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 Table of Contents  
ORIGINAL ARTICLE
Year : 2022  |  Volume : 8  |  Issue : 2  |  Page : 96-101

Clinical and angiographic characteristics of coronary artery ectasia and its correlation with high-sensitivity c-reactive protein and serum uric acid


Department of Cardiology, Osmania General Hospital, Hyderabad, Telangana, India

Date of Submission02-Jun-2022
Date of Decision23-Jun-2022
Date of Acceptance01-Jul-2022
Date of Web Publication19-Aug-2022

Correspondence Address:
Krishna Mala Konda Reddy Parvathareddy
Department of Cardiology, Osmania General Hospital, Hyderabad - 500 012, Telangana
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jpcs.jpcs_24_22

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  Abstract 


Introduction: The most plausible factor for coronary artery ectasia (CAE), a subset of coronary artery disease (CAD), is extensive inflammation. High-sensitivity C-reactive protein (hs-CRP) and serum uric acid (sUA) are well known markers of inflammation. Most of the previous studies (done in the Western population and of Middle East Asia) evaluated their role individually as a marker of inflammation in CAD. We aimed to investigate the possible association of isolated CAE with inflammation as assessed by the hs-CRP and sUA levels and check whether the inflammatory hypothesis holds good in the south Asian population. Materials and Methods: Patients admitted for coronary angiography with age ≥30 years were evaluated. Patients with both CAE and CAD were excluded. A total of 60 patients were studied. Patients with isolated CAE (30) were compared with an equal number of patients with obstructive CAD (30) and their clinical profile was studied. The hs-CRP, sUA, and novel inflammatory markers such as neutrophil–lymphocyte ratio (NLR), mean platelet volume (MPV), and red cell distribution width (RDW) were compared between the groups. Results: Of the 60 patients studied, males were 56% in the isolated CAE group and 50% in the obstructive CAD group. The hs-CRP (2.39 ± 0.41 vs. 1.41 ± 0.29, P < 0.001) and sUA levels (6.46 ± 0.58 vs. 5.36 ± 0.40, P < 0.001) were significantly elevated in the isolated CAE group compared to the obstructive CAD group. Among the novel inflammatory markers, the NLR (3.98 ± 0.42 vs. 2.91 ± 0.30, P < 0.001) and RDW (12.69 ± 0.27 vs. 12.13 ± 0.48, P < 0.001) were significantly higher in the CAE group compared to obstructive CAD group, whereas the MPV did not have a statistically significant difference (9.5 ± 0.98 vs. 9.6 ± 1.08, P = 0.525). Conclusion: The inflammatory etiology of CAE was supported by an elevated hs-CRP, sUA, and other novel inflammatory markers compared to the atherosclerotic obstructive CAD group.

Keywords: Coronary artery disease, coronary artery ectasia, high-sensitivity C-reactive protein, red blood cell distribution width, serum uric acid


How to cite this article:
Parvathareddy KM, Maale SR, Nagula P, Ravi S, Rayapu MR, Balla NV. Clinical and angiographic characteristics of coronary artery ectasia and its correlation with high-sensitivity c-reactive protein and serum uric acid. J Pract Cardiovasc Sci 2022;8:96-101

How to cite this URL:
Parvathareddy KM, Maale SR, Nagula P, Ravi S, Rayapu MR, Balla NV. Clinical and angiographic characteristics of coronary artery ectasia and its correlation with high-sensitivity c-reactive protein and serum uric acid. J Pract Cardiovasc Sci [serial online] 2022 [cited 2022 Oct 5];8:96-101. Available from: https://www.j-pcs.org/text.asp?2022/8/2/96/354131




  Introduction Top


Coronary artery ectasia (CAE) has been defined as localized or diffuse nonobstructive lesions of one of the epicardial coronary arteries with a luminal dilatation exceeding the 1.5-fold of the normal adjacent segment or vessel diameter.[1],[2] It is divided into four anatomical phenotypes according to its extension in the coronary arterial tree as proposed by Markis et al.;[3] Type I is diffuse ectasia of two or three vessels, Type II is diffuse ectasia in one vessel and focal dilatation in another vessel, Type III is diffuse ectasia of one vessel only, and Type IV is focal aneurysm.[3]

CAE is a relatively uncommon finding on coronary angiography, with a prevalence ranging from 0.3% to 5%, as per the literature.[4],[5] Several reports suggest ectasia to be more predominant in males (1.7% vs. 0.2%).[6] Although there is diversity regarding the etiopathogenesis of CAE, atherosclerosis seems to be the most frequent cause in adults.[7],[8] This hypothesis is supported by its frequent coexistence with coronary artery disease (CAD) and observation of common histopathological findings, such as lipid deposition, hyalinization, destruction, and reduction of the medial elastic fibers along with the disruption of the internal and external elastic lamina like in the atheroslcerosis.[9],[10] The component of chronic inflammation is supported by the extensive arterial damage, dilatation, and elevated markers of inflammation.[11],[12]

High-sensitivity C-reactive protein (hs-CRP) and serum uric acid (sUA) are well-known markers of inflammation in CAD. In this study, we aimed to investigate the possible association of isolated CAE with inflammation by assessing the hs-CRP and sUA levels. Most of the previous studies evaluated the role of hs-CRP and sUA levels individually, but there are not many studies evaluating the role of inflammation using both hs-CRP and sUA. These studies were done in the Western population and middle east Asia, so we aimed to evaluate if those results hold true even in the south Asian population.


  Materials and Methods Top


Patients aged ≥30 years, admitted for coronary angiography in the Department of Cardiology, Osmania General Hospital, Hyderabad, during the study period (December 2019–August 2021) were taken up for study after obtaining patient consent. After the angiography, patients were divided into two groups (patients having CAE are taken as one group and patients having obstructive CAD are taken as another group).

Study sample

The sample was 30 patients in each group.

Exclusion criteria

Patients with combined CAE and obstructive CAD [Figure 1], iatrogenic CAE due to previous coronary interventions (percutaneous coronary intervention or coronary artery bypass grafting), CAE-associated cardiomyopathies, congenital heart disease, acute myocardial infarction, acute heart failure, valvular heart disease, conduction disturbances, gastrointestinal motility disorders, thyroid disorders, liver and renal impairment, autoimmune disease, sepsis, infections, malignancy, uncontrolled hypertension, and uncontrolled diabetes mellitus (DM) were excluded.
Figure 1: Coronary angiogram showing combined coronary artery ectasia and obstructive coronary artery disease in the right coronary artery.

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Methodology

Patients presenting with typical angina or positive noninvasive screening test (Treadmill test or dobutamine stress echocardiography) for myocardial ischemia were taken for study. The demographic profile of each patient was studied. Each patient was evaluated clinically, and details regarding the cardiovascular (CV) risk factors were studied. Blood samples were analyzed using standard laboratory assays for total counts, blood glucose levels, serum creatinine, blood urea, and lipid profile. Each patient underwent electrocardiography and 2D transthoracic echocardiography. After obtaining informed written consent, coronary angiography was done through either the right femoral artery or right radial artery approach under sterile aseptic precautions using either Judkins right and left coronary catheter or the Tiger catheter. Angiographic data were analyzed for the presence of coronary ectasia, distribution of ectasia, and the number of vessels involved. The coronary arteries were analyzed regarding the extent of the lesion by diameter stenosis and extent of disease along the vessels. Blood samples for hs-CRP and sUA were sent after 24 h of angiography. For hs CRP, antecubital vein without venous stasis was used for collection of the blood sample. The collected sample is taken into tube with no anticoagulant and was analyzed with nephelometric SIEMENS Dade-Behring BN II device.[13] For sUA, the collected blood sample was centrifuged at 3000 rpm for 10 min and kept at −70°C. The level was assessed by enzymatic colorimetric assay with a clinical chemistry autoanalyzer (Modular P, Roche Diagnostics, Germany Switzerland).[14]

Statistical methods

Data were recorded on a predesigned pro forma and managed using Microsoft Excel 2007 (Microsoft Corp, Redmond, USA). Continuous variables were reported as mean ± standard deviation, median interquartile range. Categorical variables were reported as percentages. Chi-square test was done for comparison of categorical variables. The P value was two-tailed, and a value <0.05 was considered statistically significant.


  Results Top


A total of 60 patients were studied. Each group (isolated CAE and obstructive CAD) consisted of 30 patients. The following results were noted.

The mean age of patients with CAE and obstructive CAD was equal (55 ± 7 and 55 ± 8 years, respectively) [Table 1]. Males were predominant in the obstructive CAD group (56% vs. 44%), whereas in the CAE group, the sex distribution was equal. The sex distribution when compared among the groups was not statistically significant.
Table 1: Baseline characteristics of both groups

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Of the CV risk factors, smoking was more common in the obstructive CAD group compared to the CAE group (43.3% vs. 26.7%, respectively), hypertension was seen in 50% of patients of obstructive CAD compared to 43.3% in the CAE group, and diabetes was seen in half of the patients in obstructive CAD group compared to one-third in CAE group.

Of the lipid parameters, serum triglycerides were significantly higher in the CAE group compared to the obstructive CAD group (162 vs. 139 mg/dl; P = 0.026). Although the low-density lipoprotein (LDL) and high-density lipoprotein (HDL), cholesterol levels were higher in obstructive CAD compared to the CAE group, they were statistically insignificant.

Of the novel risk markers of inflammation, the neutrophil–lymphocyte ratio (NLR) was significantly elevated in the CAE group compared to obstructive CAD group (3.99 ± 0.42 vs. 2.91 ± 0.3; P = < 0.001). The mean platelet volume (MPV), a biochemical marker of platelet activation, the difference between the groups was not statistically significant (9.5 ± 0.98 vs. 9.6 ± 1.08; P = 0.525). The red cell distribution width (RDW) in patients with CAE is significantly elevated when compared with the obstructive CAD (12.69 ± 0.27 vs. 12.13 ± 0.48; P < 0.001) [Table 2]. The hs-CRP and sUA levels were higher among the patients with CAE compared to the obstructive CAD group, which was statistically significant (2.39 ± 0.41 vs. 1.41 ± 0.29 mg/L; P < 0.001) and (6.46 ± 0.58 vs. 5.36 ± 0.40 mg/dl P < 0.001), respectively [Table 3].
Table 2: Comparison of the novel risk markers of inflammation in both groups

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Table 3: Comparison of high-sensitivity C-reactive protein and serum uric acid levels in both groups

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The angiographic pattern of the ectatic segments was categorized according to the Markis et al.[3] classification. The most common pattern seen was Type 3 (33.33%, n = 10), and the least common pattern was Type 1 (15%) [Figure 2].
Figure 2: Distribution of ectasia according to Markis et al.[3] classification in the CAE group. CAE: Coronary artery ectasia.

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The ectatic segments were seen in at least two segments in the CAE group compared to the involvement of a single segment of stenosis in the obstructive CAD group (40% vs. 63.3% respectively [Table 4]. The most common involved artery in CAE is the right coronary artery (RCA) (46.1%), whereas, in the obstructive CAD group, it is LAD (42.5%) [Table 5].
Table 4: Comparison of the number of segments involved in both groups

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Table 5: Number of ectatic and stenotic segments in relation to involved arteries

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  Discussion Top


This study was an observational study to evaluate the clinical and angiographic characteristics of patients with CAE and its correlation with hs-CRP and sUA levels compared to obstructive CAD. The results showed significantly elevated hs-CRP and sUA levels in CAE compared to the obstructive CAD favoring the inflammatory hypothesis.

In our study, the mean age of the population in CAE and obstructive CAD was equal (55 ± 7 and 55 ± 8 years, respectively). The mean age of the ectasia group in most of the studies was 53–55 years, which is similar to the current study. The majority of our patients were in the 40–60 years of age group. According to most investigators, age did not seem to have any additional influence on the distribution of ectasia.[15]

In our study, the population with smoking history (current or past) are more among the CAD group than in the CAE group, although not statistically significant. It infers that smoking might have different effects in CAD and CAE. This finding of inverse correlation between smoking and CAE is similar as noted in other studies (Turhan et al.,[18] Tosu et al.,[19] Sanad et al.[20]).

Of the traditional CV risk factors, DM has a unique association with ectasia. Giannoglou et al.,[1] Williams MJ et al.,[21] Pinar Bermúdez et al.,[22] reported negative association between ectasia and DM. The meta-analysis by Huang et al.[23] concluded that DM has an inverse association with CAE and can act as a protective barrier for the manifestation of ectasia. Our observation showed the prevalence of diabetes to be lower in the CAE than in the CAD group, like in the meta analysis.[23]

As evident in the previous studies (Turhan et al.[18] and Sanad et al.[20]), dyslipidemia is more common among the CAD group compared to the CAE group. Although in our study, low HDL levels and high LDL levels were found in the CAD group, it was not statistically significant. However, mean triglyceride levels were higher in the CAD group compared to the CAE group, which was statistically significant.

At present, there is strong evidence for the relation between inflammation and CAE as demonstrated by inflammatory markers such as hs-CRP, NLR, MPV, and RDW. In agreement with the above statement, a similar observation of high NLR was noted in the CAE group compared to the CAD group. Elevated markers of neutrophil-mediated inflammation have already been demonstrated in the CAE population by Turhan et al.[18] and Li et al.[24] The MPV was found to be almost equal in both groups. An elevated MPV in the CAE group compared to normal controls was seen in a study by Sen et al.[26] The comparison of the hs-CRP levels between both groups in various studies is shown in [Table 6].
Table 6: Comparison of high-sensitivity C-reactive protein levels in both groups in various studies

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Similarly, elevated sUA levels were seen in the CAE group compared to the CAD group. The same observation was noted in Sen et al.[26]

The pathogenesis of CAE includes inflammation in the arterial wall and expansive remodeling by enzymatic degradation of the extracellular matrix by metalloproteinases and other lytic enzymes. Histopathological examination of the ectatic segment revealed atherosclerotic changes and thinner tunica media of the artery. Compared to the previous studies, we evaluated both hs-CRP, serum UA levels, and novel markers of inflammation in patients with CAE and compared them to the levels in patients with CAD [Table 7]. The inflammatory hypothesis seems to be most justifiable for the occurrence of CAE based on elevated inflammatory markers, as seen in our study.
Table 7: Comparison of the present study with previous studies

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On angiography, the ectatic segments were categorized according to Markis et al.[3] classification. The most common was Type III. It was similar to previous studies (Sanad et al.,[20] and Demir et al.[27])

We found that RCA was the most common vessel to be involved with ectasia [Figure 3] and LAD in the obstructive CAD group [Figure 4]. There was no involvement of the left main coronary artery in the CAE group. Similar findings with regard to CAE were noted in Sanad et al.[20] and Turhan et al.[18]
Figure 3: Coronary angiogram of a 56-year-old male presented with chronic stable angina showing coronary artery ectasia in the right coronary artery.

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Figure 4: Coronary angiogram of a 60-year-old female showing obstructive coronary artery disease with severe stenosis in the proximal left anterior descending artery and left circumflex artery.

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Limitations

The study population is less and is a single-center study. Other inflammatory markers like ICAM-1, E-selectin, MMPs, were not assessed. Healthy controls were not selected for comparison. Prognostic values of hs-CRP and sUA levels in CAE patients were not analyzed.


  Conclusion Top


Coronary artery ectasia (CAE), a subset of CAD, has inflammatory etiology supported by an elevated hs-CRP and sUA levels when compared to the atherosclerotic obstructive CAD. Large population studies are needed to confirm this causal association.

Ethics clearance

Institutional Ethics Committee has approved the study.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

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Giannoglou GD, Antoniadis AP, Chatzizisis YS, Damvopoulou E, Parcharidis GE, Louridas GE. Prevalence of ectasia in human coronary arteries in patients in northern Greece referred for coronary angiography. Am J Cardiol 2006;98:314-8.  Back to cited text no. 1
    
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Doi T, Kataoka Y, Noguchi T, Shibata T, Nakashima T, Kawakami S, et al. Coronary artery ectasia predicts future cardiac events in patients with acute myocardial infarction. Arterioscler Thromb Vasc Biol 2017;37:2350-5.  Back to cited text no. 5
    
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Richards GH, Hong KL, Henein MY, Hanratty C, Boles U. Coronary artery ectasia: Review of the non-atherosclerotic molecular and pathophysiologic concepts. Int J Mol Sci 2022;23:5195.  Back to cited text no. 8
    
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Dereli S, Çerik İB, Kaya A, Bektaş O. Assessment of the relationship between C-reactive protein-to-albumin ratio and the presence and severity of isolated coronary artery ectasia. Angiology 2020;71:840-6.  Back to cited text no. 12
    
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Ozbay Y, Akbulut M, Balin M, Kayancicek H, Baydas A, Korkmaz H. The level of hs-CRP in coronary artery ectasia and its response to statin and angiotensin-converting enzyme inhibitor treatment. Mediators Inflamm 2007;2007:89649.  Back to cited text no. 17
    
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Tosu AR, Yurtdaş M, Özdemir M, Selçuk M, Aladağ N, Ceylan Y, et al. Evaluation of the Serum Levels of Uric Acid and C-reactive Protein in Isolated Coronary Artery Ectasia. Koşuyolu Heart Journal 2014;17:105-9.  Back to cited text no. 19
    
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Sanad O, Al-Keshk E, Ramzy A, Tabl MA, Bendary A. Characteristics of coronary artery ectasia and its association with carotid intima-media thickness and high sensitivity C-reactive protein. Int J Cardiol Cardiovasc Res 2016;3:24-30.  Back to cited text no. 20
    
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Pinar Bermúdez E, López Palop R, Lozano Martínez-Luengas I, Cortés Sánchez R, Carrillo Sáez P, Rodríguez Carreras R, et al. Coronary ectasia: Prevalence, and clinical and angiographic characteristics. Rev Esp Cardiol 2003;56:473-9.  Back to cited text no. 22
    
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Huang QJ, Zhang Y, Li XL, Li S, Guo YL, Zhu CG, et al. Clinical features of coronary artery ectasia in the elderly. J Geriatr Cardiol 2014;11:185-91.  Back to cited text no. 23
    
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Ammar W, Kappary M, Baghdady Y, Shehata M. Matrix metalloproteinase-9 (MMP9) and high sensitivity C-reactive protein (hs-CRP) in coronary artery ectasia. Egypt Heart J 2013;65:289-93.  Back to cited text no. 25
    
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Sen N, Tavil Y, Yazici HU, Hizal F, Açikgöz SK, Abaci A, et al. Mean platelet volume in patients with coronary artery ectasia. Med Sci Monit 2007;13:CR356-9.  Back to cited text no. 26
    
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Demir M, Demir C, Keçeoğlu S. The relationship between vitamin D deficiency and coronary artery ectasia. Postepy Kardiol Interwencyjnej 2014;10:238-41.  Back to cited text no. 27
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]
 
 
    Tables

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



 

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