more preferable in this manner owing to two factors:First, although some conditions such as exercise and dehydration may increase the absolute number of neutrophils and lymphocytes, NLR is less commonly affected and second, and more importantly, it is a ratio calculated from the counts of products of two different but complementary immune pathways, Neutrophils are effective in ongoing active nonspecific inflammation through the secretion of various inflammatory enzymes and mediators including elastase, myeloperoxidase, and free oxygen radicals. In contrast to the phagocytic and killing effects of neutrophils, lymphocytes fulfill the regulatory function of the immune system.[12]

Increased neutrophil count was found to be associated with infarct size and adverse angiographic outcomes in patients with myocardial infarction while low lymphocyte count was related to adverse outcomes in patients with myocardial infarction and chronic heart failure. Since NLR reflects both immune pathways and is probably less affected by confounding conditions, it may be more predictive than either parameter alone.[13]

Sarli et al. in 2013 showed that NLR was higher in patients with isolated CAE and in patients with CAD than in patients with normal coronary angiography. In addition, it was demonstrated in the same study that NLR was associated with severity of CAE according to Markis classification.

[14]

Balta et al. in 2013 investigated the role of NLR in 181 patients that were divided into three groups; they found that NLR was significantly higher in both CAE and CAD groups compared to the normal coronary angiography group.[15]

Işık et al. in 2013 indicated that NLR level 2.37 measured on admission had 77% sensitivity and 63% specificity in predicting isolated CAE.[16]

In practice, CAE frequently coexists with severe atherosclerosis. Some recent publications have looked at the relationship between isolated CAE and NLR.

However, the relationship between NLR and CAE with coexisting CAD has not been extensively studied. Here, we showed that patients with isolated CAE had significantly higher NLR values than patients with normal coronary angiography. We also demonstrated that patients having CAE with CAD had higher NLR values than patients with normal coronary angiography, Elevated neutrophil counts and NLR values in CAD and CAE may mirror severity of inflammation in coronary arteries. Thus, this study provided strong evidence for the role of inflammation in CAE.

Platelet-to-lymphocyte ratio

In our study, regarding to PLR, we found that there was significant difference when we compared both types of CAE (isolated CAE, atherosclerotic CAE) and the control group (normal coronary arteries) P = 0.007 and P = 0.009, respectively, and there is also significant difference when we compared isolated CAE and atherosclerotic CAE (P = 1.00), we also found by the ROC curve that; PLR at a level 110.5 measured on admission had 82.5% sensitivity and 60% specificity in predicting CAE, combination between PLR and MPV had sensitivity 82.5% and specificity 60% in predicting CAE, combination between PLR and Hs-CRP had sensitivity 87.5% and specificity 60% in predicting CAE, finally combination between PLR and NLR had sensitivity 82.5% and specificity 60% in predicting CAE, we also found the presence of an associations between PLR and severity of ectasia (according to Markis classification), and the presence of significant association between PLR and types of CAE, as there is significant negative correlation between PLR and types of CAE (R = −0.605, P ≤ 0.001).

Kundi et al. in 2016 who studied 330 patients who had undergone coronary angiography for suspected coronary artery disease had found that PLR was significantly higher in patients with isolated CAE than in those with normal coronary angiography and CAD.[17]

Harun et al. in 2016 indicated that PLR level 96 measured on admission had 69% sensitivity and 65% specificity in predicting isolated CAE.[17]

PLR is a new prognostic marker that integrates the risk prediction of these two parameters (platelets and lymphocytes) into one (PLR). It gives an idea about both the aggregation and inflammation pathways, and it may be more valuable than either platelet or lymphocyte count alone in the prediction of coronary atherosclerotic burden.[18]

In fact, PLR gives information about both aggregation and inflammatory pathways. PLR can be superior to the platelet or lymphocyte counts alone for prediction of isolated CAE, since both inflammation and endothelial damage play a role in the pathogenesis of CAE.[19]

Mean platelet volume

Regarding to MPV, in our study, we found that there was significant difference when we compared both types of CAE (isolated CAE and atherosclerotic CAE) and the control group (normal coronary arteries), but there is no significant difference when we compared isolated CAE and atherosclerotic CAE. Furthermore, we found by the ROC curve that a MPV at a level 8.25 measured on admission had 72.5% sensitivity and 55% specificity in predicting CAE and the combination between Hs-CRP and MPV can predict CAE with sensitivity 90% and specificity 85% (95% CI, AUC = 0.924, P < 0.001) and the combination between MPV and PLR can predict CAE with sensitivity 82.5% and specificity 60% (95% CI, AUC = 0.757, P = 0.001) and the combination between NLR and MPV can predict CAE with sensitivity 57.5% and specificity 85% (95% CI, AUC = 0.771, P = 0.001), we also investigated the presence of associations between MPV and severity of ectasia (according to Markis classification), we found significant association between MPV and types of CAE, as there is significant negative correlation between PLR and types of CAE (R = −0.614, P ≤ 0.001).

This was in agreement with Demir et al. in 2013 who studied on 374 patients who had undergone coronary angiography for suspected coronary artery disease and had founded that MPV was significantly higher in patients with CAE and CAD than in normal coronary angiography group.[20]

Large platelets contain denser granule, express more adhesion molecules, produce more thromboxane, and have more thrombotic potential than smaller platelets, MPV is a simple marker that reflects platelet size and activity.[21]

In the study of Sen et al. in 2007, MPV was greater in 67 patients with CAE than in a control group. In this study, MPV was greater in CAE patients.[22]

Varol et al. in 2009 evaluated MPV in CAE. MPV was again greater in patients with CAE.[23]

Increased platelet activity is associated with increased MPV. Large platelets that contain more dense granules are metabolically and enzymatically more active than small platelets and have higher thrombotic potential.[24]

Patients with CAE had a greater MPV than those with normal coronary arteries but not greater than those with CAD. The increase in platelet volume parallels the increase of metabolic and enzymatic activity, including increased thromboxane A2 and B2 activity per volume and glycoprotein IIb–IIIa expression. These platelets have an increased response to ADP and decreased response to prostacyclin aggregation. Wide platelets are dense and alpha granules such as platelet factor-4, P-selectin, and platelet-derived growth factor, which contribute chemotactic and vascular neointimal proliferation as mitogenic factors, are larger than in normal platelets. These factors affect cell adhesion, aggregation, and thrombosis via inflammation and endothelial function.[25]

High-sensitivity C-reactive proteins

Regarding to Hs-CRP, when we compared both types of CAE (isolated CAE and atherosclerotic CAE) and the control group (normal coronary arteries) we found significant difference but there is no significant difference when we compared isolated CAE and atherosclerotic CAE, also we found by the ROC curve that a Hs-CRP at a level 2.35 measured on admission had 95% sensitivity and 85% specificity in predicting CAE, combination between Hs-CRP and NLR can predict CAE with sensitivity 77.5% and specificity 90%, combination between Hs-CRP and MPV can predict CAE with sensitivity 90% and specificity 85%, combination between Hs-CRP and PLR can predict CAE with sensitivity 87.5% and specificity 60%, we also investigated the associations between Hs-CRP and severity of ectasia (according to Markis classification) and we found significant association between Hs-CRP and types of CAE, as there is significant negative correlation between Hs-CRP and types of CAE (R = −0.686, P ≤ 0.001), also In our study, by entering NLR, PL.

This was in agreement with Demir et al. in 2014 who studied on 213 patients who had undergone coronary angiography for suspected CAD and had founded that high sensitive CRP was significantly higher in patients with CAE and CAD than in normal coronary angiography group, and also there is significant correlation between Hs-CRP and severity of CAE.[20]

On contrary with Veselka et al. in 2002 who reported that the CRP level was not related to the extent of coronary atherosclerosis assessed by coronary angiography, a history of MI or stable angina, in patients referred for coronary angiography, or abnormal exercise test results, this difference can be explained using Hs-CRP in our study not CRP in the this study.[26]

Hunt et al. in 2001 confirmed by electron beam computed tomography that of those generally known risk factors of atherosclerosis, only low-density lipoprotein–cholesterol, and not CRP, was related to the extent of coronary calcifications.[27]

It, therefore, seems that the purported relationship between inflammatory biomarkers and the appearance or progression of coronary atherosclerosis might be spurious, possibly due to small-sample-size studies, methodology, or technical details for measuring these markers, and lack of controls without CAD. Thus, this association should be reevaluated in further prospective cohort studies with larger sample sizes, and preferably in CAD patients and suitable controls.

Acute-phase proteins are a class of proteins whose serum concentrations increase (positive acute-phase proteins) in response to inflammation. CRP is the first positive acute-phase protein being described and a sensitive systemic marker of the inflammation.[28]

That's why all patients with inflammatory diseases were excluded from our study for Hs-CRP to be valid as a marker for atherosclerotic process.

There is increasing evidence pointing to the role of inflammation in every phase of atherosclerosis. The inflammatory protein Hs-CRP directly contributes to the atherosclerotic process. Conversely, increased atherosclerotic burden increases the Hs-CRP levels. Hs-CRP is stored within the intima of the early atherosclerotic lesions, and it is chemotactic for the monocytes.[29]

Although the underlying inflammatory mechanisms in coronary artery disease are well known, the role of inflammation in the pathogenesis of isolated CAE are yet to be cleared. The postmortem histopathological results obtained from the histopathological studies conducted for this purpose have demonstrated that the vascular inflammation in patients with CAE is more large scale and severe than in coronary artery disease. This condition probably involves all the vascular layers along the coronary circulation and plays a role in the pathogenesis of CAE. In Demir et al. in 2014, Hs-CRP levels in patients with CAE and CAD were higher in comparison to individuals with normal coronary arteries.[20]

Study limitations

  • The main limitation of our study is the relatively small sample size
  • Another limitation is that there is no evaluation of the prognostic value of laboratory parameters in patients with CAE
  • We only studied patients prospectively, and it would have been better if we had followed the patients to further discover the association of these parameters with adverse cardiac events
  • Usage of a single blood sample will not predict the persistence of laboratory parameters over time. Patients' being hypotensive during the procedure might lead to a wrong diagnosis of CAE
  • A further limitation is evaluation of coronary angiography visually and calculating the vessel diameter quantitatively with quantitative coronary angiography in case of any conflict for CAE. We did not employ intravascular ultrasound or optical coherence tomography.


Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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    Figures

  [Figure 1], [Figure 2]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]



 

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