Here we show a natural history of WCA in LAD of a young man by serial CAG in a 7-year interval, and the lesion features were visualized by OCT imaging. Our case indicates an acquired cause of WCA and most likely resulted from recanalized thrombus. This supports the finding in another report, in which WCA development was observed in the right coronary artery by serial CAG in a 6-year interval, and the lesion characteristics were observed by intravascular ultrasound (IVUS) [4]. Till now, only these two case reports described the natural history of WCA by serial CAG.
One pathological mechanism proposed for WCA is congenital[5]. However, there is lack of data showing that WCA has a genetic predisposition or hereditary characteristic. The OCT image features of WCA is summarized as follows: (1) Intertwined thin channels separated by fibrous tissue without cross-communications among them; (2) Undisrupted arterial wall integrity without dissection; and (3) High signal intensity and low signal attenuation[1]. Although it is not conclusive, no cross-communications is proposed as a key feature in distinguishing congenital WCA from other etiologies, such as thrombus recanalization[1]. In the current case which is acquired, we also found no cross-communications among the lager and the smaller channels by OCT. However, the smaller channel itself has multiple microchannels and cross-communications exist among them. Taking into account the limited number of published case reports, we consider that no cross-communications among the channels is just one type of WCA, thus could not be used as a criterion for differential diagnosis.
The other proposed pathological mechanism for WCA is acquired factors, including thrombus recanalization, spontaneous coronary artery dissection (SCAD) or bridging collaterals of chronic total coronary occlusions (CTO). It is not rare that neovascular channels form in the CTO segments, but histologic studies show their diameters range from 160 to 230 µm[6]. As the diameters of two main channels (2000 µm and 1000 µm, respectively) in the current case were much larger than that of neovascular channels in CTO lesions, they are unlikely resulted from recanalization of a CTO. In addition, SCAD is known as a nonatherosclerotic disease and women comprise 87–95% of the patients[7]. Thus, we may exclude the etiology of healed SCAD as CAG indicated an atherosclerotic lesion in the same location 7 years ago. Consequently, recanalization of thrombosis is most likely to be the underline mechanism for this case. Taken together with the previously reported case[4], which also observed a natural history of WCA, we speculate that WCA is most likely an acquired coronary artery disease.
In the past, WCA was deemed to be a benign abnormality and usually do not need intervention[8]. It is now recognized that WCA may lead to ischemia and even myocardial infarction and surgical or percutaneous revascularization is indicated in such patients [1]. The literature review of case reports (37 cases) showed that 24 (50.4%) cases were single vessel disease, and 18 (48.6%) cases underwent revascularization. Among them, 5 (13.5%) cases received coronary artery bypass graft (CABG) and 13 (35.1%) cases underwent percutaneous coronary intervention (PCI)[1]. Thus, PCI is a therapeutic option for most of WCA patients with documented ischemia when the anatomy is suitable. We suggest two technical points when PCI is planned for WCA: (1) Use polymer sleeve CTO guidewires to cross the lesion with sliding and rotating technique. If it does not work, penetration technique with coiled CTO guidewires may be considered; and (2) Confirm that the multi-channels share the media and the guidewire locates inside the media by intravascular imaging, so that the stent could be safely expended without risk of perforation.