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J Thorac Cardiovasc Surg 2003;125:1548-1550
© 2003 The American Association for Thoracic Surgery
Brief Communications |
From the Thoracic and Cardiovascular Surgery Department, University Hospital of Caen, France,a and the Vascular Surgery Department, University Hospital of Siena, Italy.b
Received for publication Aug 10, 2002. Accepted for publication Sept 9, 2002. Address for reprints: Massimo Massetti, MD, Thoracic and Cardiovascular Surgery Department, University Hospital, 14033, Caen, France (E-mail: massetti-m{at}chu-caen.fr).
Acute myocardial ischemia or infarction as a result of retrograde coronary artery dissection is a well-known complication after acute type A aortic dissection.
1 Although the prevalence of chronic coronary artery disease among patients with acute dissection of the ascending aorta has been reported to be between 8% and 41%, 2 retrograde dissection of the aortic root reaching the coronary ostia is the most typical cause of acute coronary malperfusion observed in this condition. 1 However, other mechanisms of myocardial ischemia, related to the diastolic expansion of the false aortic channel, have been described by Borst. 3
We present here the case of a patient with acute type A aortic dissection in whom an acute coronary malperfusion was sustained by an atypical mechanism of flow obstruction.
Clinical summary
A 49-year-old man with a history of hypertension and sarcoidosis was transferred from an outlying hospital to our institution in severe cardiogenic shock. Two hours previously, he had experienced the sudden onset of acute chest pain, followed within a few minutes by shortness of breath and severe hypotension. A 12-lead electrocardiogram showed diffuse ST-segment depression and T-wave inversion with an anterior ST elevation (without a related Q wave). A transthoracic echocardiogram was not of diagnostic quality because of a poor acoustic window. Intravenous heparin, inotropic support, and mechanical ventilation had been given without any change in the patient's condition. Systemic fibrinolysis was administered without improvement. At the time of arrival at our institution, the patient had a blood pressure of 68/45 mm Hg and an irregular pulse of 110 beats/min. The peripheral pulses were weak but symmetric. Preoperative creatine kinase MB levels were not significantly elevated.
Transesophageal echocardiography was performed to obtain an analysis of the left ventricular segmental wall motion before urgent coronary angiography; surprisingly, it demonstrated the presence of an intimal flap in the ascending aorta with a circumferential distal disruption of the inner aortic wall layers. The cylindric flap presented a proximal invagination movement through the aortic valve, inside the left ventricle, during diastole (Figure 1). This diastolic intussusception of the tubular flap determined the flow obstruction of the coronary ostia and the subsequent myocardial malperfusion. Global biventricular wall motion abnormalities and a left ventricular ejection fraction of 0.25 were demonstrated. We decided to operate on the patient without delay.
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On opening the aorta, we found a circumferential tear of the intima that had caused the described proximal intussusception. Above the level of the right coronary ostium, the tubular flap was partially lacerated, making residual coronary arterial perfusion still possible. The aorta below the sinotubular junction was spared. Surgical treatment consisted of the complete resection of the dissected portion of the ascending aorta and, after generous mobilization of the aortic arch and of the heart (by freeing the inferior vena cava at its diaphragmatic passage), a direct aortoaortic anastomosis with a 4-0 polypropylene suture. Despite the short duration of the aortic repair, the use of controlled reperfusion, and the absence of bleeding complications (although the patient had received systemic fibrinolysis), weaning from cardiopulmonary bypass was complex as a result of poor left ventricular performance. Cardiac compression by sternal closure was not tolerated; delayed sternotomy closure was therefore necessary. Inotropic requirements decreased from the immediate postoperative period to the 5th postoperative day just before chest closure (on 6th postoperative day), indicating patient stabilization. Postoperative creatine kinase MB level (peak creatine kinase MB 45 IU/L) returned to normal, and significant recoveries form segmental wall motion abnormalities were observed: left ventricular end-systolic volume decreased from 170 to 120 mL/m2, left ventricular end-diastolic volume decreased from 99 to 57 mL/m2, and left ventricular ejection fraction increased from 0.25 to 0.4.
The subsequent postoperative course was uneventful. The patient recovered well from the operation and was discharged on postoperative day 17. Histologic examination of the aortic wall specimen showed cystic medial necrosis.
Discussion
In 1962, Hufnagel and Conrad 4 first described the circumferential disruption of the inner aortic wall layers of the ascending aorta and its subsequent distal invagination. They named this particular presentation of acute aortic dissection intimointimal intussusception. To date, all cases described in the literature 5 have shown a distal invagination. In our patient the presence of a proximal invagination determined this atypical presentation with coronary malperfusion. In the presence of an established diagnosis of acute aortic dissection, the presence of coronary malperfusion and myocardial ischemia can be easily ruled out by simple diagnostic and laboratory investigations. Conversely, aortic dissection is not often considered a cause of myocardial malperfusion; thus misdiagnosis, which represents one of the main preoperative risks for these patients, may frequently occur. 1 This was the case for our patient, to whom systemic thrombolytic treatment was given before a diagnosis of acute aortic dissection was made.
The subsequent surgical treatment was strongly influenced by this inadvertent treatment, which induced us to avoid any prosthetic material to replace the ascending aorta and imposed a closed technique of anastomosis to avoid hypothermic circulatory arrest. It should be said, however, that the limited longitudinal extension of the dissection was well suited to the repair technique.
This procedure does not fulfill the radical criteria advocated by some authors in the settings of acute type A dissection. 6 However, it should be underlined that the resection included the entire dissected portion of the aorta and that the parts left in place exhibited a completely normal aspect.
References
This article has been cited by other articles:
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  S-M KO MDCT findings of acute aortic dissection with diastolic prolapse of the intimal flap into the left ventricle Br. J. Radiol., May 1, 2009; 82(977): e95 - e97. [Abstract] [Full Text] [PDF]
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 W. Whitley, K. A. Tanaka, E. P. Chen, and K. E. Glas Acute Aortic Dissection with Intimal Layer Prolapse into the Left Ventricle Anesth. Analg., April 1, 2007; 104(4): 774 - 776. [Full Text] [PDF]
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