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.