Spontaneous coronary artery dissection (SCAD) is a rare and potentially life-threatening condition that can cause rapid deterioration and fatal myocardial infarction. By definition, SCAD implies formation of a false lumen around the true lumen of the artery, which may or may not communicate with the true lumen. By compression of the true lumen, this may cause a blockage of the coronary flow, resulting in myocardial infarction (MI). Early recognition is important as the dissection can progress unpredictably upstream or downstream. Potential associations have been made between this condition and female gender, pregnancy, cystic medial necrosis, cocaine abuse, and collagen vascular disorders. We present a case report of a relatively healthy individual with no significant past medical history who presented with stroke, with the work-up revealing MI from SCAD. The patient was treated successfully using percutaneous coronary intervention.
A 60-year-old Caucasian male with no significant past medical history and no allergies was admitted with a complaint of left-sided numbness followed by weakness in the left arm and leg. The patient was an active smoker who had smoked one pack per day for several years. His family history was negative for heart attack, stroke, diabetes, hypertension, or any other disorders, including collagen vascular diseases. The clinical impression was acute cerebrovascular accident within three hours. Computed tomography without contrast ruled out any bleed and the patient was given tissue plasminogen activator. Subsequent magnetic resonance imaging of the brain showed an acute infarct in the posterior limb of the right internal capsule, although magnetic resonance angiography was unrevealing. During his subsequent hospitalization, the patient regained power in his left upper and lower extremities.
Work-up was initiated to find the cause, including finding a possible hypercoaguable state. The patient did not complain of significant chest pain, but had an abnormal electrocardiogram with Q-waves in the anterolateral leads. Troponin I was 0.04 ng/ml. Two-dimensional echocardiography showed anterolateral hypokinesis to akinesis with an ejection fraction of 35–40 %, suggesting anterolateral MI. The patient was started on a heparin drip, which was subsequently stopped. The patient was continued on aspirin, clopidogrel bisulfate, and beta-blockers, and a plan was made for cardiac catheterization. The thought process was that a clot in the left ventricle was formed because of MI which might have embolized, causing acute stroke.
Left heart catheterization was performed and showed an aortic pressure of 116/76 mmHg, a left ventricular pressure of 100/2 mmHg, and a left ventricular end-diastolic pressure of 5 mmHg. There was no gradient across the aortic valve. Catheterization showed that the left main coronary artery (LMCA) was of a decent size with mild irregularities. No significant disease was found in the LMCA. The left anterior descending artery (LAD) was a good-sized 3 mm vessel with what seemed like a spontaneous coronary dissection at the second diagonal branch (see Figure 1). The second diagonal branch had a fairly long dissection involving the ostium as well as the proximal area. The distal LAD had mild diffuse disease and no dissection. The first diagonal branch was a good size with fairly diffuse disease starting from the ostium. The left circumflex artery (CFx) was a non-dominant, fairly large vessel with about 30–40 % ostium disease. The CFx in the atrioventricular groove was a medium-sized vessel with mild irregularities. A stent was placed in the spontaneous coronary dissection in the mid-LAD area, with no post-catheterization complications (see Figure 2). Subsequent images showed complete resolution of dissection (see Figure 3).
This case represents a unique manifestation of SCAD which possibly led to MI, resulting in clot formation in the akinetic left ventricle which possibly embolized systemically, leading to acute stroke.
SCAD is thought to account for about 0.1–0.28 % of all patients with acute coronary syndrome or sudden cardiac death.1 The pathophysiology of SCAD is thought to be a result of a bleed into the vessel wall from the lumen itself.2 The process may be initiated in the media and adventitia of the vessel wall. The resulting hematoma may expose the endothelium to added stress, causing intimal tear. The hematoma results in luminal compression, limiting antegrade flow. Various associations of SCAD include a younger and predominantly female population, particularly in the peri- and post-partum periods, increased shear stress such as after exercise or sneezing, and cocaine abuse. Heritable connective tissue disorders, such as Marfan’s syndrome and Ehlers-Danlos syndrome, and autoimmune connective tissue disorders and vasculitides have been associated with SCAD. Cystic medial necrosis has been reported in some post mortem cases of SCAD.
Medical management alone is insufficient and may be a bridge to endovascular stenting. Beta-blockers may be employed. The role of thrombolytic and antiplatelet agents is controversial.
Stenting the SCAD is very challenging, with a risk of inserting the guidewire into the false lumen. Sometimes, the dye might not penetrate the false lumen sufficiently. If an entry point is identified by angiography, a stent can be applied to this proximal entry point, creating a sort of seal.3 However, in a significant number of cases the dissection is too long for a single stent to be sufficient; in these cases, multiple continuous stents may be employed to hold the dissection in place.
In the case described above, a single stent to the entry point of the dissection was employed to seal the lesion, which resolved the problem. The dissection involved a good-sized vessel with a caliber of 3mm. Authorities on the subject advocate conservative management with beta-blockers for SCAD in vessels with a caliber of less than 2 mm. In our case, intravascular ultrasound (IVUS) was not employed to delineate the entry point. IVUS has been advocated by some authorities to define the entry point before attempting to pass the guidewire and stent the lesion.
In our patient, SCAD was most likely the cause of MI. SCAD is a relatively rare condition that still presents a challenge to the interventional cardiologist.4 There should be a high index of suspicion in high-risk cases such as young females, peri-partum cases, and patients with drug abuse or a family history of connective tissue diseases. The case discussed above is unique in that no such association was present except possibly a history of smoking, which has not been associated with this condition. It is also interesting to note the downstream effects of SCAD, with possible clot formation in the left ventricle with sytemic embolization, leading to very unique presentation of SCAD.
Efforts are ongoing to better understand and approach this condition. More cardiologists are encouraged to report this condition. In this regard, the DISCOVERY registry is an important initiative which aims to log these cases and better define the true significance of SCAD.1