The American Heart Hospital Journal


Current knowledge on the epidemiology and natural history of coronary ectasia derives from several large angiographic series, where patients have been divided according to the presence or absence of the atherosclerotic lesion. Although the clinical presentation and the long-term cardiac complications are mostly associated with the severity of the co-existing coronary lesions, in the subset of CAE patients without coronary stenosis the mechanisms that are likely related to acute coronary syndromes are spasm occurrence within the CAE or at its borders, thrombus formation in ectatic segment in the presence of flow disturbances together with possible distal microembolization. In CAE, MI is caused by repeated distal dissemination of microemboli or by in situ thrombosis of the dilated vessel. Recent studies have also suggested that the ectatic wall may be a source of thrombogenic substances;9


stenosis, suggesting the difference in the incidence of CAE reported. The right coronary artery is the most commonly affected, followed by the left circumflex or left anterior descending artery. Three-vessel or left main involvement is rare.8


also an increased


prevalence of circulating anti-endothelial cell antibodies provides the evidence of a possible role of autoimmunity in certain cases of CAE.10


Flow alterations in particular ‘slow


flow’ are an inherent characteristic of CAE and this has been directly evaluated,11


using the Doppler wire to measure blood


flow velocity and coronary flow reserve in patients with isolated CAE. Moreover, several studies12


demonstrated that


presence of CAE was associated with higher TIMI frame count, indicating slower coronary flow. It is interesting that a significantly lower myocardial blush grade was observed in patients with CAE despite brisk epicardial flow, thereby suggesting a significant microvascular impairment.13


The


main histologic features of CAE are lipid deposition with foam cells, fibrous caps, and extensive destruction of musculoelastic elements of the media; these findings are similar to those described for aortic aneurysms but the two forms of disease are not always associated.


Although the molecular mechanism underlying coronary ectasia has yet to be elucidated, several studies suggest the pivotal role of the increased level of metalloproteinases (MMPs), which are actively involved in the proteolysis of the extracellular matrix proteins. In fact, differing from patients with obstructive coronary lesions, CAE patients have a higher percentage of the 5A/5A polymorphism of the metalloproteinase-3 (MMP-3) causing an imbalance between MMPs and their endogenous tissue inhibitors.14 Matrix MMPs are also implicated in blood–brain barrier (BBB) disruption, and in degradation of extracellular matrix proteins and myelin components that are the major finding of the pathogenesis of multiple sclerosis (MS). In particular an imbalance in levels of MMPs and tissue inhibitors of


Summer 2011


Case Report


MMP (TIMP) has been implicated in the pathogenesis of MS, an inflammatory, demyelinating disease of the central nervous system (CNS), with BBB breakdown. Since monocytes form a major cell population in acute MS lesions and may facilitate their entrance into the CNS by secretion of MMP. In fact, previous studies show that MS is associated with elevated levels of MMP and TIMP expressing blood monocytes that may contribute to MS pathogenesis.15–17 This increased proteolysis could theoretically predispose to an increased risk for plaque rupture and a subsequent acute coronary event with a diagnosis made at the time of urgent angiography. However, when AMI occurs in a case of CAE, current reperfusion therapies (thrombolysis, primary stenting, manual thrombectomy) due to the large arterial size and a massive intracoronary thrombus, when used alone, are limited in terms of preventing the development of distal embolization and the ‘no reflow phenomenon.’


Case Report


A 45-year-old man, with hypercholesterolemia and MS was admitted to our emergency department for a chest pain lasting two hours and ST segment elevation on D2-D3-aVF-V5-V6 D1- and aVL leads. After a loading dose of 300 mg of aspirin, 600 mg of clopidogrel, and a 5,000 IU bolus dose of unfractioned heparin (UFH) the patient was transferred in the catheterization laboratory in order to perform an urgent coronary angiography. The coronary angiography showed: left main, normal without significant narrowing; anterior descending and circumflex arteries, large vessels with diffuse ectasia without significant narrowing (see Figure 1); right coronary artery (RCA), dominant vessel: diffuse ectasia with large thrombotic endoluminal involvement in the middle segment (TIMI 1, Thrombus Score 2); and occlusion of a large acute lateral branch (TIMI 0) (see Figure 2A). Engagement of the right coronary artery was performed using a Judkins Right 4 (6 French-Mach1 Boston Scientific) guiding catheter via transradial left approach. A Balance Middle Weight 0.014 inch (Abbott) guidewire was used to cross the occlusion of acute lateral branch persisting after distal positioning of the wire. An embolic protection device (Filter Wire EZ-Boston Scientific Corp., 2011 Stierlin Court, Mountain View, CA 94043-4655 US) was positioned in the distal segment of the right coronary artery to minimize distal embolization (see Figure 2B). In order to manage the high thrombotic burden in a very large and ectatic coronary vessel (quantitative coronary angiography [QCA] of proximal segment: 7.1 mm), multiple thrombus aspirations were performed (total = 4) with Export XT Catheter (Medtronic Inc., 710 Medtronic Parkway Minneapolis, US) (see Figure 2B) followed by an intracoronary locally delivered injection of a 10 ml abciximab (ReoPro, Eli Lilly) bolus across a rapid exchange therapeutic perfusion catheter (Clear Way RX,


Diffuse Coronary Ectasia Complicated by Myocardial Infarction 49


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