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European Heart Journal Advance Access originally published online on January 16, 2006
European Heart Journal 2006 27(9):1026-1031; doi:10.1093/eurheartj/ehi725
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© The European Society of Cardiology 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Coronary artery ectasias: imaging, functional assessment and clinical implications

Athanassios Manginas* and Dennis V. Cokkinos

First Department of Cardiology, Onassis Cardiac Surgery Center, 356 Syngrou Avenue, Athens 17674, Greece

Received 22 September 2005; revised 1 December 2005; accepted 23 December 2005; online publish-ahead-of-print 16 January 2006.

* Corresponding author. Tel: +30 210 9493341; fax: +30 210 9493235. E-mail address: nassoseft{at}yahoo.com


   Abstract
Top
 Abstract
Introduction
 Underlying pathology and...
 Imaging
 Flow alterations
 Clinical sequelae and prognosis
 Treatment
 Conclusions
 References
 
Coronary artery ectasia is a relatively common entity characterized by inappropriate dilatation of the coronary vasculature. The exact mechanism of its development is unknown, but evidence suggests a combination of genetic predisposition, common risk factors for coronary artery disease and abnormal vessel wall metabolism. It frequently coexists with aneurysms elsewhere, mostly involving the aorta. In this review, the flow disturbances that are associated with this condition and the imaging modalities, which can be used for diagnosis and prospective follow-up are described. The prognosis of coronary ectasias is controversial and prospective studies focusing on conservative or invasive strategies to prevent cardiac complications are needed.

Key Words: Coronary artery disease • Ectasia • Aneurysm • Coronary flow


   Introduction
Top
 Abstract
 Introduction
Underlying pathology and...
 Imaging
 Flow alterations
 Clinical sequelae and prognosis
 Treatment
 Conclusions
 References
 
Coronary artery ectasia (CAE) has been observed by pathologists and cardiologists for more than two centuries. As its first description by Morgagni1 this not so infrequent form of coronary artery disease has puzzled the clinicians regarding its cause, clinical sequelae and treatment. In the current review we searched the MEDLINE database for all relevant articles, containing the key words ‘coronary ectasia’ and ‘coronary aneurysm’ without specific selection criteria. The reference list of identified papers was also searched. With the widespread use of coronary angiography the incidence of CAE in patients undergoing this diagnostic procedure was clearly delineated. Although the incidence may overestimate the true frequency in the general population, CAE has been found in 1–5% during coronary angiography.2–7 In the largest series from the CASS registry, Swaye et al.2 found CAE in 4.9% of more than 20 000 coronary angiograms they reviewed. The incidence of CAE in an Indian patient cohort with ischaemic heart disease has been reported to exceed 10%.8

The most commonly used angiographic definition of CAE, albeit arbitrary, is the diameter of the ectatic segment being more than 1.5 times larger compared with an adjacent healthy reference segment.2–3 However, as the distribution of CAE is quite variable and not always focal, normal reference segments may not be readily apparent, and this definition potentially underestimates the true incidence of the disease. More detailed definition characteristics, for example employing larger diameter ratio or incorporating angiographic flow alterations, may enhance detection accuracy during angiography but also may further underestimate the true incidence of the disease.

More than half of CAE are due to coronary atherosclerosis, but occasionally they are related to other pathological entities.9 As the first report of coronary dilatation in a patient with syphilitic aortitis,1 CAE has been observed in association with connective tissue disorders such as scleroderma,10 Ehlers–Danlos syndrome11 and polyarteritis nodosa12 but also with bacterial infections13 and the Kawasaki disease.14 In a small percentage of patients CAE can be congenital in origin.15 The differentiation between congenital and acquired coronary aneurysms may often be difficult, despite the exclusion of other associated diseases.9 Acquired CAE should also be differentiated from coronary aneurysms following coronary interventions. These include true or pseudo-aneurysms during coronary balloon angioplasty, but more importantly following coronary stent placement, atherectomy and brachytherapy.16–18 Occasionally large ulcerated coronary plaques can be misinterpreted angiographically as coronary aneurysms. Their true cause can be usually revealed with intravascular ultrasound (IVUS).19

Recent studies have documented the association of CAE with the presence of aneurysms in other vascular beds as well, probably owing to a common underlying pathogenetic mechanism. CAE has been seen more frequently in patients with aneurysms of the abdominal and ascending aorta, the popliteal arteries, veins, and the pulmonary artery.20 In a retrospective study by Stajduhar et al.,21 20.8% of patients operated on for abdominal aortic aneurysm had CAE, compared with 2.9% of patients who were operated on for occlusive peripheral vascular disease. Similar findings have been reported by most,22–24 but not all investigators.2,5 Our group recently extended this association to patients operated on for aneurysm of the ascending aorta, reporting a five-fold increase in the frequency of angiographically detected CAE, compared with a concomitantly studied cohort of patients with suspected coronary artery disease.25


   Underlying pathology and causative mechanisms
Top
 Abstract
 Introduction
 Underlying pathology and...
Imaging
 Flow alterations
 Clinical sequelae and prognosis
 Treatment
 Conclusions
 References
 
The specific causative mechanisms of abnormal luminar dilatation in CAE are essentially unknown. However, as the histopathological characteristics are similar to coronary atherosclerosis, it is not surprising that the hypotheses for the origin of CAE revolve around the vascular endothelium and the biological properties of the arterial wall. Virmani23 and other investigators have provided detailed pathological characterization of CAE, including lipid deposition with foam cells, fibrous caps and significant loss of musculoelastic vascular wall components as main histological abnormalities.4,22 CAE has to be differentiated from post-stenotic dilatation, in which an increase in wall stress, added to the atherosclerotic destruction of the media, may result in progressive arterial dilatation.26 In a minority of cases, CAE is observed in the absence of significant atheromatous burden. Despite the intact intima, extensive media degeneration and hyalinization, possibly as a result of chronic vascular inflammation, are stressed as the common denominator in all cases with CAE.27

On a pathophysiological basis, Sorrell28 suggested a probable mechanism that can predispose to ectasia, i.e. chronic overstimulation of endothelium by NO or NO donors. Enhanced NO production has also been documented, via the iNOS pathway, following an increase in the local interstitial concentration of acetylcholine.29 ‘Clustering’ of CAE has been observed in Vietnam veterans exposed to Agent Orange,30 suggesting a possible link between NO overstimulation and medial thinning leading to CAE. The components of this chemical compound, directly or indirectly, antagonizes acetylcholinesterase, thus producing higher levels of acetylcholine and enhanced NO production. Although contra intuitive, ectatic coronary segments can undergo intense coronary spasm in response to exogenous administration of vasoreactive medications such as ergonovine and acetylcholine. Despite controversy, if spasm may occur within the CAE31 or at its borders,32 this phenomenon, together with possible distal microembolization, may account for the rare development of acute coronary syndromes in patients with CAE without coronary stenoses (‘dilated coronaropathy’), who also manifest ischaemia at exercise.9

Another mechanism, proposed by Lamblin et al.,24 focuses on the system of metalloproteinases, which are actively involved in the proteolysis of the extracellular matrix proteins. These investigators found in patients with CAE, compared with to patients with obstructive coronary lesions, a higher percentage of the 5A/5A polymorphism of the metalloproteinase-3 (MMP-3). Although the serum levels of the MMP-3 were not measured, it is possible that overexpression of MMP-3 may lead to enhanced vessel wall degradation of various matrix proteins, such as proteoglycans, laminin, fibronectin and collagen Types III, IV, V, and IX and subsequent excessive vessel wall dilatation. These results are in line with recent evidence suggesting the presence of higher MMP-3 levels and an imbalance of MMP/TIMP in patients with generalized CAE.33 As CAE commonly coexist with coronary stenoses, overproduction of the MMPs may contribute to the development of acute coronary syndromes, and these findings if verified may offer in the future therapeutic insights through MMP inhibition. In addition, the inflammatory vascular hypothesis is further strengthened by observations linking the presence of CAE with elevated plasma levels of hsCRP,34,35 Il-636 and V-CAM, I-CAM, and E-selectin.37

Taken all the above findings together, one might speculate that CAE occurs due to two different mechanisms in two distinct patient groups: (i) rarely in subjects without coronary atherosclerosis as a result of exogenous interstitial NO vascular overstimulation and (ii) commonly in patients with concomitant coronary artery disease due to severe and chronic arterial inflammation.


   Imaging
Top
 Abstract
 Introduction
 Underlying pathology and...
 Imaging
Flow alterations
 Clinical sequelae and prognosis
 Treatment
 Conclusions
 References
 
For the last four decades, since Daoud22 stated ‘indeed no case of coronary aneurysm has yet been diagnosed antemortem’, coronary angiography remains the gold standard for the assessment of CAE. In order to clarify anatomical variations, Markis proposed a classification of CAE based on the extent of ectatic involvement. In decreasing order of severity, diffuse ectasia of two or three vessels was classified as Type I, diffuse disease in one vessel and localized disease in another vessel as Type II, diffuse ectasia of one vessel only as Type III and localized or segmental ectasia as Type IV.4 In addition, CAE has been classified according to the anatomical shape of the ectatic segment in fusiform or saccular types.20 Older studies preferred the term ‘coronary aneurysm’ for the more discrete and saccular-type ectatic segments, reserving the term ‘ectasia’ for the fusiform diffuse vessel involvement.4,38 All three coronary vessels can be affected by CAE, but in ~75% of patients an isolated artery is ectatic.3 In patients with concomitant coronary artery disease, the proximal and mid segments of the right coronary artery are the most frequently involved, followed by the left anterior descending artery and the circumflex artery.2,3 The reason for the higher right coronary artery predisposition to CAE is not well understood. Of interest, diffuse, fusiform type CAE tends to have more frequently bilateral distribution and association with abdominal aortic aneurysms but it coexists with obstructive coronary lesions less frequently, compared with discrete saccular type CAE.3,9,21 In a small percentage of patients, CAE does not coexist with coronary stenoses. In this subgroup, more frequently involves part or the whole length of the artery in a diffuse form (‘dilated coronaropathy’).9 Coronary angiography by documenting the severity and extent of concomitant coronary artery disease may also provide significant prognostic information, as discussed subsequently. To date, there are no studies examining the anatomical changes that may occur in CAE over time. From a small angiographic series of nine patients, we noted that the CAE diameter remained stable over a mean follow-up of 36 months. Although speculative, this finding may suggest that the pathophysiological mechanisms responsible for their development operated temporarily long before their angiographic documentation (unpublished data).

IVUS is an excellent tool to assess luminal size and characterize arterial wall changes. Ge et al.,19 observed a significant atheromatous burden in the majority of CAE, with plaque areas evenly distributed between proximal and distal reference segments, as well as within the aneurysmal segment. Percent stenosis, however, was significantly lower within the CAE, due to larger vessel area, stressing the difficulty in assessing the degree of stenosis when it appears within an ectatic segment. Of importance, IVUS correctly differentiated true from false aneurysms caused by plaque rupture.39 Emptied plaque cavities may appear angiographically as CAE and the distinction are of clinical importance, as false aneurysms may lead to acute coronary syndromes.40

Recently, magnetic resonance imaging (MRI) has been successfully used to assess coronary anatomy in patients with CAE41 (Figure 1) and Kawasaki syndrome.42 This modality, together with electron beam computerized tomography, may prove to be of particular value for the non-invasive prospective evaluation of CAE, as regards both morphology and flow.


Figure 7251
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  		Figure 1 Coronary magnetic resonance angiograms employing ‘black blood’ (left) or ‘white blood’ (middle) contrast and a corresponding coronary angiogram (right) from a patient with an ectatic right coronary artery (maximum diameter of the ectatic segment 5.2 mm). Adapted with permission from Mavrogeni et al.41

 

   Flow alterations
Top
 Abstract
 Introduction
 Underlying pathology and...
 Imaging
 Flow alterations
Clinical sequelae and prognosis
 Treatment
 Conclusions
 References
 
Disturbances in blood flow filling and washout are an inherent characteristic of CAE. They represent the direct result of inappropriate coronary dilatation and are clearly associated with the severity of CAE.9 Angiographic signs of turbulent and stagnant flow include delayed antegrade dye filling, a segmental back flow phenomenon and local deposition of dye (stasis) in the dilated coronary segment.4,9

Slow flow has been recently directly evaluated. In a detailed study, Akyurek et al.43 used the Doppler wire (Flowire) to measure blood flow velocity and coronary flow reserve in patients with isolated CAE and in a control group. They reported within the CAE, compared with the control group, a trend for lower resting blood flow velocity. Following intracoronary administration of papaverine, a potent hyperemic stimulus, the coronary flow reserve was 1.51 in the CAE compared with 2.67 in the control arteries (P<0.001), suggesting a combination of epicardial flow disturbances and microvascular dysfunction as the cause of myocardial ischaemia. A point of interest was the estimated resting absolute volumetric flow within the CAE, found approximately 3 times higher compared with control patients. On a conceptual basis, this finding contradicts previous data using coronary sinus lactate and exercise stress test, that documented myocardial ischaemia in areas supplied by ectatic arteries.9,44 A possible explanation may be the spurious estimation of volumetric flow with the Flowire in a dilated coronary segment with obviously non-laminar flow.9

Recently, we used the TIMI frame count method (TFC), an index of coronary flow velocity along the entire epicardial coronary artery and reported a higher TFC (slower flow) in CAE.45 We subsequently reported similar findings using magnetic resonance flow velocity.46 More studies are needed in this aspect, including transthoracic Doppler evaluation, as the acceleration of slow flow may be a therapeutic target.


   Clinical sequelae and prognosis
Top
 Abstract
 Introduction
 Underlying pathology and...
 Imaging
 Flow alterations
 Clinical sequelae and prognosis
Treatment
 Conclusions
 References
 
In the majority of cases (~85%), CAE accompanies atherosclerotic coronary disease.2–4,6 The clinical presentation and the long-term cardiac complications are mostly associated with the severity of the coexisting coronary lesions. In this population, it has been repeatedly shown that CAE does not confer an additional risk to that which is attributed to coexisting coronary stenoses.2–4 In the largest series from the CASS study, the presence of CAE did not affect the adjusted 5-year survival of patients with coronary artery disease (75 vs. 81%).2

In a recent report from our group corresponding to more modern medical management, the 2-year survival in the two groups, with and without CAE, was also similar (96.7 vs. 94.8%).3 Very recently, Baman et al.,47 using more stringent criteria for identifying patients with CAE, reported a significant adverse outcome among 276 patients they studied, with a 5-year mortality of 29.1%. Although autopsy reports frequently document thrombus within a CAE, the true incidence of thrombotic occlusion is unknown, requiring a large prospective angiographic study. Non-invasive methods, especially MRI, may offer a means of prospectively following these patients.

The clinical course of the patients with isolated CAE (with no or non-significant coronary stenoses) deserves special attention. Despite the absence of flow limiting coronary lesions in this small group of patients, Krueger et al.9 convincingly documented the presence of angina, positive exercise stress test and pacing-induced myocardial ischaemia in patients with ‘dilated coronaropathy’. In addition, unstable coronary syndromes may occur despite absence of stenoses: In our study, 38.7% of patients with isolated CAE were reported as having a history of myocardial infarction in the corresponding myocardial territory.3 Overall, however, cardiac event rate in this patient group appears to be low and clinical follow-up suggests a relatively favorable prognosis. As reported previously2 mortality approximates 2% per year.


   Treatment
Top
 Abstract
 Introduction
 Underlying pathology and...
 Imaging
 Flow alterations
 Clinical sequelae and prognosis
 Treatment
Conclusions
 References
 
Contrary to atherosclerotic coronary artery disease, there is a scarcity of data adequately addressing the medical management of patients with CAE. Previous studies based on the significant flow disturbances within the ectatic segments, suggested chronic anticoagulation as main therapy.28,48 However, this treatment has not been prospectively tested, and could not be recommended unless supported by subsequent studies.27 Heparin infusion as well as fibrinolysis, have been successfully used for recanalization in isolated cases of acute thrombotic occlusions, occasionally revealing absence of flow-limiting stenoses.49,50

The coexistence of CAE with obstructive coronary lesions in the great majority of patients and the observed incidence of myocardial infarction, even in patients with isolated coronary ectasias, have led to the generalized administration of aspirin in all patients with CAE.2,51 The role of combined antiplatelet therapy, with the addition of ADP inhibitors, has not yet been evaluated in prospective randomized studies.

Medications with vasodilating properties against coronary spasm have also been proposed.28 Of importance, nitrates, presumably by causing further coronary epicardial dilation, have been shown to exacerbate myocardial ischaemia and are discouraged in patients with isolated CAE.9 To date, there are no vasoactive medications that have been tested, in order to be widely recommended to patients with CAE.

As CAE represents a form of atherosclerotic heart disease, intense risk factor modification for primary and secondary prevention is obviously necessary. Sudhir et al.52 reported that CAE is 6 times more frequent among patients with familial hypercholesterolemia than in a control group, suggesting a link between abnormal lipoprotein metabolism and aneurysmal coronary artery disease.

For patients with coexisting obstructive lesions and symptoms or signs of significant ischaemia despite medical therapy, percutaneous and/or surgical coronary vascularization can safely and effectively restore normal myocardial perfusion. Ochiai et al.53 many years ago reported excellent acute and long-term results of balloon angioplasty in lesions adjacent to coronary aneurysms and these findings also agree with our clinical observations. One point of special consideration is the need for adequate stent expansion and wall apposition. This, at times can be accomplished only with IVUS (Figure 2). Although we did not encounter acute complications using the IVUS, extra care is recommended during introduction and withdrawal of the device, in order to avoid stent dislocation. The implantation of covered vs. bare metal stents offers superior acute angiographic result excluding the ectatic segment, but long term benefit has not been adequately proven.54 Coronary artery bypass grafting has been used for many years for the treatment of significant coronary artery disease co-existing with ectatic coronary segments. The presence of thrombus within the CAE and the question of the necessity to remove large aneurysms has led to the introduction of a variety of operative procedures, including proximal and distal ligation, aneurysmorrhectomy and even aneurysm resection.55 The post-operative outcome, however, was uniformly good.56


Figure 7252
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  		Figure 2 Coronary angiogram of the left anterior descending artery (right anterior oblique projection) showing a severe mid-segment stenosis (black arrow) adjacent to a coronary ectatic segment, before stent placement (left), after stent placement (middle), and intracoronary ultrasound image (right) within the proximal ectatic segment exhibiting inadequate apposition of stent struts (asterisks) against the vessel wall (white arrows) despite stent overexpansion.

 

   Conclusions
Top
 Abstract
 Introduction
 Underlying pathology and...
 Imaging
 Flow alterations
 Clinical sequelae and prognosis
 Treatment
 Conclusions
References
 
CAEs represent a not uncommon form of atherosclerotic coronary artery disease, seen in ~5% of patients undergoing coronary angiography. Many unanswered questions remain regarding their exact aetiology, prognosis and therapy. The introduction of genetic studies, new non-invasive modalities, especially MRI, and the systematic testing of modern antiplatelet and vasoactive medications, may offer significant means of improving their prognosis.

Conflict of interest: none declared.


   References
Top
 Abstract
 Introduction
 Underlying pathology and...
 Imaging
 Flow alterations
 Clinical sequelae and prognosis
 Treatment
 Conclusions
 References
 

  1. Morgagni JB. De sedlbus, et causis morborum per anatomen indagatis. Tomus primus, Liber II, Epist 27, Article 28, Venetiis, 1761.
  2. Swaye PS, Fisher LD, Litwin P, Vignola PA, Judkins MP, Kemp HG, Mudd GJ, Gosselin AJ. Aneurysmal coronary artery disease. Circulation 1983; 67: 134–138.[Abstract/Free Full Text]
  3. Demopoulos V, Olympios C, Fakiolas C, Pissimissis E, Economides N, Adamopoulou E, Foussas S, Cokkinos DV. The natural history of aneurysmal coronary artery disease. Heart 1997; 78: 136–141.[Abstract/Free Full Text]
  4. Markis JE, Joffe CD, Cohn PF, Feen DJ, Hermann MV, Gorlin R. Clinical significance of coronary arterial ectasia. Am J Cardiol 1976; 37: 217–222.[CrossRef][ISI][Medline]
  5. Hartnell GG, Parnell BM, Pridie RB. Coronary artery ectasia – its prevalence and clinical significance in 4993 patients. Br Heart J 1985; 54: 392–395.[Abstract/Free Full Text]
  6. Farto–e–Abreu P, Mesquita A, Silva JA, Seabra Comez R. Coronary artery ectasia: clinical and angiographic characteristics and prognosis. Rev Port Cardiol 1993; 12: 305–310.[Medline]
  7. Aintablian A, Hamby RT, Hoffman I, Kramer RJ. Coronary ectasia: incidence and results of coronary bypass surgery. Am Heart J 1978; 96: 308–315.
  8. Sharma SN, Kaul U, Sharma S, Wasiv HS, Manchanda SC, Bahl VK, Talwar KK, Rajani M, Bhatia ML. Coronary arteriographic profile in young and old Indian patients with ischaemic heart disease: a comparative study. Indian Heart J 1990; 42: 365–369.[Medline]
  9. Krueger D, Stierle U, Herrmann G, Simon R, Sheikhzadeh A. Exercise-induced myocardial ischaemia in isolated coronary artery ectasias and aneurysms (‘Dilated Coronaropathy’). J Am Coll Cardiol 1999; 34: 1461–1470.[Abstract/Free Full Text]
  10. Chaithiraphan S, Goldberg E, O'Reilly M. Multiple aneurysms of coronary artery in sclerodermal heart disease. Angiology 1973; 24: 86–93.[Free Full Text]
  11. Shiro I, Bannerman RM, Graf CJ, Brennan JC. Ehlers–Danlos syndrome with multiple arterial lesions. Am J Med 1969; 47: 967–977.[CrossRef][ISI][Medline]
  12. Tang PHL, Segal AJ. Polyarteritis nodosa of infancy: fatal late complications. JAMA 1970; 217: 666–670.
  13. Davidson A, Eshaghpour E, Young N, Mintz GS. Late thrombosis of a coronary artery mycotic aneurysm. Am Heart J 1991; 121: 1549–1550.[CrossRef][ISI][Medline]
  14. Hiraishi S, Yashiro K, Oguchi K, Kusano S, Ishii KK, Nakazawa K. Clinical course of cardiovascular involvement in the mucocutaneous lymph node syndrome-relation between the clinical signs of carditis and development of coronary arterial aneurysm. Am J Cardiol 1981; 47: 32.
  15. Seabra-Gomes R, Somerville J, Ross DN, Emanuel R, Parker DJ, Wong M. Congenital coronary artery aneurysms. Br Heart J 1974; 36: 329–335.[Free Full Text]
  16. Bell MR, Garrati KN, Bresnahan JF, Edwards WD, Holmes DR. Relation of deep arterial resection and coronary aneurysms after directional coronary atherectomy. J Am Coll Cardiol 1992; 20: 1474–1481.[Abstract]
  17. Noguchi T, Itoh A, Miyazaki S, Yasuda S, Moii I, Daikoku S, Goto Y, Nonogi H. Images in cardiovascular medicine. Intravascular ultrasound diagnosis of a coronary aneurysm after Palmaz-Schatz stent implantation. Circulation 1999; 99: 162–163.[Free Full Text]
  18. Condado JA, Waksman R, Gurdiel O, Espinosa R, Gonzalez J, Burger B, Villoria G, Acquatella H, Crocker IR, Seung KB, Liprie SF. Long-term angiographic and clinical outcome after percutaneous transluminal coronary angioplasty and intracoronary radiation therapy in humans. Circulation 1997; 96: 727–732.[Abstract/Free Full Text]
  19. Ge J, Liu F, Kearney P, Gorge G, Haude M, Baumgart D, Ashry M, Erbel R. Intravascular ultrasound approach to the diagnosis of coronary artery aneurysms. Am Heart J 1995; 130: 765–771.[CrossRef][ISI][Medline]
  20. Befeler B, Aranda JM, Embi A, Mullin FL, El-Sherif N, Lazzara R. Coronary artery aneurysms. Study of their etiology, clinical course and effect on left ventricular function and prognosis. Am J Med 1977; 62: 597–607.[CrossRef][ISI][Medline]
  21. Stajduhar KC, Laired JR, Rogan KM, Wortham DC. Coronary arterial ectasia: increased prevalence in patients with abdominal aortic aneurysm as compared to occlusive atherosclerotic peripheral vascular disease. Am Heart J 1993; 125: 86–92.[CrossRef][ISI][Medline]
  22. Daoud AS, Pankin D, Tulgan H, Florentin RA. Aneurysms of the coronary artery-report of ten cases and review of literature. Am J Cardiol 1963; 11: 228–237.[CrossRef][ISI][Medline]
  23. Virmani R, Robinowitz M, Atkinson JB, Forman MB, Silver MD, McAllister HA. Acquired coronary arterial aneurysms: an autopsy study of 52 patients. Hum Pathol 1986; 17: 575–583.[ISI][Medline]
  24. Lamblin N, Bauters C, Hermant X, Lablanche JM, Helbecque N, Amouyel P. Polymorphisms in the promoter regions of MMP-2, MMP-3, MMP-9 and MMP-12 genes as determinants of aneurysmal coronary artery disease. J Am Coll Cardiol 2002; 40: 43–48.[Abstract/Free Full Text]
  25. Papadakis M, Leontiadis E, Manginas A, Voudris V, Pavlides G, Karatasakis G, Foussas S, Michalis A, Cokkinos D.V. Frequency of coronary artery ectasias in patients operated on for ascending aortic aneurysms. Am J Cardiol 2004; 94: 1433–1435.[Medline]
  26. Rodbars S, Ikeda K, Montes M. An analysis of mechanisms of poststenotic dilatation. Angiology 1967; 18: 349–353.[Free Full Text]
  27. Rath S, Har-Zahav Y, Battler A, Agranat O, Rotstein Z, Rabinowitz B, Neufeld HN. Fate of nonobstructive aneurysmatic coronary artery disease: angiographic and clinical follow-up report. Am Heart J 1985; 109: 785–791.[CrossRef][ISI][Medline]
  28. Sorrell VL. Origins of coronary artery ectasia. Lancet 1996; 20: 136–137.[CrossRef]
  29. Vanhoutte PM. Endothelium and control of vascular function. Hypertension 1989; 13: 658–667.[Abstract/Free Full Text]
  30. England JF. Herbicides and coronary artery ectasia (letter). M J Aust 1981; 68: 260.
  31. Bove AA, Vlietstra RE. Spasm in ectatic coronary arteries. Mayo Clin Proc 1985; 60: 822–826.[Medline]
  32. Suzuki H, Takeyama Y, Hamazaki Y, Namiki A, Koba S, Matsubara H, Hiroshige J, Murakami M, Katagiri T. Coronary spasm in patients with coronary ectasia. Cathet Cardiovasc Diagn 1994; 32: 1–7.[Medline]
  33. Finkelstein A, Michowithz Y, Abashidze A, Miller H, Keren G, George J. Temporal association between circulating proteolytic, inflammatory and neurohormonal markers in patients with coronary ectasia. Atherosclerosis 2005; 179: 353–359.[CrossRef][ISI][Medline]
  34. Adiloglu AK, Can R, Nazli C, Ocal A, Ergene O, Tinaz G, Kisioglu N. Ectasia and severe atherosclerosis: relationships with chlamydia pneumoniae, helicobacterpylori, and inflammatory markers. Tex Heart Inst J 2005; 32: 21–27.[Medline]
  35. Turban H, Erbay AR, Yasar AS, Balci M, Bicer A, Yetkin E. Comparison of c-reactive protein levels in patients with coronary artery ectasia versus patients with obstructive coronary artery disease. Am J Cardiol 2004; 94: 1303–1306.[Medline]
  36. Tokgozoglu L, Ergene O, Kinay O, Nazli C, Haselik G, Hoscan YU. Plasma interleukin-6 levels are increased in coronary artery ectasia. Acta Cardiol 2004; 59: 515–519.[Medline]
  37. Turhan H, Erbay AR, Yasar AS, Aksoy Y, Bieer A, Yetkin G, Yetkin E. Plasma soluble adhesion molecules; intercellular adhesion molecule-1, vascular cell adhesion molecule-1 and E-selection levels in patients with isolated coronary artery ectasia. Coron Artery Dis 2005; 16: 45–50.[Medline]
  38. Tunick PA, Slater J, Kronzon I, Glassman E. Discrete atherosclerotic coronary artery aneurysms: a study of 20 patients. J Am Coll Cardiol 1990; 15: 279–282.[Abstract]
  39. Gerrand TJ, Mintz GS, Popma, Lewis SA, Vaughn NA, Leon MB. Intravascular ultrasound diagnosis of a coronary pseudoaneurysm following percutaneous transluminal coronary angioplasty. Am Heart J 1993; 125: 880–882.[Medline]
  40. Fuster V, Stein B, Ambrose JA, Badimon JJ, Chesebro JH. Atherosclerotic plaque rupture and thrombosis: evolving concepts. Circulation 1990; 82: 47–59.
  41. Mavrogeni S, Manginas A, Papadakis E, Foussas S, Douskou M, Baras P, Seimenis I, Cokkinos DV. Correlation between magnetic resonance angiography (MRA) and quantitative coronary angiography (QCA) in ectatic vessels. J Cardiovasc Magn Reson 2004; 6: 17–23.[Medline]
  42. Mavrogeni S, Papadopoulos G, Douskou M, Kaklis S, Seimenis I, Baras P, Nikolaidou P, Bakoula C, Karanasios E, Manginas A, Cokkinos DV. Magnetic resonance angiography is equivalent to X-ray coronary angiography for the evaluation of coronary arteries in Kawasaki disease. J Am Coll Cardiol 2004; 43: 649–652.[Abstract/Free Full Text]
  43. Akyurek O, Berkalp B, Sayin T, Kumbasar D, Kervancioglu C, Oral D. Altered coronary flow properties in diffuse coronary artery ectasia. Am Heart J 2003; 145: 66–72.[CrossRef][ISI][Medline]
  44. Sayin T, Doven O, Berkalp B, Akyurek O, Gulec S, Oral D. Exercise-induced myocardial ischaemia in patients with coronary artery ectasia without obstructive coronary artery disease. Int J Cardiol 2001; 78: 143–149.[CrossRef][ISI][Medline]
  45. Papadakis M, Manginas A, Cotileas P, Demopoulos V, Voudris V, Pavlides G, Foussas S, Cokkinos DV. Documentation of slow coronary flow by the TIMI frame count in patients with coronary ectasia. Am J Cardiol 2001; 88: 1030–1032.[CrossRef][ISI][Medline]
  46. Mavrogeni S, Manginas A, Papadakis E, Douskou M, Cokkinos D, Katsiva V, Foussas S, Voudris V, Giakoumelos A, Seimenis J, Baras P, Cokkinos DV. Coronary flow evaluation by TIMI frame count and magnetic resonance flow velocity in patients with coronary artery ectasia. J Cardiovasc Magn Reson 2005; 7: 545–550.[Medline]
  47. Baman TS, Cole JH, Devireddy CM, Sperling LS. Risk factors and outcomes in patients with coronary artery aneurysms. Am J Cardiol 2004; 93: 1549–1551.[Medline]
  48. Swanton RH, Thomas MC, Coltart DJ, Jenkins BS, Webb Peploe MM, Williams BT. Coronary artery ectasia: a variant of occlusive arteriosclerosis. Br Heart J 1978; 40: 393–400.[Abstract/Free Full Text]
  49. Tanabe Y, Itoh E, Nakagawa I, Suzuki K. Pulse-spray thrombolysis in acute myocardial infarction caused by thrombotic occlusion of an ectatic coronary artery. Circ J 2002; 66: 207–210.[Medline]
  50. Lau GT, Brieger D, Freedman SB. Infarction due to right coronary artery thrombus. Clin Cardiol 2004; 27: 96.[Medline]
  51. AL-Harthi SS, Nouh MS, Arafa M, Al-Nozha M. Aneurysmal dilatation of the coronary arteries: diagnostic patterns and clinical significance. Int J Cardiol 1991; 30: 191–194.[CrossRef][ISI][Medline]
  52. Sudhir K, Ports TA, Amidon TM, Goldberger JJ, Bhushan V, Kane JP, Yock P, Malloy MJ. Increased prevalence of coronary ectasia in heterozygous familial hypercholesterolemia. Circulation 1995; 91: 1375–1380.[Abstract/Free Full Text]
  53. Ochiai M, Yamagushi T, Tagushi J, Ohno M, Yoshimura H, Kashida M, Kuwako K, Isshiki T, Kurokawa K. Angioplasty of stenoses adjacent to aneurysmal coronary artery disease. Jpn Heart J 1990; 31: 749–757.[Medline]
  54. Stefanadis C, Toutouzas K, Tsiamis E, Toutouzas P. New stent design for autologous venous graft-covered stent preparation: first human application for sealing of a coronary aneurysm. Catheter Cardiovasc Interv 2002; 55: 222–227.[Medline]
  55. Vijayanagar R, Shafii E, DeSantis M, Waters RS, Desai A. Surgical treatment of coronary aneurysms with and without rupture. J Thorac Cardiovasc Surg 1994; 107: 1532–1535.[Free Full Text]
  56. Harandi S, Johnston SB, Wood RE, Roberts WC. Operative therapy of coronary arterial aneurysm. Am J Cardiol 1999; 83: 1290–1293.[CrossRef][Medline]

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