DISCUSSION
Percutaneous coronary intervention (PCI) in SCAD patients is associated
with high rates of complications. Iatrogenic coronary artery dissection
(ICAD) is very infrequent, but a tremendous complication after coronary
angiography in the general population, <0,2%.(3) Prakash et al. found the incidence to be 2%
during diagnostic coronary angiography alone and up to 14,3% among
patients with PCI on SCAD. (3) PCI in the presence of
SCAD is technically more challenging. Maneuvering inside the coronary
arteries can provoke propagation of the dissection ante- or retrogradely
no infrequently, which in turn results in expansion of the area of
myocardial ischemia. Forced and intense injection of the contrast medium
must be avoided. (4,5)
Although rare, iatrogenic retrograde extension of the dissection into
the ascending aorta (0,02 – 0,6% of diagnostic and interventional
percutaneous procedures) is reported.(6) Dunning et
al. have found a significantly increased rate in aortocoronary
dissections in procedures performed for acute myocardial infarction
(AMI) (0,19%) compared with non-AMI cases (0,01%).(7,8) To our knowledge, this is the first reported
case of type A aortic dissection after PCI for AMI due to SCAD. More
frequently, iatrogenic type A aortic dissection involves the right
coronary artery because it is more susceptible to trauma from a guide
catheter than the LM. (7) In our case, the dissection
extended from the LM to the aorta because of preexisting SCAD in the
left coronary artery system.
Aortocoronary dissection is usually suspected at the time of coronary
intervention. According to Dunning et al. criteria, the aortocoronary
dissection is distinguished into three classes: Class I when the aortic
dissection involves the ipsilateral cusp. Class II, when it includes
cusp and extends up to the aorta for less than 40mm and Class III as for
Class II but at length over 40mm. (8) There are no
guidelines for treating aortic dissection caused by PCI.(9) The best treatment in Classes I and II seems to be
the stenting of the coronary artery, including the respective ostium
trying to seal the entry point of the dissection. Then consider
conservative management with intensive clinical follow-up. Additional
imaging controls are necessary only in unstable patients and if there is
evidence of progression of the lesion. In contract, Class III mandates
more aggressive surgical management. (7,8,10) In our
case, the presence of abundant pericardial effusion the day after PCI
comprised a high index of suspicion of progression of the known
retrograde aortocoronary dissection. The CT scan revealed a Class III
aortocoronary dissection: dissection with IMH of the ascending aorta
extending from the left coronary sinus to the inferior limit of the
innominate artery origin (Figure 3A). Besides the fact that the patient
was stable and there was no evidence of active flow of contrast media in
the false lumen, the delay of surgery just reconfirmed the necessity of
emergent intervention in Class III aortocoronary dissection. Indeed, as
shown on the revaluation with CT scan on day thirteen, there was an
increase of the aortic hematoma despite the initial invariable CT image
on day eight of hospitalization.