Discussion of Questions

Question A. Woven coronary disease is a rare conformational coronary disorder. It is characterized by the subdivision of the coronary artery lumen into multiple small independent channels, that merge again into the distal lumen. It usually initiates in the proximal third of the coronary and extends a few centimeters, but there are cases that evolve to almost the full extension of the vessel. It was first described by Sane and Vidaillet, in 1988, as a congenital anomaly, when they observed that the patient's RCA was divided into two major branches which crossed each other in the atrioventricular groove and then fused again near the acute marginal branch as a figure of eight¹. The etiology and pathogenesis of this disease are still unknown. Initially, some authors believed it was caused by spontaneous coronary dissection or even chronic thrombosis with late recanalization². However, latter publications that studied the coronaries with optical coherence tomography (or OCT) proved that the dissection theory was wrong, since the vessels have multi-fenestrations with an intact wall, without any branches coming out of them³. Moreover, histopathological findings of an anomalous segment of an RCA dismissed the dissection hypothesis. It was demonstrated that the lumen was divided in small separated vessels that conserved integrity of their walls, and they did not communicate with each other, showing no signs of dissection, nor thrombus⁴.

Question B. Because of its rarity, it is not always easy to differentiate this condition. Diagnosis must be made for coronary dissection, recanalized thrombus formation, complicated plaque with thrombus formation, and bridging collaterals². As a result of misdiagnosing woven coronary arteries, unnecessary cardiac intervention such as coronary angioplasty may be performed².This ultimately places the patient at an increased risk for arterial damage and other complications^5,6. In multivessel symptomatic patients, CABG maybe the best treatment option bypassing the diseased segment.

Question C. Since most cases are usually findings on angiograms, optimized medical therapy has been the treatment of choice. Prophylactic use of acetylsalicylic acid in patients with woven coronary anomaly is reasonable. Follow-up of those patients are crucial to understand the need for intervention. There are few studies that reported regular follow-up of the medical therapy patients, but all of them report good outcomes without the need for interventions. The multiple lumen tortuosity may increase the difficulty of percutaneous coronary intervention (PCI), thus CABG may be the best alternate choice if optimized medical therapy fails⁷. There are only two reports of PCI treatment and only three reports of CABG treatment so far, but none of them have woven multiarterial coronary disease. This is the first report to describe a case of a patient with multivessel woven disease, that was successfully treated with CABG.

Question D. There are only 25 cases reported so far and most of them report single vessel disease in young male patients, more frequently affecting the RCA. There are only three cases reported involving two vessels and only one reporting three vessel involvement other than ours.

Comments

Woven coronary disease is considered a benign condition, since most of the cases reported so far are findings on cardiac angiograms⁸. However, some authors have published reports of patients with angina and acute coronary syndromes related to the affected arteries and even sudden cardiac death⁴.

Although the distal coronary flow is usually preserved, the distance of the thin channels and the twirling of the channels can predispose the vessel to thrombus formation⁹. There are also theories that correlate higher atherosclerosis process at the affected segment due to reduced coronary laminar flow within the thin channels and a greater shear stress. This may ultimately increase the chance of thrombus formation¹⁰.

This theory is sustained by the previous histological findings showing that those vessels had diffuse mild intimal fibrosis with one of them displaying 80% of luminal stenosis due to a concentric intimal fibrous plaque.

There are also reports that show evidence of silent ischemia with echocardiograms presenting segmented akinesia and scintigraphy with non-viable myocardium related to the woven diseased vessel¹⁰.