CASE PRESENTATION
A 59-year-old female smoker with a history of hyperlipidemia was
admitted for ST-segment elevation myocardial infarction (STEMI) in a
peripheral hospital. Transthoracic echocardiography (TTE) revealed
hypokinesis of the lateral wall, however systolic function was preserved
(left ventricular ejection fraction (LVEF) 55%).
She was immediately transferred to the catheterization laboratory, where
coronary angiography revealed type II spontaneous coronary artery
dissection (SCAD) of the left coronary system, initiating from the
distal part of the left main coronary artery (LMCA) (Figure 1A B,).
Initially stenting of the ramus intermedius was performed. During
stenting manipulations of the first diagonal and left anterior
descending (LAD) artery, the dissection extended retrogradely into the
LM and left coronary sinus (Figure2A). An additional stent was therefore
inserted to the LMCA until its ostium. Specifically, a 3.5mm x 26mm
stent followed by overdistension with a noncompliant balloon 4mm x 2mm
was introduced into the LMCA, with partial protrusion of its foci into
the aortic lumen. Because of the unimpeded flow in the circumflex
coronary artery, the dissection was left unhandled. No apparent residual
stenosis was seen after the procedure (Figure 2B).
The following day, transthoracic echocardiography (TTE) identified a
notable pericardial effusion leading to prompt pericardiocentesis, which
evacuated 540cc of bloody content. An urgent CT angiography revealed an
aortic intramural hematoma <1cm in size extending
longitudinally along the anterolateral side of the ascending aorta, from
the aortic root up to the origin of the innominate artery (DeBakey type
II). The aorta was 44-45mm in diameter.
Despite attempts to manage this conservatively with strict blood
pressure control on the coronary care unit, a repeat CT scan 12 days
later revealed expansion of the intramural aortic hematoma, and residual
pericardial effusion (Figure 3). Repeat TTE revealed worsening LV
systolic dysfunction (LVEF 40%) and hypokinesis of the lateral and
anterior-apical cardiac walls, suggesting compromised flow in the left
coronary system. The patient was escalated and transferred to the
cardiothoracic centre for definitive management.