Traditionally it is recognized that coronary angiography grossly under diagnoses SCAD. Whilst this is not particularly true when a dissection or intimal flap is clearly visible on angiography, this occurs most particularly in SCAD which has resulted in diffuse stenosis with an intramural hematoma without a flap. There are many case reports in the literature where SCAD was “invisible” on angiography and the diagnosis was elucidated only on intravascular imaging.

An angiographic classification for SCAD has recently been proposed by Saw [13], with three types of angiographic subtypes. Type 1 is the stereotypical angiographic appearance with a radiolucent flap (Fig 8.1a). Type 2 involves usually the mid to distal segments with often an abrupt change in vessel calibre, often extending into the terminal segment (Fig. 8.1b). Type 3 describes a focal segment of “atherosclerotic” lesion, usually in a localized segment of an artery, with compromise of side branches but usually otherwise no atherosclerotic lesion in other segments (Fig. 8.1c).

Most conventional angiography series tend to suggest an under-diagnosis when there is a low index of suspicion amongst angiographers. However, in an unusual twist, when OCT was systemically employed for angiographically suspected SCAD lesions [14], some cases transpired to be intracoronary thrombus manifesting as filling defect, even diffuse atherosclerotic lesions. In short, when a radiolucent dissection flap is seen angiographically, the diagnosis of SCAD is reasonably specific; in the absence of a dissection flap, angiography alone is not sufficiently sensitive enough to rule out SCAD, particularly the “diffuse stenosis” subtype caused by intramural hematoma mimicking atherosclerosis (Table 8.2).

The appearance of SCAD on IVUS was first reported by Maehara et al. [15] in 2002. These IVUS studies were important in establishing the two cardinal and pathognomonic features for SCAD on intravascular imaging: intimal dissection flap and intramural hematoma. As originally suggested from autopsy studies, spontaneous intramural hematoma was the first diagnostic feature for SCAD. The finding of an intimal flap progressed the understanding of SCAD, and raised several pathogenetic mechanism. One, a spontaneous separation developed between the arterial layers, allowing the development of a false lumen, eventually leading to the dual lumen. Second, a hematoma occurred spontaneously, with the expanding hematoma eventually rupturing into true lumen causing an intimal tear from the pressurized cavity.

The enhanced resolution of OCT over IVUS has now meant however that OCT may be the intracoronary imaging of choice in SCAD, although a definitive comparison between IVUS and OCT in SCAD is yet to be performed. The first comparison between the two modalities was reported by Poon et al. [16], who suggested potential superiority of OCT over IVUS. A subsequent eight patient series by Paulo et al. [17] demonstrated that the two modalities may be complementary.

The biggest limitation to OCT in the use of SCAD is the depth of penetration, particularly in the setting of thrombus and significant intramural hematoma where the external reference diameter is difficult if not impossible to assess. Indeed, in two recent OCT SCAD series (Paulo [17] and Nishiguchi [12]), thrombus and significant residual blood render OCT uninterpretable. In Paulo’s eight patient series, IVUS provided better definition on the external layer, better assessment of the heterogeneity within the intramural hematoma, and allowed for longer segments to be imaged. A summary of the characteristics of each imaging modality is presented in Table 8.2.