Case Report
Figure 1: Spontaneous Coronary Artery Dissection in the Left Anterior Descending Artery Just Before Branching of the Second Diagonal Branch Caption notes
The American Heart Hospital Journal
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.
Discussion
SCAD is thought to account for about 0.1–0.28 % of all patients with acute coronary syndrome or sudden cardiac death.1
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
126 Spontaneous Coronary Artery Dissection Presenting with Stroke
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
Winter 2011
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