Case Presentation: A 58 year old male with no previous cardiac history presented to the emergency department (ED) with acute onset of substernal chest pain. An electrocardiogram (ECG) showed inferior ST-segment depressions, and cardiac troponins peaked at 1.05 ng/mL (normal 0.00-0.10 ng/mL). Cardiac catheterization revealed diffuse coronary artery ectasia (CAE), with marked dilation of the right coronary artery (RCA), left anterior descending (LAD), and left circumflex arteries (Image 1). The ectatic vessels, especially the distal RCA, demonstrated slow flow. He otherwise had mild coronary artery disease. A transthoracic echocardiogram (TTE) showed normal function without wall motion abnormalities. The patient was started on warfarin and aspirin, as well as a beta blocker and high dose statin. Three months after discharge, he again felt severe substernal chest pain while walking and presented to the ED. ECG was consistent with an inferior ST-segment myocardial infarction. Of note, his international normalized ratio (INR) was subtherapeutic. Cardiac catheterization again showed slow flow in the ectatic RCA without an intervenable lesion. He was then placed on triple therapy with clopidogrel, aspirin, and warfarin. He has remained on triple therapy and without further cardiac symptoms, now nine months after his initial presentation.
Discussion: CAE is characterized by dilation of diffuse segment(s) of the coronary arteries to at least 1.5 times the normal diameter. CAE is typically asymptomatic and incidentally discovered during cardiac catheterization or other imaging of the cardiac vessels, and the incidence has been reported to be between 0.3%-5%. The RCA is most commonly affected, followed by the LAD. The etiology is likely multifactorial. CAE is strongly associated with atherosclerotic disease, hypertension, and dyslipidemia. Connective tissue diseases, vasculitis, and iatrogenic vessel injury have also been implicated.
Patients with CAE have a higher incidence of major adverse cardiac events (MACE), likely due to increased turbulent flow, stasis, and endothelial dysfunction in the ectatic vessels. In one study, patients who presented with myocardial infarction (MI) and were found to have CAE had a 3.25 fold greater risk of recurrent MACE after 49 months, compared to similar patients without CAE.
Evidence to guide management of CAE is still scarce. One retrospective study has found that warfarin monotherapy significantly decreased adverse cardiac events in CAE patients compared to no anticoagulation. Another study showed that dual antiplatelet therapy halved the incidence of cardiac events in patients with CAE, compared to no anticoagulation.
Conclusions: Coronary artery ectasia is relatively uncommon. Patients with CAE are at greater risk for MACE and will likely benefit from anti-coagulation; however, further studies are needed to determine the optimal anticoagulation strategy.