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.