Discussion
SCAD mainly affects middle-aged women comprising 87% to 95% of all cases with a mean age ranging between 44 to 53 years. There also have been few cases reported in teens and elderly as well. Out of all patients who present with ACS, SCAD’s prevalence is estimated to be 4%. In addition, SCAD accounts for up to 35% of ACS in women under 50 years of age, a number that may be underestimated given that SCAD is often both underdiagnosed and misdiagnosed. According to multiple studies, SCAD often co-exists with other conditions and is initiated by various triggers. In a descending order of prevalence, such co-existing conditions may include FMD, hypertension, connective tissue disorders, migraine, genetic susceptibility, and pregnancy. Some of the triggers may include hormone imbalance, significant emotional distress, intense exercise, medications and illicit substances [8, 10-11].
One of the developing and well-supported explanations for the pathophysiologic emergence of SCAD is the “outside-in” hypothesis. It attributes the initiating event to a primary hemorrhage of a vaso vasorum within the medial coronary layer. As a sequelae, the new-born hematoma may either self-dissolve or further expand in a longitudinal and circumferential fashion, creating a false lumen that eventually accumulates to compress and narrow the true lumen causing ischemic symptoms. SCAD is classified into 4 types based on angiographic appearance. Type 1 is pathognomonic arterial wall staining by contrast dye with multiple radiolucent lumens. Type 2 is diffuse, long, and smooth stenosis of variable degrees. Type 3 often mimics atherosclerotic lesions and is the most often to be misdiagnosed requiring further characterization and specialized imaging. Type 4 is complete occlusion of distal coronaries mimicking coronary embolism (Figure 5)9 . The majority of SCAD cases present as type 2, which is mainly seen in the mid-to-distal left anterior descending coronary artery lesions [10].
Although advancements in the understanding of SCAD’s pathophysiology have been made, the predilection to certain sides and segments of the coronary arteries remains unclear. SCAD tends to present in the distal coronary arteries and its smaller branches. Specifically, it has the propensity to affect the mid-to-distal portions of the LAD. [8,10]. In a study by Jackson et al that focused on the pathophysiologic mechanisms through optical coherence tomography of 65 SCAD cases, the percentage affecting the left main stem and the proximal LAD coronary artery were 1% and 4%, respectively. In comparison, the percentage found within the distal portions of the LAD coronary artery was 45% [12]. Studies have yet to explore this regional favoritism of SCAD, but it is thought to be influenced by physical mechanics of blood flow, native structural differences within certain areas of the tunica media, or a combination of both. Thus far, the literature has not revealed such explanations to any epidemiological or genetic basis for a high prevalence within the aforementioned coronary segments.
Although guideline-supported treatment of SCAD, once confirmed by coronary angiography, is stent; a growing number of clinicians and centers opt to manage conservatively without PCI, especially if coronary flow is preserved and the lesion is distal. As high as 95% of such cases commonly undergo spontaneous resolution within 30 days [13]. Conservative management is favored because of the unpredictable outcomes of PCI as well as the myriad of complications including PCI failure due to unwanted false lumen interactions with the wire or the stent itself, or iatrogenic expansion of the dissection which happens in up to one third of cases.In a study by Tweet et al, proximal and ostial left main coronary arteries in SCAD had the lowest rates of conservative treatment compared to lesions in the mid-to-distal portions.[14]. Therefore, patients with proximal SCAD lesions, such as ours, are at a propagated disadvantage given the innate risks associated with intra-angiographic and post-PCI outcomes.