Case Report
Iatrogenic Subtle Acute Aortic Dissection During Coronary Angioplasty for In-Stent Restenosis. Value of Intravascular
Ultrasoun
September 2004
Acute aortic dissection (AD) constitutes a life-threatening entity that requires early recognition and management.1–3 AD is a dynamic process with a broad clinical spectrum of presentation. In most patients AD occurs spontaneously as the result of cystic medial necrosis of the aortic wall.1–3 However, iatrogenic AD is also being increasingly recognized following cardiac surgery, balloon conterpulsation or coronary interventions.4–9 The occurrence of AD complicating coronary angiography is exceedingly rare. Iatrogenic AD during coronary interventions is also rare with an estimated incidence of 0.03–0.06%.4–9
The new diagnostic imaging techniques provide an excellent visualization of the aortic wall and have a very high sensitivity and specificity for the diagnosis of AD.2,3 These techniques have been also very helpful for guiding clinical decision making in patients with iatrogenic AD.2,7,9 However, despite such technical advances the diagnosis of AD remains notably challenging. Conditions such as aortic intramural hematomas, penetrating atherosclerotic ulcers and intimal tears without hematoma,10 are currently considered variants of AD that can elude clinical recognition.2,3,10 Likewise, minor iatrogenic aortic wall injuries may also be overlooked when only typical features of classic AD are considered.
In this report we describe a patient with a limited, subtle, iatrogenic AD following a coronary angioplasty procedure. Intravascular ultrasound (IVUS) was able to recognize and characterize this confined AD and also ensured adequate stent coverage of its coronary entry door. Both transesophageal echocardiography and magnetic resonance imaging failed to detect any significant aortic wall abnormality.
Case Report. A 46-year-old man with unstable angina was referred to our hospital for cardiac catheterization. One year ago he suffered an inferior myocardial infarction and 6-months later started with effort angina. At that time an occluded right coronary artery was successfully treated with two stents and another stent was required to treat a severe lesion on the mid left circumflex coronary artery. He remained asymptomatic until 3 months ago when he complained again of effort angina.
Physical examination was unremarkable. The electrocardiogram showed sinus rhythm and Q waves on inferior leads. Coronary angiography revealed a total occlusion (TIMI 0 flow) of the mid right coronary artery (RCA) just at the site where the proximal stent could be appreciated on fluoroscopy (Figure 1–1). The most proximal segment of the RCA also had a moderate stenosis with haziness. The distal RCA was well visualized by collateral circulation. The length of the occlusion was estimated to be of 20 mm. The left anterior descending coronary artery was normal and the circumflex coronary artery had an excellent angiographic appearance at the previously stented site. Left ventriculography revealed mild inferior hypokinesis with an ejection fraction of 60%.
During the attempts to recanalize the occluded RCA different wires where used. Eventually the Shinobi guidewire (Cordis Corporation, Miami Lakes, Florida) (sitting on a balloon catheter advanced proximal to the occlusion site) was able to cross the occlusion. Several inflations were performed at the level of the two stents with a 3 mm diameter balloon catheter (Crosssail, Guidant, ACS, Diegem, Belgium). A good result was obtained at the treated segment but the moderate lesion in the proximal RCA appeared to be more severe and presented a type B coronary dissection. Furthermore, a faint linear image of contrast retention was observed at the ostium of the RCA which also extended for a few milimeters into the right sinus of Valsalva. At this moment the patient complained of chest paint but no electrocardiographic changes were appreciated. The possibility of a iatrogenic AD of the aortic root was suspected. Therefore, a 3 x 18 Bx Sonic (Cordis Europe, Roden, The Netherlands) stent was implanted to cover the proximal RCA but also ensuring that the stent protruded 1–2 millimeters into the aortic root. Then, a 3.5 mm balloon was inflated up to 14 atmospheres to over-expand and flare the proximal margin of the stent. An excellent result was obtained at the level of the proximal RCA but the linear, localized image of contrast staining persisted on the aortic wall (Figure 1–2 and 1–3). Therefore, an IVUS interrogation (Ultracross, Boston Scientific Corporation, Sunnyvale, Calif.) of the proximal and mid RCA was performed. The two stents on the mid RCA still contained some residual neointima but had a large lumen. The new stent implanted in the proximal RCA showed full expansion and apposition along its entire length (Figure 2) and had a cone-shaped morphology. The proximal 1 mm of the stent clearly protruded within the aorta. This segment was carefully interrogated with IVUS after slightly retracting the guiding catheter in order to obtain a disengaged position. Then, the aortic wall immediately cranial to the right coronary ostium was interrogated. Special care was taken to slightly rotate the guiding catheter to visualize the aortic wall from different views. A crescentic-shaped aortic wall thickening was readily visualized (Figure 2). This image was characteristic of an intramural aortic hematoma11,12 with echogenic layering. Neither an aortic intimal tear nor an intimal dissection could be visualized. The remaining wall of the ascending aorta was absolutely normal. Transesophageal echocardiography, specifically performed to examine the right sinus of Valsalva, was unable to detect any significant abnormalities of the aortic wall. Nevertheless, the origing of the RCA could be easily identified by the bright echoes of the slightly protruding stent. A magnetic resonance imaging study performed 24 hours later also failed to detect any abnormalities on the aortic root. The patient remained asymptomatic during hospitalisation but experienced a mild rise in creatine kinase (488 U, 200 upper normal limit). He was discharged 4 days after admission on aspirin and clopidogrel. At 3-month follow-up he remained asymtomatic and had a negative exercise test.
Discussion. Coronary dissection is a common complication of balloon coronary angioplasty that may be readily managed with coronary stenting.13 Proximal progression of the dissection into the aortic root, however, is a unique complication that may represent a challenging therapeutic dilemma.4-7 Management of classic AD involving the ascending aorta requires surgical repair to prevent death from rupture or cardiac tamponade.1–3 However, in a previous report we suggested that the outcome of these iatrogenically induced aortic intimal tears is favourable when they remain stable and localized.7,8 Before adopting a conservative approach, however, one must fully ensure that the coronary entry door has been properly sealed with stents.7,8 Currently, sequential non-invasive imaging techniques provide reassuring information on this regard confirming the stable nature of the dissection3,7and supporting a “watchful waiting” strategy. Should any progression of AD be noted, a shift in management to an interventional strategy, aiming to the definitive repair the AD, need to be contemplated.
The mechanism responsible for the occurrence of AD during coronary interventions remains obscure.4–7 In most patients, however, an unnoticed, vigorous injection of contrast medium into the subintimal space appears to play a major role. In some cases, the entry site is located within the coronary artery, secondary to an intimal dissection caused by the guidewire, the balloon or the tip of the guiding catheter. From this location the contrast media advances retrogradely, cleaving the laminar plane of the media in two, and disperses into the aortic root. This further emphasizes the importance of sealing the coronary entry door. Aggressive attempts to recanalize coronary occlusions enhance the likelihood of subintimal disruption.4-7 In fact, most previously reported cases involve occlusions of the RCA.4–7 In our patient, the underlying substrate of in-stent restenosis could also have played a role, although the excellent angiographic results of repeated coronary interventions in this setting are well established.
In the International Registry of AD (IRAD)9 a iatrogenic etiology was demonstrated in 34 patients. Cardiac surgery was responsible for most cases of type A dissection, whereas coronary interventions accounted for most cases of type B dissections. Compared with spontaneous AD patients with iatrogenic AD were older and had a higher incidence of coronary risk factors and atherosclerosis. This study emphasized that the diagnosis of iatrogenic AD was difficult to make due to its atypical presentation and the relative lack of classical signs of AD.
Stevenson et al.10 recently suggested that despite the high sensitivity of modern imaging techniques, some patients with missed diagnosis of “subtle” classes of AD variants are increasingly being recognized. In these patients with subtle AD, an intimal tear without extensive undermining of the intima or intimal “flap” is recognized at operation. Most of such patients with undiagnosed AD had undergone multiple imaging techniques preoperatively. However, a characteristic aortic bulge is visualized on aortography. They suggested that in patients with suspected AD not proven by non-invasive imaging techniques further studies, including aortography in multiple views, should be performed.
IVUS provides accurate visualization of the aortic wall and is especially suited for patients with suspected AD and normal aortograms.11 Previous reports have described the value of IVUS in classic forms of AD11 and in patients with intramural hematomas.12 IVUS may also be of value in the diagnosis of traumatic aortic rupture where even subtle forms of intimal tears should be recognized. Moreover, the potential value of IVUS to guide fenestration interventional procedures in selected patients with AD and side-branch ischemia has been recently reported.14 To the best of our knowledge, however, the present report constitutes the first description of the value of IVUS in iatrogenic AD, both to confirm the diagnosis and to guide therapy. Our findings confirm that subtle and localized forms of iatrogenic AD may be overlooked by current non-invasive imaging techniques because still a better resolution is required in this setting. In patients with subtle iatrogenic AD a high index of clinical suspicion is warranted. Staining of contrast on the aortic wall during coronary procedures can not be disregarded as an incidental feature but should rise the possibility of subtle and confined iatrogenic AD. Careful analysis of the aortic root using several angiographic views is required. Persistent staining of the aorta associated with chest pain is sufficient for the diagnosis and should prompt therapy. However, IVUS may provide further insights and confirm the diagnosis in selected patients. Moreover, IVUS provides a unique visualization of the stent used to seal the entry door: expansion, apposition and location of the upper margin of the stent with respect to aortic-coronary junction.
1. Roberts WC. Aortic dissection: anatomy, consequences and causes. Am Heart J 1981;101:195–214.
2. Erbel R, Alfonso F, Boileau C, et al. Task Force on aortic dissection. European Society of Cardiology. Diagnosis and management of aortic dissection. Europ Heart J 2001;22:1642–1681.
3. Cigarroa JE, Isselbacher EM, DeSanctis RW, Eagle KA. Diagnostic imaging in the evaluation of suspected aortic dissection: old standards and new directions. N Engl J Med 1993;328:35–43.
4. Geraci AR, Krishnaswami V, Selman MV. Aortocoronary dissection complicating coronary arteriography. J Thorac Cardiovasc Surg 1973;65:695–698.
5. Moles VP, Chappuis F, Simonet F, et al. Aortic dissection as complication of percutaneous coronary angioplasty. Cathet Cardiovasc Diagn 1992;26:8–11.
6. Pande AK, Gosselin G, Leclerc Y, Leung TK. Aortic dissection complicating coronary angioplasty in cystic medial necrosis. Am Heart J 1996;131:1221–1223.
7. Alfonso F, Almería C, Fernández-Ortíz A, et al. Aortic dissection occurring during cioronary angioplasty: Angiographic and transesophageal echocardiographic findings. Cathet Cardiovasc Diagn 1997;42:412–415.
8. Alfonso F. Management of aortic dissection complicating coronary interventions. Cathet Cardiovasc Diagn 1998;43:491-492-493 (letter).
9. Januzzi JL, Sabatine MS, Eagle KA, et al. Iatrogenic aortic dissection. Am J Cardiol 2002;89:623–626.
10. Svensson LG, Labib SB, Eisenhauer AC, Butterly JR. Intimal tear without hematoma. An important variant of aortic dissection that can elude current imaging techniques. Circulation 1999;99:1331–1336.
11. Weintraub AR, Erbel R, Görge G, et al. Intravascular ultrasound imaging in acute aortic dissection. J Am Coll Cardiol 1994;24:495–503.
12. Alfonso F, Goicolea J, Aragoncillo P, et al. Diagnosis of aortic intramural hematoma by intravascular ultrasound imaging. Am J Cardiol 1995;76:735–738.
13. Alfonso F, Hernandez R, Goicolea J, et al. Coronary stenting for acute coronary dissection after coronary angioplasty: implications of residual dissection. J Am Coll Cardiol 1994;24:989–999.
14. Chavan A, Hausmann D, Dresler C, et al. Intravascular ultrasound-guided percutaneous fenestration of the intimal flap in the dissected aorta. Circulation 1997;96:2124–2127.
