Since it was first reported in 1931 , only 220 cases of SCAD have been documented in the literature, likely an underestimate because 60% to 80% of cases present as sudden cardiac death .
SCAD has been reported predominantly in young women, particularly during pregnancy and puerperium. The incidence in postmenopausal women is rare; a review of the existing literature is notable for only three other cases of SCAD in postmenopausal women above the age of 60 years . Of the three, one had diabetes and rheumatoid arthritis and one had severe systolic hypertension. The third women had no identifiable predisposing factors.
Our patient was postmenopausal, without any associated significant atherosclerotic disease, severe hypertension or other co-morbidities; and at 62 years of age, our patient is one of the oldest documented cases of SCAD on record.
The etiology of SCAD is likely multifactorial, the common insult being the weakening of the arterial wall, predisposing it to dissection. The proposed pathophysiologic mechanisms include inflammation and rupture of atherosclerotic plaques, enzymatic lysis of the arterial wall by peri-adventitial eosinophilic infiltrates in non-atherosclerotic vessels, changes in hormonal milieu associated with pregnancy and puerperium, presence of underlying vascular and connective tissue disorder, and mechanical weakening of the arterial wall caused by shear and stress associated with physical activity and cocaine use .
In atherosclerotic arteries, plaque inflammation and rupture can cause disruption of the intimal medial junction resulting in an intimal flap and subsequent intramural hematoma formation . Coronary artery spasm vasospasm has also been thought to result in SCAD, however it remains unclear whether the vasospasm leads to dissection or the dissection itself leads to secondary vasospasm . In the case of our patient, coronary angiography was remarkable for a single, non-critical proximal atherosclerotic lesion, with no impairment in coronary flow, followed by dissection with luminal compromise. It is our hypothesis that in this particular patient, the culprit lesion leading to ischemic symptoms and the ST elevation seen at the time of presentation was likely the result of a primary spontaneous dissection of the left anterior descending artery associated with secondary vasospasm.
Clinical presentations can span the clinical spectrum from unstable angina, to myocardial infarction and sudden cardiac death . There has been an increasing recognition of cases due to the increasing use and availability of imaging modalities including angiography, intravascular ultrasound and computed tomography angiography . Coronary angiography is considered the diagnostic test of choice . On angiography, the typical appearance is that of a radiolucent line that represents the intimal medial flap, separating the flow between the true and false lumens. However, an intimal flap may or may not be visualized .
The literature on SCAD largely consists of case reports and case series; in the absence of clinical trials and guidelines, treatment decisions continue to be a challenge. Regardless of the management employed, the primary concern is to maintain the patency of the true lumen . For patients presenting with an acute coronary syndrome, initial medical therapy should include antiplatelet and anti-ischemic agents along with anticoagulation with heparin . If the suspicion for coronary artery dissection is high, fibrinolytics should be avoided. This can be challenging in the postmenopausal setting where the most common cause of atherothrombosis continues to be atherosclerotic coronary artery disease. Fibrinolytics, although they may help re-establish anterograde flow in the true lumen , carry the risk of increasing flow into the false lumen and propagating the dissection . In patients with ongoing ischemia, revascularization with percutaneous coronary intervention or a coronary artery bypass graft should be undertaken; the decision to opt for either is largely based on the extent and location of the dissection . After the resolution of the acute phase, a search into the etiology of the dissection should be pursued to guide future management. In addition to aspirin and beta blockers, patients with underlying coronary artery disease should receive cholesterol-lowering medication, whereas those who are at a risk for or who have underlying coronary vasospasm should be started on a calcium channel blocker . Patients with SCAD during pregnancy or the peripartum period should be counseled on the increased risk of dissection associated with increasing parity and age .
Possible late complications include progression of the dissection and formation of pseudoaneurysms . Patients should be followed for any symptoms of recurrent ischemia . Stress testing with nuclear perfusion imaging is preferred over coronary angiography as a means of surveillance .
The overall survival for patients with SCAD has been reported as around 90%, with no significant difference in outcome being reported regardless of the treatment modalities employed .