Case Presentation. A 63-year-old Caucasian male with multiple cardiovascular risk factors including hypertension, dyslipidemia, history of smoking and a positive family history experienced an antero-apical myocardial infarction (MI) 12 years ago followed by a clinically stable and uneventful course. Approximately 6 months before the actual event, the patient presented with increasing anginal symptoms and underwent percutaneous revascularization. At that time, ventriculography documented a hypokinetic apex and a global ejection fraction of 62%. Coronary angiography revealed a distal chronic occlusion of the left anterior descending coronary artery (LAD), severe stenoses of the first diagonal branch (DB1), an occluded first and a severely narrowed second posterolateral branch (PLB2) of the circumflex coronary artery. The DB1 and PLB2 were successfully treated with sirolimus-eluting stents using a Launcher EBU 4.0 6 Fr guide catheter (Medtronic, Inc., Minneapolis, Minnesota) and the patient was discharged. He remained free of symptoms for about 6 months before again developing angina for which he was readmitted for invasive coronary artery evaluation. Coronary angiography was performed by an experienced operator (several years of catheterization laboratory experience, over 5,000 interventions). Arterial access via the right femoral artery was uncomplicated. However, because of a marked kinking of the pelvic arteries, a 30 cm sheath had to be placed. The left main coronary artery was selectively cannulated with a diagnostic 5 Fr Judkin’s Infiniti Left-4 catheter (Cordis Corp., Miami Lakes, Florida), and the right coronary artery with a diagnostic 5 Fr Judkin’s Infiniti Right-4 catheter (Cordis). The right coronary artery (RCA) was free of stenoses. Although there was no evidence of restenosis within the stents in DB1 and PLB2, the angiogram revealed a rapid progression of atherosclerosis in the distal left main artery (60% stenosis), the LAD (serial 50% stenoses) and the proximal circumflex (80% stenosis); the latter was considered to be the culprit lesion. The patient received 8,000 U of heparin intravenously, but no glycoprotein IIb/IIIa receptor antagonist. After three attempts to intubate the left main coronary artery with a 6 Fr Amplatz Launcher Left-2, the patient suddenly complained of a migrating pain starting in the neck to the back; he then rapidly became hypotensive and developed a slow junctional backup rhythm (45 bpm) requiring administration of atropine (1 mg intravenously).
Venous femoral access was obtained, and volume resuscitation was begun. An angiogram of the thoracic aorta revealed a double-contoured ascending aorta (Figure 1); the entire aorta appeared dilated. Coronary angiography demonstrated no dissection entry. An immediately performed transesophageal echocardiography confirmed the diagnosis of an acute aortic dissection with a supracoronary entry not affecting the coronary arteries, with only mild aortic regurgitation due to a detachment of the left and non-coronary commissure of the valve (Figure 2). The dissection extended to the descending aorta.
The patient was sent to the operating room without delay. After an unsatisfactory reconstruction attempt of the aortic valve, an Edwards Lifesciences (Irvine, California) Model 2900 Nr 27 prosthesis was implanted, the supracoronary thoracic aorta and half of the aortic arch was replaced (24 mm Vascutec Gelweave™, Sulzer Vascutec, Renfreshire, Scotland), and venous bypass grafting to the posteroventricular branch and LAD were performed. The patient’s recovery was uneventful. Histological workup of the aortic fragments demonstrated myxoid degeneration, as well as a disturbed architecture of the elastic fibers and patchy fibrosis of the aortic wall in all fragments that were examined (Figure 3). The patient showed no clinical features of a hereditary connective tissue disease. Furthermore, a skin biopsy was normal and revealed no signs suggesting the presence of Marfan’s or Ehlers-Danlos Syndrome.
Discussion. Acute aortic dissection during cardiac catheterization is a very rare complication. It has been reported with an overall incidence of 0.02%, more often in the emergency setting of acute myocardial infarction (AMI, 0.19%) than in an elective setting (0.01%).1 The incidence is generally higher during percutaneous interventions (overall 0.03%) than with diagnostic procedures (0.10% in AMI, < 0.01% in elective settings).1 In most of the previously reported cases, the entry point originated within a dissected coronary artery (predominantly RCA) with progressive retrograde dispersion within the subintimal space in the aortic root. Only a few reports of isolated dissection of the aorta without involvement of coronary arteries are published in the literature.2
Several risk factors may be involved under such circumstances. Susceptibility to dissection may be related to an underlying structural weakness of the media. Predisposing conditions include hypertension, Marfan’s, and Ehlers-Danlos Syndrome, congenitally unicuspid and bicuspid aortic valves and cystic medial necrosis.3 The role of cystic media necrosis, however, is controversial, as low grades of degeneration are nonspecific and commonly occur with aging.4,5 Severe atherosclerosis has been suggested to weaken the media through impaired nutrition and ulcerated plaques that may serve as entry points for pulsatile blood flow.6 Indeed, an unusually kinked iliacal vessel, as in the case presented here, may reflect abnormal vasculature.
In addition, operator-related risk factors such as the use of Amplatz catheters were reported to be involved in a disproportionate number (44%) of catheter-induced dissections.1 Moreover, subintimal passage of a guidewire or inadvertent handling of guide catheters may open the subintimal space. Furthermore, vigorous hand injection of contrast medium may provide further dispersion. In the acute setting, cardiac catheterization for AMI can be considered an independent risk factor. Haste of the operator to rapidly achieve myocardial reperfusion, as well as an increased state of vascular inflammation that typically occurs in AMI, may facilitate such a complication. In the presented case, an experienced operator made three gentle attempts to intubate the left coronary artery with little dye injection prior to dissection; neither vigorous injection of the contrast agent nor aggressive manipulation with the catheter was involved. The Amplatz catheter was chosen (as opposed to the EBU, which was used in the intervention 6 months earlier) in order to access the very calcified and tortuous right circumflex artery (RCX) with better backup to perform the intervention on these complex serial RCX lesions. If the entry of the dissection is within a coronary artery and the dissection does not extend > 40 mm up the ascending aorta, attempts can be made to seal the entry with an intracoronary stent.1
In some cases, the aneurysm may resolve spontaneously in the first month without need for surgery.7 Progression of the dissection through the entire ascending aorta, and particularly to the descending aorta, or failure of entry sealing with a stent are indications for urgent surgical treatment. In this patient, the entry was above the left coronary ostium, suggesting that slipping of the tip of the Amplatz catheter along the ascending aorta created the intimal flap. Histology of several fragments of the aorta revealed a fresh dissection in the outer half of the media, which showed irregular and focally missing elastin fibers and myxoid degenerations in certain areas. As these changes occurred in all segments examined, these findings strongly point to this patient suffering from some sort of structural tissue disorder rather than representing a histological artifact.
In summary, this case demonstrates an iatrogenic acute aortic dissection with a supracoronary entry without involvement of the coronary arteries, which most likely occurred as a result of a combination of factors including an underlying structural tissue disorder of the vessel wall, a dilated aorta, as well as the use of the rather “aggressive” Amplatz guide catheter. Fortunately, in this case, swift and appropriate measures were undertaken and the patient recovered well after emergency replacement of the supracoronary thoracic aorta and half of the aortic arch. Acknowledgements. The authors would like to acknowledge Dr. B. Sasse for provision of the histological slides, and Prof. R. Jenni for provision of the echocardiographic images.
- Dunning DW, Kahn JK, Hawkins ET, O'Neill WW. Iatrogenic coronary artery dissections extending into and involving the aortic root. Catheter Cardiovasc Interv 2000;51:387–393.
- Mauser M, Ennker J, Fleischmann D. Dissection of the sinus valsalvae aortae as a complication of coronary angioplasty. Z Kardiol 1999;88:1023–1027.
- Spittell PC, Spittell JA Jr, Joyce JW, et al. Clinical features and differential diagnosis of aortic dissection: Experience with 236 cases (1980 through 1990). Mayo Clin Proc 1993;68:642–651.
- Carlson RG, Lillehei CW, Edwards JE. Cystic medial necrosis of the ascending aorta in relation to age and hypertension. Am J Cardiol 1970;25:411–415.
- Schlatmann TJ, Becker AE. Histologic changes in the normal aging aorta: Implications for dissecting aortic aneurysm. Am J Cardiol 1977;39:13–20.
- Wilson SK, Hutchins GM. Aortic dissecting aneurysms: Causative factors in 204 subjects. Arch Pathol Lab Med 1982;106:175–180.
- Perez-Castellano N, Garcia-Fernandez MA, Garcia EJ, Delcan JL. Dissection of the aortic sinus of Valsalva complicating coronary catheterization: Cause, mechanism, evolution, and management. Cathet Cardiovasc Diagn 1998;43:273–279.