A 75-year-old Afro-Caribbean male presented with a non-ST-elevation myocardial infarction. Coronary angiography showed generally grossly dilated coronary arteries with a large lobular thrombus in the distal right coronary artery. We briefly review this case and discuss the definition, pathophysiology and treatment for coronary artery ectasia. J INVASIVE CARDIOL 2008;20:E23–E25 Key Words: percutaneous coronary intervention; thrombosis; acute coronary syndrome

       Case Report. A 75-year-old Afro-Caribbean male presented to our hospital with typical ischemic chest pain associat ed wi th a rai sed t roponin I l eve l of 3.5. His electrocardiogram (ECG) on admission showed anterolateral T-wave inversion. The diagnosis of non-ST-elevat ion myocardial infarction (NSTEMI) was made. He was treated with nitrates, low-molecular weight heparin, aspirin and clopidogrel. Past medical history included a previous non-Qwave inferior MI in 1994. He had no history of significant childhood fever.
       Coronary angiography in 1994 showed mildly dilated coronary vessels with minor plaque irregularities only in the right coronary artery (RCA). The left anterior descending artery (LAD) was unobstructed. There was minor plaque disease in the circumflex artery (CX). Unfortunately, the cine angiography films were destroyed after 10 years according to the local hospital’s policy. A direct comparison of the angiographic pictures with the present films was therefore not possible.

Figure 1B.

Figure 1. Diffuse coronary artery ectasia with acutely occluded right coronary artery ( A ), and thrombotic material in the circumflex artery ( B ).

Figure 1A.

Diffuse coronary artery ectasia with acutely occluded right coronary artery ( A )

       On this admission, coronary angiography was performed via the right radial artery. The RCA was occluded in its mid course (Figure 1A). The LAD and CX were grossly dilated throughout. Thrombus was likely present in the CX (Figure 1B).
       After deploying a PT Choice Xtra Support Wire^™ ( Boston Scientific Corp., Natick, Massachusetts) in the RCA, the occlusion was opened using a 4.0 x 10 mm Maverick^™ balloon (Boston Scientific). The RCA was grossly dilated and a large lobular thrombus was present in the distal vessel (Figure 2). A 4.0 x 15 mm Driver^™ bare-metal stent (Medtronic Inc., Minneapolis, Minnesota) was inserted into the mid RCA. The original balloon was dilated in the distal RCA, with no effect.
       The patient was given a bolus of abciximab followed by an infusion for 48 hours to help resolve the thrombus. He was then started on full-dose enoxaparin and had a repeat angiogram 6 days later. Thrombus in the RCA and CX had reduced in size (Figure 3). Autoimmune antibody (antinuclear [ANA], antineutrophil cytoplasmic [ANCA], anti- DNA, antiextractable nuclear antigen [ENA], rheumatoid factor) and treponemal screen were negative. The patient was commenced on life-long warfarin and discharged 14 days after presentation. Additional drugs on discharge included a beta-blocker, a statin and an angiotensin-converting enzyme inhibitor.

Figure 3.

Angiogram 6 days after initial treatment, showed decreased size of intracoronary thrombi after therapy with glycoprotein IIb/IIIa inhibitor and low-molecular heparin.

Figure 2.

Patent right coronary artery (RCA) and 3 large thrombi in distal RCA (marking of deflated balloon visible). A 4.0 x 15 mm bare-metal stent was successfully deployed in its midcourse.

       Discussion. Diffuse coronary artery ectasia (CAE) is a relatively common angiographic finding with an average incidence of 1–5%.¹ There are few case reports on this subject.^2–4 The degree of severity of ectasia seen in our case is unusual. According to the angiographic definition used in the Coronary Artery Surgery Study,⁵ a vessel is considered to be ectasic when its diameter is ≥ 1.5 times that of the adjacent normal segment in segmental ectasia.⁹ The majority (~85%) of CAEs are due to coronary atherosclerosis, but occasionally, they are related to other pathologies such as syphilitic aortitis, connective tissue disorder (scleroderma, Ehlos-Danlos syndrome, polyarterit is nodosa)⁹ and Kawasaki’s disease. Very rarely, they are of congenital origin.
       The underlying causative mechanism for CAE remains unknown, however, overstimulation of the endothelium with NO or NO donors has been suggested. Other explanations for CAE include higher metalloproteinase 3 (MMP-3) levels and an imbalance of MMP/TIMP. Higher levels of CRP, IL- 6 and adhesion molecules such as V-Cam, I-Cam and Eselectin were also found in patients with CAE,⁹ suggesting the disease to be an active inflammatory process.
       Most frequently, the proximal and mid segments of the RCA are involved in CAE.¹⁰ Although there is a measurable incidence of previous MI, patients with mild CAE show no worse outcomes when compared to nonectatic patients⁶ in contrast to those with coronary artery aneurysms who have a 5-year mortality rate of 29%.¹¹ Reduced flow within the dilated segments has been demonstrated and might predispose patients to thrombotic occlusions of the affected artery.¹² Treatment of CAE should focus on anticoagulation to avoidslow-flow-induced thrombosis. No study has yet shown a benefit of a anticoagulation regimes of warfarin, mono or dual antiplatelet therapy. Nitrates, presumably by causing further endothelial dilatation and consecutive reduction in blood flow, should be avoided in patients with CAE.¹³ Aggressive risk-factor modification for primary and secondary prevention of atherosclerotic heart disease should be initiated.