|Year : 2019 | Volume
| Issue : 1 | Page : 72-76
Prevalence and clinical profile of angiographic coronary artery ectasia among North Indian population
Rasheed Ahmed1, Gaurav Khandelwal2, Agam Bansal2, Anoop Jain3, Krati Khandelwal4, Rohit Singla3
1 Department of Cardiology, Heart and General Hospital, Jaipur, Rajasthan, India
2 Department of Cardiology, AIIMS, Bhopal, Madhya Pradesh, India
3 Department of Cardiology, SMS, Jaipur, Rajasthan, India
4 Department of Cardiology, Santokba Durlabhji Memorial Hospital, Jaipur, Rajasthan, India
|Date of Web Publication||4-Feb-2019|
23 New MLA Colony, Jawahar Chowk, Bhopal - 462 003, Madhya Pradesh
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Background: Coronary artery ectasia (CAE) has been widely recognized as not so infrequent form of coronary artery disease. Few retrospective studies from the Indian subcontinent have reported its prevalence to be varying from 1.9% to 10%. No large-scale study has been done among North Indian population. Methods: A prospective analysis of all coronary angiograms performed at our catheterization laboratory, between June 2012 and February 2014, was done. CAE was defined and classified according to the Markis classification. For every patient included, epidemiological, clinical, and appropriate laboratory data were obtained. Results: One hundred and twenty-four out of 3,014 coronary angiograms (4.1%) showed CAE. Mean age of the study population was 55.5 years. About 86.3% were male, 50.8% were current smokers, 27.4% had hypertension, 16.1% had diabetes mellitus, and 32.3% had dyslipidemia. The most common clinical presentation was ST-segment elevation myocardial infarction, observed in 44.4% of cases. Right coronary artery (RCA) was the most frequent coronary artery to be involved. Markis Class 3 was the most frequent pattern of CAE observed. Conclusion: The prevalence of coronary ectasia among North Indian patients undergoing coronary angiography was 4.1%. Of them, 16.9% angiograms showed isolated CAE. RCA was the most common affected vessel (58.1%). Large-sized studies to delineate treatment for this common entity are needed.
Keywords: Angiography, coronary artery ectasia, North India
|How to cite this article:|
Ahmed R, Khandelwal G, Bansal A, Jain A, Khandelwal K, Singla R. Prevalence and clinical profile of angiographic coronary artery ectasia among North Indian population. J Nat Sc Biol Med 2019;10:72-6
|How to cite this URL:|
Ahmed R, Khandelwal G, Bansal A, Jain A, Khandelwal K, Singla R. Prevalence and clinical profile of angiographic coronary artery ectasia among North Indian population. J Nat Sc Biol Med [serial online] 2019 [cited 2020 Dec 5];10:72-6. Available from: http://www.jnsbm.org/text.asp?2019/10/1/72/251510
| Introduction|| |
Coronary artery ectasia (CAE) was first described by Morgagni in 1761. Since then, it has been widely recognized as not so infrequent form of coronary artery disease (CAD). This pathological entity is defined as dilatation of a part or whole of the coronary artery 1.5 times or more the diameter of an adjacent normal segment. It is commonly associated with atherosclerotic CAD. Occasionally, it has been seen with other pathological entities such as syphilitic aortitis, connective tissue disorders such as scleroderma, Ehlers–Danlos syndrome, and Polyarteritis Nodosa, bacterial infections, and Kawasaki disease. In a small percentage of patients, CAE can be congenital in origin. Its exact pathophysiology and natural history still remains an enigma. Till date, it continues to baffle the clinicians regarding its cause, clinical sequelae, and appropriate treatment.
With the widespread use of coronary angiography worldwide, the incidence of CAE in patients undergoing this diagnostic procedure has been studied across the globe.,,,,, These studies have found its incidence varying from 1% to 5%. Few studies have also been done from the Indian subcontinent,,,, all retrospective in nature. The incidence of CAE in an Indian patient cohort with ischemic heart disease was observed to exceed 10%, following a post hoc analysis. In another recent study done in South India, the incidence of CAE without concomitant CAD was shown to be 1.9%. Besides, one more study from South India showed prevalence of CAE to be 4.5%, with 85% of these having coexistent CAD. The exact incidence of CAE in the general population may be overestimated by these studies as it is much less likely to be discovered in patients without symptomatic CAD. The present study was done to prospectively evaluate the incidence of CAE in North Indian patients undergoing coronary angiogram for various reasons since no large-scale study from North India is available. We simultaneously tried to correlate various patient and angiographic characteristics with CAE.
| Methods|| |
A prospective analysis was conducted on all coronary angiograms performed at the catheterization laboratory of Sawai Man Singh Medical College and Hospital, Jaipur (Rajasthan), which is one of the largest government tertiary care centers of North India, between June 2012 and February 2014. A total of 3,014 coronary angiograms were evaluated. These angiograms were done in patients with suspected or known CAD and to rule out CAD in patients with valvular/congenital heart disease. Angiographic assessment was done by visual and quantitative methods. The definition of CAE employed was that used in the Coronary Artery Surgery Study (CASS), where a vessel was considered ectatic when its luminal diameter exceeded 1.5-fold the adjacent normal segment. Ectasia was classified according to the Markis classification – Type I: diffuse ectasia in two or three vessels, Type II: diffuse ectasia in one vessel and localized disease (i.e., aneurysm) in another, Type III: diffuse ectasia in only one vessel, and Type IV: coronary aneurysm in one vessel.
For every patient included, epidemiological, clinical parameters and appropriate investigations such as electrocardiogram, echocardiography, and lipid profile were obtained. Dyslipidemia was defined as the presence of either of the four parameters: (1) total cholesterol >200 mg/dl, (2) low-density lipoprotein (LDL) cholesterol >130 mg/dl, (3) high-density lipoprotein (HDL) cholesterol <40 mg/dl for males and <50 mg/dl for females, and (4) triglyceride >150 mg/dl. Patients were not evaluated further for various cardiovascular complications following hospital discharge.
Continuous variables are expressed as mean ± standard deviation and categorical variables as percentages.
| Results|| |
During the study period, 3,014 coronary angiograms were performed. One hundred and twenty-four coronary angiograms (4.1%) showed CAE [Figure 1] and [Figure 2]. Demographic data of the patients are depicted in [Table 1]. Mean age of the study population was 55.5 ± 10.9 years. Among them, 107 (86.3%) were male, 63 (50.8%) were current smokers, 34 (27.4%) had hypertension, 20 (16.1%) had diabetes mellitus, and 40 (32.3%) had dyslipidemia with elevated serum LDL and triglycerides and low HDL levels and 15 (12.1%) had positive family history of CAD.
|Figure 1: Coronary angiogram showing diffuse ectasia in the right coronary artery|
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|Figure 2: Coronary angiogram showing localized aneurysm in the left anterior descending coronary artery|
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Clinical presentation of CAE patients [Table 2] was anterior wall ST-segment elevation myocardial infarction (STEMI) in 38 (30.7%), non-ST-segment elevation ACS in 32 (25.8%), chronic stable angina pectoris (CSAP) in 29 (23.4%), inferior wall STEMI in 17 (13.7%), atypical angina in 5 (4%), and valvular heart disease in 3 (2.4%) of cases.
Twenty-one (16.9%) angiograms showed isolated CAE with no coronary obstructive lesions. In another Indian study reviewing 4,950 coronary angiograms, 270 patients were found to have coronary ectasia (5.45%). Of them, 52 patients had isolated coronary ectasia (19.19%).
Overall, the right coronary artery (RCA) was the most common affected vessel (58.1%), followed by the left circumflex coronary artery (LCX) in 40.3% and the left anterior descending coronary artery (LAD) in 37.9% of the patients. Considering the distribution of ectasia versus aneurysm among the three coronary arteries [Figure 3], aneurysm was seen predominantly in LAD artery (56.5%), whereas ectasia was commonly seen in RCA 57 (53.3%), followed by LCX 38 (35.5%) and LAD 12 (11.2%). [Figure 4] shows the distribution of these CAE patients according to the Markis classification. Markis Class III was the most frequent in this study cohort.
|Figure 3: Distribution of diffuse ectasia (n = 107) versus aneurysm (n = 62) among the three coronary arteries|
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|Figure 4: Distribution of the 124 coronary artery ectasia patients according to the Markis classification|
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| Discussion|| |
CAE is defined as local or generalized aneurysmal dilatation of the coronary arteries and likely represents an exaggerated form of expansive vascular remodeling. The majority of CAEs are strongly associated with local and systemic atherosclerosis, and it has been observed commonly in response to atherosclerotic plaque growth., Enzymatic degradation of the extracellular matrix of the media is the major pathophysiologic process that leads to ectasia.
The prevalence of CAE has been widely studied in different regions of the world. Studies from South India show its angiographic prevalence to be around 4.5% and prevalence of pure CAE without CAD to be 1.9%. A small study from North India, in a post hoc analysis, revealed the prevalence of CAE in patients of ischemic heart disease to be around 10%. A recent Northeast Indian study found the angiographic prevalence of CAE to be about 5.45% and isolated coronary ectasia to be 1.05%. This is the first large study in North India which has prospectively tried to evaluate the prevalence of CAE in patients undergoing coronary angiography for various reasons. We found prevalence of CAE to be 4.1% in 3,014 consecutive coronary angiographies.
CAE in previous studies has shown to have a predilection for RCA,,, except one study. The same trend was also observed in the present study, with 58.1% of CAE patients having evidence of dilatation of RCA. Why RCA is predisposed to CAE, as opposed to other coronary arteries, is an unanswered question. Atherosclerotic disease, which has been correlated with CAE, may affect any of the coronaries with no special predilection for RCA. Hence, some other yet unidentified factor may be responsible for this observation. Besides, CAE may involve more than one coronary artery. Twenty-nine percent of patients in this study had multivessel CAE, as seen in other studies also.
Overall, CAE was most frequent in RCA. However, localized aneurysm formation rather than diffuse ectasia was seen predominantly in LAD in this study. The same pattern was observed in a recent study from South India. However, another study from Pakistan revealed contrary findings, in which both diffuse ectasia and focal disease were more common in RCA. Since patient population was single centered, the data on different countries could be different due to genetic and environmental differences on atherosclerosis.
Increased prevalence of ectasia and aneurysmal disease in familial hypercholesterolemia (FH) suggests a link between plasma lipoproteins and coronary aneurysms. The prevalence of CAE in FH was proposed as structural weakening or active lysis of connective tissue elements in the arterial wall resulting from interaction with LDL cholesterol. In this study, 40 (32.3%) patients had dyslipidemia. This figure is comparable with other studies in the Indian subcontinent.,
Diabetes mellitus has been reported to be independently but inversely associated with CAE. In this study, 16% of patients had diabetes mellitus. Background prevalence of diabetes mellitus in North India is roughly similar. Hence, the presence of diabetes does not represent a strong risk factor for the development of CAE.
In the present study, 27.4% of patients with CAE suffered from hypertension and 50% were current smokers. These risk factors for CAD have been shown to be associated with CAE in other studies also.,,, Histopathological studies could have delineated to a better degree the prevalence of CAE derive from each etiologic factor. Possibly, in most cases, overlapping etiologic factors result in the development of CAE.
Studies have shown that the clinical spectrum of CAE is variable, including stable angina pectoris, unstable angina, and myocardial infarction. Few CAE patients may develop it in the absence of CAD. It has also been linked with various connective tissue disorders. The most common clinical presentation in this study was STEMI (44.4%). Other studies from Indian subcontinent have shown CSAP as predominant clinical syndrome., Association with STEMI appears coherent in lieu of tendency for thrombosis in ectatic vessels with sluggish blood flow and associated local atherosclerotic changes.
The treatment of CAE is controversial. Some authors recommended long-term anticoagulation therapy while others recommended only antiplatelet therapy with aspirin in asymptomatic individuals. Role of nitrates or calcium channel blockers for angina is controversial. Considering the strong association of dyslipidemia and atherosclerosis with CAE, the use of lipid-lowering agents may be beneficial to this group of patients. Some authors advocate IVUS for correct assessment of percentage diameter stenosis and differentiation of true from false aneurysms. A recent study found medical, percutaneous coronary intervention, and coronary artery bypass grafting equally effective for ectasias.
There have been very limited data regarding revascularization of stenotic ectatic coronary arteries. Drug-eluting balloon-expandable stents are often used wherever possible. Self-expanding stents (SESs) permit to obtain a complete apposition of stent struts by its constant gentle outward force. Newer generation SES STENTYS stent made from nitinol with nickel–titanium alloy self-expands and confirms to vessel lumen over time. The covered balloon-expandable Jostent has been shown to be an effective device for exclusion of coronary aneurysms. Due to the huge amount of thrombus, rheolytic coronary mechanical thrombectomy and aspiration thrombectomy may be beneficial in improving epicardial and myocardial reperfusion. In many cases, intracoronary thrombolysis or Group IIb/IIIa has shown good result in dealing with huge thrombus burden. In the symptomatic patient not suitable for stent insertion, surgical excision or ligation of the aneurysm with bypass graft of the affected coronary arteries may be the procedure of choice. Coronary artery aneurysm of at least three to four times, the size of the original vessel diameter is considered as an absolute indication for surgical intervention by many, because of the propensity for complications such as compression, rupture, or thrombosis.
The present study has some important limitations. Since we did not follow-up patients after hospital discharge, the natural history of these lesions cannot be discerned from the present study. It would be interesting to see if markers of increased atherosclerotic vascular damage such as carotid intima-media thickness and flow-mediated dilation of brachial artery are altered in this group of patients. Further, like other studies, this study cannot tell us about the exact prevalence of CAE in general population at large.
| Conclusion|| |
CAE was found to be present in 4.1% of patients out of 3,014 coronary angiograms, in this study of North Indian population. This agrees with the result of few other large-scale studies from Indian subcontinent,, and worldwide. It is one of the largest studies representing CAE incidence and pattern in patients undergoing angiography for various reasons. The prognosis of CAE is controversial and appropriate treatment debatable. Further work, especially prospective studies, delineating its natural history and management is needed.
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| References|| |
Lazzarin P, Pasero G, Marson P, Cecchetto A, Zanchin G. Takayasu's arteritis. A concise review and some observations on a putative case reported by Giovanni Battista Morgagni (1761) Reumatismo. 2005;57:305–313.
Manginas A, Cokkinos DV. Coronary artery ectasias: Imaging, functional assessment and clinical implications. Eur Heart J 2006;27:1026-31.
Swaye PS, Fisher LD, Litwin P, Vignola PA, Judkins MP, Kemp HG, et al.
Aneurysmal coronary artery disease. Circulation 1983;67:134-8.
Demopoulos VP, Olympios CD, Fakiolas CN, Pissimissis EG, Economides NM, Adamopoulou E, et al.
The natural history of aneurysmal coronary artery disease. Heart 1997;78:136-41.
Markis JE, Joffe CD, Cohn PF, Feen DJ, Herman MV, Gorlin R, et al.
Clinical significance of coronary arterial Ectasia. Am J Cardiol 1976;37:217-22.
Hartnell GG, Parnell BM, Pridie RB. Coronary artery ectasia. Its prevalence and clinical significance in 4993 patients. Br Heart J 1985;54:392-5.
Farto e Abreu P, Mesquita A, Silva JA, Seabra-Gomes R. Coronary artery ectasia: Clinical and angiographic characteristics and prognosis. Rev Port Cardiol 1993;12:305-10.
Aintablian A, Hamby RI, Hoffman I, Kramer RJ. Coronary ectasia: Incidence and results of coronary bypass surgery. Am Heart J 1978;96:309-15.
Sharma SN, Kaul U, Sharma S, Wasir HS, Manchanda SC, Bahl VK, et al.
Coronary arteriographic profile in young and old Indian patients with ischaemic heart disease: A comparative study. Indian Heart J 1990;42:365-9.
Nyamu P, Ajit MS, Joseph PK, Venkitachalam L, Sugirtham NA. The prevalence and clinical profile of angiographic coronary ectasia. Asian Cardiovasc Thorac Ann 2003;11:122-6.
Harikrishnan S, Sunder KR, Tharakan J, Titus T, Bhat A, Sivasankaran S, et al.
Coronary artery ectasia: Angiographic, clinical profile and follow-up. Indian Heart J 2000;52:547-53.
Sultana R, Sultana N, Ishaq M, Samad A. The prevalence and clinical profile of angiographic coronary ectasia. J Pak Med Assoc 2011;61:372-5.
Coronary Artery Surgery Study (CASS): A randomized trial of coronary artery bypass surgery. Survival data. Circulation 1983;68:939-50.
Malviya A, Jha PK, Mishra A. Isolated coronary artery ectasia: Clinical, angiographic, and follow up characteristics. Indian Heart J 2017;69:619-23.
Aksu T, Uygur B, Durukan Koşar M, Güray U, Arat N, Korkmaz S, et al.
Coronary artery ectasia: Its frequency and relationship with atherosclerotic risk factors in patients undergoing cardiac catheterization. Anadolu Kardiyol Derg 2011;11:280-4.
Antoniadis AP, Chatzizisis YS, Giannoglou GD. Pathogenetic mechanisms of coronary ectasia. Int J Cardiol 2008;130:335-43.
Li JJ, Li Z, Li J. Is any link between inflammation and coronary artery ectasia? Med Hypotheses 2007;69:678-83.
Androulakis AE, Andrikopoulos GK, Kartalis AN, Stougiannos PN, Katsaros AA, Syrogiannidis DN, et al.
Relation of coronary artery ectasia to diabetes mellitus. Am J Cardiol 2004;93:1165-7.
Mohan V, Sandeep S, Deepa R, Shah B, Varghese C. Epidemiology of type 2 diabetes: Indian scenario. Indian J Med Res 2007;125:217-30.
] [Full text]
Fukuhara S, Takase E, Fujimoto T, Takami Y, Yamamoto K, Nishida T, et al.
Coronary ectasia resulting in thrombotic coronary occlusion after warfarin interruption: A case report. J Cardiol 2005;46:195-200.
Sorrell VL, Davis MJ, Bove AA. Current knowledge and significance of coronary artery ectasia: A chronologic review of the literature, recommendations for treatment, possible etiologies, and future considerations. Clin Cardiol 1998;21:157-60.
Garrand TJ, Mintz GS, Popma JJ, Lewis SA, Vaughn NA, Leon MB, et al.
Intravascular ultrasound diagnosis of a coronary artery pseudoaneurysm following percutaneous transluminal coronary angioplasty. Am Heart J 1993;125:880-2.
Vasu N, Narayanan S, Ajit MS. Clinical outcome of various management strategies in coronary artery ectasia. Indian Heart J 2017;69:319-21.
Moretti C, Omedè P, Presutti DG, D'Ascenzo F, De Simone V, Colaci C, et al.
Shaping an ectatic coronary artery: Stentys implantation. Int J Cardiol 2014;171:459-61.
Szalat A, Durst R, Cohen A, Lotan C. Use of polytetrafluoroethylene-covered stent for treatment of coronary artery aneurysm. Catheter Cardiovasc Interv 2005;66:203-8.
[Figure 1], [Figure 2], [Figure 3], [Figure 4]
[Table 1], [Table 2]