Ann Thorac Surg 2008;86:453-456. doi:10.1016/j.athoracsur.2008.03.078
© 2008 The Society of Thoracic Surgeons
Original Articles: Adult Cardiac
Novel Insights Into the Mechanisms and Treatment of Intramural Hematoma Affecting the Entire Thoracic Aorta
Michael Grimm, MD*,
Christian Loewe, MD,
Roman Gottardi, MD,
Martin Funovics, MD,
Daniel Zimpfer, MD,
Suzanne Rodler, MD,
Marion Dorfmeister, MD,
Maria Schoder, MD,
Johannes Lammer, MD,
Seyedhossein Aharinejad, MD,
Martin Czerny, MD
Departments of Cardiothoracic Surgery and Interventional Radiology, University of Vienna Medical School, Vienna, Austria
Accepted for publication March 28, 2008.
* Address correspondence to Dr Grimm, Waehringer Guertel 18-20, Vienna, A-1090, Austria (Email: michael.grimm{at}meduniwien.ac.at).
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Abstract
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Background: The purpose of this study was to address a previously not described mechanism underlying intramural hematoma (IMH) of the entire thoracic aorta and to test the hypothesis whether endovascular stent graft placement in this particular mechanism could be beneficial.
Methods: Within a 5-year period, we treated 8 patients with IMH affecting the entire thoracic aorta. The presumed site of initial plaque rupture was chosen as target for endovascular stent graft placement.
Results: In all patients, a small atherosclerotic plaque at the free lateral wall or at the concavity of the distal aortic arch could be identified as initial site of IMH. Endovascular stent graft placement was performed successfully in all patients. By covering the suspected primary lesion, resorption of IMH especially within the ascending aorta could be achieved. Mean follow-up is 16 months (range, 1 to 25).
Conclusions: Plaque rupture may be identified as the cause of IMH in a previously unrecognized subgroup of patients. If at the convexity of the distal arch, supra-aortic branches prevent retrograde extension toward the ascending aorta. If at the free lateral wall or at the concavity, IMH may affect the entire thoracic aorta, owing to the lack of the natural barrier of the supra-aortic branches. Endovascular stent graft placement of this plaque-associated IMH may be more effective and less invasive than conventional surgery to treat the entire thoracic aortic disease.
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Introduction
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Intramural hematoma (IMH) of the aorta has been recently defined as a subtype of acute aortic wall dissection with no detectable intimal tear and, consequently, lack of false lumen flow [1]. Lack of presence of intimal disruption or flap is the prerequisite for IMH diagnosis [2]. A mostly crescentic high attenuation area with lack of contrast enhancement along the aortic wall is specific for this type of lesion [3]. If the ascending aorta is affected by IMH, conventional surgery rather than the risk factor–guided conservative treatment is the state of the art [4]. With the recent advances in imaging, in particular by electrocardiographic (ECG)-gating techniques, a more precise evaluation of IMH is possible. The presumed mechanism of IMH, rupture of vasa vasorum [5], however, may be doubted as in many IMH patients a small primary entry tear can be found. Therefore, such IMH patients who currently undergo high-risk conventional surgery could benefit from endovascular stent graft placement as a safe and effective treatment modality [6–8].
This study addresses a previously not described mechanism underlying IMH of the entire thoracic aorta and to test the hypothesis whether endovascular stent graft placement in this particular mechanism could be beneficial.
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Patients and Methods
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Between 2003 and 2008, 8 patients (6 male, 2 female) were referred to our department with IMH diagnosis affecting the entire thoracic aorta (mean age, 73 years; range, 53 to 86). All patients were referred within 48 hours of initial acute thoracic pain. Mean numeric EuroSCORE (European System for Cardiac Operative Risk Evaluation) was 13.3 (11 to 16), and mean logistic EuroSCORE was 44.5 (22.7 to 67.5). The Ethics Committee approved the study and waived the need for patient consent.
Imaging
All computed tomography (CT) examinations were performed on a 64-row CT scanner (Brilliance 64; Philips, Eindhoven, the Netherlands). To allow pulsation free visualization of the thoracic aorta up to the aortic root, a retrospective ECG-gating technique was used.
All CT angiograms were performed in the arterial phase during the intravenous administration of nonionic iodinated contrast material. A bolus triggering technique assessed the contrast medium transit time. The region of interest was the distal arch/descending aorta. A threshold of 150 HU (absolute) was used. In a biphasic fashion, 130 mL contrast agent was administered: the first 30 mL was injected at a flow rate of 6 mL/s followed by the second 100 mL administered at 5 mL/s. A saline flush of 40 mL was given to all the patients after the contrast medium injection to optimize contrast utilization. With a post-threshhold delay of 8 s, ECG-gated CT angiography of the entire aorta was performed using the following imaging parameters: a slice collimation of 64 x 0.625 and a pitch of 0.29 were used. The matrix size was 512 x 512. Images were reconstructed with a slice thickness of 1.4 and a slice increment of 1 mm as well as with a slice thickness of 3 and a slice increment of 2 mm without using the ECG-triggering ("untagged images"). Additionally, image redistribution according to the heart action was performed after scanning (retrospective ECG-triggering). Usually, images were triggered in a mid phase at 55% of a R-R interval. If pulsation artefacts occurred, other phases of the heart cycle were reconstructed. For every phase, two series were reconstructed (1.4/1 mm as well as 3/2 mm).
Stent Graft Placement
Stent grafts were placed under anesthesia. In all patients, a common femoral artery access was chosen. A 5F pigtail catheter was advanced through the right brachial artery into the aortic arch to reconfirm characterization of the morphology and extent of the lesion. After systemic heparinization therapy with 80 IU/kg, arteriotomy was performed and the catheter was advanced under fluoroscopic guidance. The stent graft was deployed during systemic hypotension with a systolic pressure of 60 mm Hg.
Stent grafts
Two different, commercially available stent graft systems were used. The Talent and the modified Valiant endovascular stent graft (Medtronic, Santa Rosa, California) were used in 7 patients. The Relay stent graft (Bolton Medical, Sunrise, Florida) was used in 1 patient. For both systems, the diameter of the stent graft was calculated from the largest diameter of the proximal or distal neck, and an oversizing factor of 10% was calculated.
Quality control
Immediately after stent grafting, patients underwent a completion CT scan to verify the effectiveness of the procedure. Within the initial 3 days after stent grafting, CT scans were repeated daily. Subsequently, a final CT scan was performed the day before discharge from hospital, then at 1, 3, and 6 months, and twice a year thereafter.
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Results
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Evaluation of IMH Mechanism
By using the imaging technique described above, rupture of a small atherosclerotic plaque at the free lateral wall or at the concavity of the distal aortic arch was identified as the underlying cause of the disease (Fig 1A and B;
Fig 2A and B). One patient required extension of the proximal landing zone by autologous double transposition, as described [9], before stent graft placement.
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Fig 1. (A) The computed tomography scan at diagnosis reveals a small atherosclerotic plaque at the lateral wall as the underlying cause of the disease. The arrow points at the plaque. (B) The intramural hematoma is seen within the ascending aorta.
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Fig 2. (A) The computed tomography scan at diagnosis reveal a small atherosclerotic plaque at the concavity of the distal aortic arch as the underlying cause of the disease. The arrow points at the plaque. (B) The intramural hematoma is seen within the ascending aorta.
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Short-Term Outcome
Stent grafting was successful, and complete cover of the suspected underlying cause of the disease was demonstrated by angiography in all patients. In 1 patient, balloon dilatation was performed to achieve sufficient alignment to the lesser curvature of the aortic arch. No procedure-related complications, including ischemia of the aortic branches, were noted. In 1 patient with pericardial effusion, subxyphoidal drainage was performed immediately after stent grafting.
Within the initial 3 days after stent graft placement, completion CT scans showed a progressive resorption of IMH especially within the ascending aorta in all patients, indicative of effective treatment (Fig 3A and B;
Fig 4A and B). The same mechanism could be observed in the descending aorta in 6 patients. In the remaining 2 patients, a classic type B dissection distal to the stent graft was observed after 1 week.
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Fig 3. (A) The patient shown in Figure 1 is shown after stent graft placement with successful coverage of the suspected underlying pathology. (B) Complete resorption of the intramural hematoma within the ascending aorta is seen.
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Fig 4. (A) The patient shown in Figure 2 is shown after stent graft placement with successful coverage of the suspected underlying pathology. (B) Complete resorption of the intramural hematoma within the ascending aorta is seen.
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Midterm Outcome
Mean follow-up was 16 months (range, 1 to 25). Patients have had an uneventful follow-up to date. Complete remodeling of the ascending aorta was observed in all patients. Endovascular leaks have not occurred so far.
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Comment
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The results suggest that when advanced imaging is applied, plaque rupture may be identified as the cause of IMH in a previously unrecognized subgroup of patients. If at the convexity of the distal arch, supra-aortic branches prevent retrograde extension toward the ascending aorta. If at the free lateral wall or at the concavity, IMH may affect the entire thoracic aorta, owing to the lack of the natural barrier of the supra-aortic branches.
Intramural hematoma accounts for almost 6% of acute aortic syndromes and is therefore a relevant pathology in incidence and consequence [1]. The treatment strategies of IMH remain controversial as the natural history of the disease is not fully understood [10–13]. If the ascending aorta is affected, especially in case of rapid progression or already detectable pericardial effusion, consent exists that these patients should undergo emergency replacement of the ascending aorta, similar to treatment of acute type A aortic dissection [4].
In contrast to classical type A dissection—with a detectable primary entry tear within the proximal portion of the thoracic aorta—during ascending aortic replacement for IMH, a primary entry tear is not detectable during open replacement. In this particular setting, it remains uncertain, whether the initiative mechanism of this life-threatening disease has been treated properly. Thus, these patients remain at risk of having further adverse events related to an unidentified lesion in other aortic segments distal to the treated area. More aggressive, complete arch replacement is often based on individual decision, resulting in substantial extension of surgery and potential risk of consequent collateral injury.
By using an advanced imaging system, we have detected rupture of a small atherosclerotic plaque at the free lateral wall or at the concavity of the distal aortic arch as the underlying disease mechanism in 8 patients admitted to our center with IMH diagnosis. We postulate that—after the plaque rupture—antegrade or retrograde progression, or both, of the pathology affects the aortic wall. If the primary lesion is located at the convexity of the aortic arch, we suggest that the supra-aortic branches may serve as a natural anatomical barrier against retrograde progression, thus resulting in predominant antegrade development as observed in type B dissection (Fig 5A, B). However, in case of a primary lesion located at the free lateral wall or at the concavity of the distal aortic arch, the lack of a natural anatomical barrier may permit retrograde progression down to the level of the aortic root (Fig 6A, B). This mechanism seems valid for both variants of acute aortic syndromes, IMH as well as dissection.
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Fig 5. (A, B) Computed tomography scan at diagnosis of a patient with a type B dissection with the primary entry tear being located at the convexity of the proximal descending aorta (arrow), showing the classical antegrade component as well as the retrograde component of the dissection ending at the level of the left subclavian artery owing to its function as an anatomical barrier.
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Fig 6. (A, B) Computed tomography scan at diagnosis of a patient with a type B dissection with the primary entry tear being located at the concavity of the distal aortic arch (arrow), showing the classical antegrade component as well as a retrograde type A dissection extending into the aortic root owing to no existing anatomical barriers in this region.
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Limitations and Potential Contraindications for This New Treatment Approach
The major limitation of this study is the low number of patients in a single-center study. Definitely, the IMH treatment proposed here deserves further studies. We do believe that all patients in whom a clearly defined point of entry cannot be demonstrated are not candidates for this approach, as endovascular therapy may be counterproductive and harmful. This should be a prerequiste for this approach.
Summarizing, we conclude that plaque rupture may be identified as the cause of IMH in a previously unrecognized subgroup of patients. If at the convexity of the distal arch, supra-aortic branches prevent retrograde extension toward the ascending aorta. If at the free lateral wall or at the concavity, IMH may affect the entire thoracic aorta, owing to the lack of the natural barrier of the supra-aortic branches. Endovascular stent graft placement of this plaque-associated IMH may be more effective and less invasive than conventional surgery to treat the entire thoracic aortic disease.
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References
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Abstract
Introduction
