Ann Thorac Surg 2004;77:1075-1077
© 2004 The Society of Thoracic Surgeons
Case report
Pinhole rupture of aortic root aneurysm with severe atherosclerotic change
Hidenori Sako, MD, PhDa*,
Tetsuo Hadama, MD, PhDa,
Osamu Shigemitsu, MD, PhDa,
Shinji Miyamoto, MD, PhDa,
Hirofumi Anai, MD, PhDa,
Tomoyuki Wada, MD, PhDa,
Naoki Hijiya, MD, PhDb
a Departments of Cardiovascular Surgery Oita Medical University, Oita, Japan
b Pathology, Oita University, Oita, Japan
Accepted for publication April 14, 2003.
* Address reprint requests to Dr Sako, Department of Cardiovascular Surgery, Oita University, School of Medicine, 1-1 Idaigaoka, Hasama, Oita 879-5593, Japan
e-mail: sakoh{at}med.oita-u
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Abstract
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We report two cases of the rupture of calcified aortic root aneurysms that were successfully treated by emergency operations. One patient underwent Bentall's operation, and for the other, we performed a valve-sparing operation. Because their aneurysms revealed pear-like configurations with aortic regurgitation, the findings were consistent with annuloaortic ectasia (AAE). However, both cases were unlike typical AAE in that the aortic walls showed severe atherosclerotic change, with little sign of cystic medial necrosis. It was very interesting that each rupture point was a very small pinhole originating from one of the atherosclerotic ulcers.
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Introduction
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Annuloaortic ectasia (AAE) shows dilatation of the ascending aorta and the sinus of Valsalva with aortic regurgitation. It is commonly complicated with aortic dissection because of the laceration of the aortic intima [1]. One of the major pathologic changes in AAE is cystic medial necrosis [1, 2]. We encountered two cases of the rupture of aortic root aneurysms with hemopericardium. Although the patients' clinical diagnoses were compatible with AAE, their aortic walls showed severe atherosclerotic changes, with little sign of cystic medial necrosis. Each rupture point was a very small pinhole originating from one of the atherosclerotic ulcers.
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Case reports
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Case 1
A 53-year-old man was admitted to our hospital with sudden-onset severe chest pain and a fainting attack. On physical examination, his heart rate was 110 beats per minute with regularity, and his blood pressure (BP) was 97/58 mm Hg. A grade II/IV early diastolic decrescendo aortic regurgitant murmur was heard. His white blood cell count was elevated to 13,300 per cubic millimeter, and no anemia was observed. Computed tomography (CT) of the chest showed hemopericardium and aneurismal change of the aortic root. Severe calcification of the aneurismal wall was observed, and the maximum diameter of the aneurysm was 70 mm (Figs 1B, 1C). Although the calcification of the root aneurismal wall was very severe, there was little calcification and no aneurismal change in the descending or abdominal aorta. Echocardiography revealed moderate aortic regurgitation and dilatation of the ascending aorta extending down to the sinuses of Valsalva and the aortic annulus, consistent with AAE. The patient underwent an emergency operation. Before median sternotomy, cannulations through the right axillary artery and the left femoral artery were established. Venous drainage was accomplished with a single cannula in the right atrial appendage. The operative findings showed a pear-like root aneurysm with hemopericardium (Figs 1A, 1B). The rupture point was a very small pinhole occluded with thrombus (Figs 1A, 1C). Cardiopulmonary bypass was begun, and the ascending aorta was cross-clamped after confirming that there was no fragile atheromatous plaque at the clamping site using intraoperative echography. The inside of the aneurismal wall showed severe arteriosclerosis, and the pinhole rupture point was originating from one of the atherosclerotic ulcers (Figs 1A, 1C). The aortic root was replaced with a tube graft (Gelseal [Vascutek Ltd, Inchinnan, United Kingdom], 26 mm) and a 25-mm prosthetic valve (St. Jude Medical, St. Paul, MN). Both coronary arteries were reconstructed with the Carrel patch method. The postoperative course was uneventful. The pathologic findings revealed severe atherosclerotic changes and the transmural rupture of the aortic wall. There was little sign of cystic medial necrosis in the peripheral, less atherosclerotic section of the resected specimen (Fig 1D).
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Fig 1. (A, C) Operative findings revealed a pear-like aortic root aneurysm. The aneurysmal wall showed severe atherosclerotic changes. Arrows indicate a pinhole rupture point. (B) Chest computed tomography on admission showed calcified aneurysm of the aortic root and hemopericardium. (D) Pathologic findings showed severe atherosclerotic changes of the aortic wall, but there were no signs of cystic medial necrosis. (In = intima; Ad = adventitia; Th = thrombus.)
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Case 2
An 81-year-old hypertensive man was hospitalized because of sudden-onset severe chest pain. On admission, his heart rate was 120 beats per min, his BP was 60/32 mm Hg, and slight anemia was observed. Although electrocardiography revealed severe aortic regurgitation and an old myocardial infarction of the inferior wall, no coronary angiogram was performed because of his shock status. Chest-enhanced CT showed an aortic root aneurysm about 70 mm in diameter and hemopericardium. There were severe calcifications from his ascending aorta to the aortic arch and scattered calcifications in his descending and abdominal aorta. Both the right axillary artery and the left femoral artery were chosen for arterial perfusion, and venous drainage was accomplished with a single cannula in the right atrial appendage. During cardiopulmonary bypass, the axillary flow was kept dominant over the femoral flow to prevent cerebral embolism by the atheromatous plaque from the abdominal aorta. The ascending aorta was cross-clamped after checking the clamping site using intraoperative echography. The findings during operation showed aneurismal dilatation of the ascending aorta and the right coronary sinus of Valsalva. The atherosclerotic change of the aneurismal wall was very severe, and a pinhole rupture point was located on the anterior wall of the aneurysm, occluded with thrombus (Figs 2A, 2B). Although the right coronary sinus of Valsalva was dilatated, the aortic valve leaflets were almost normal. Therefore, a valve-sparing operation was performed. The ascending aorta and the right coronary sinus of Valsalva were resected and replaced with a 26-mm gelatin-sealed prosthetic graft. The right coronary artery was directly anastomosed to the graft by the Carrel patch method. After the operation, right hemiparesis was observed temporally and improved gradually. The resected specimen pathologically showed severe atherosclerotic changes of the aortic wall, with little sign of cystic medial necrosis in the less atherosclerotic section (Fig 2C).
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Fig 2. (A, B) The aneurysmal wall showed severe atherosclerotic changes. Rupture point was closed with thrombus at operation (arrows). (C) Aneurysmal wall showed severe atherosclerotic changes. (In = intima; Ad = adventitia; Th = thrombus.)
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Comment
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We encountered two cases of the rupture of aortic root aneurysms with hemopericardium. Although the patients' clinical diagnoses were compatible with AAE, their pathologic findings revealed severe atherosclerotic changes of the aneurismal wall, with little sign of cystic medial necrosis. Each rupture point originated from one of the atherosclerotic ulcers of the aneurismal wall. These findings were compatible with penetrating atherosclerotic ulcers of the aorta. Shennan [3] was the first to describe penetrating atherosclerotic ulceration of the thoracic aorta in 1934, and his observations were enhanced by Stanson and colleagues [4] in 1986. They described a progression of the atherosclerotic process in which an ulcer penetrates through the internal elastic lamina and extends into the media. In their surgical pathology series, medial dissection was the most commonly observed fate of penetrating ulcers. They also reported that the extension of an ulcer may produce a complete transmural aortic rupture [3, 4]. The pathologic findings in our cases showed severe atherosclerotic changes of the aneurismal wall and the transmural rupture of the atherosclerotic ulcers. These findings were compatible with their description. Ulceration has been described along the whole length of the aorta, but the most common sites are the middle and distal descending thoracic segments [5–7], and only a few cases of penetrating atherosclerotic aortic ulcers originating in proximal portions of the ascending aorta have been reported [5, 8]. Therefore, our two cases were very rare. On the other hand, atherosclerotic ulcers have been found in aortas of increased diameter compared to normal size [5]. Because the aortas of both patients were markedly dilatated, they likely had great potential for atherosclerotic ulcers. Although these cases were clinically compatible with AAE, there was little sign of medial degeneration in the peripheral, less atherosclerotic section of the resected specimen. The patients should have initially had cystic medial necrosis in the aneurismal wall, and severe atherosclerotic change probably modified and obscured the medial degeneration.
Although our two patients were successfully treated, the second patient unfortunately showed temporary hemiparesis. When a patient's abdominal aorta is calcified, we usually choose both the right axillary artery and the right or left femoral artery for arterial perfusion and keep the axillary flow dominant over the femoral flow, because the retrograde perfusion from the femoral artery may blow atheromatous plaques of the abdominal aorta up to the cerebral artery and cause cerebral embolisms. In the second case, atheromatous plaques of the ascending aorta or the aortic arch probably caused the cerebral damage. When there are fragile atheromatous plaques from the ascending aorta to the aortic arch, it is very difficult to prevent cerebral embolisms completely.
We have reported two cases of pinhole ruptures of severely calcified aortic root aneurysms. Although their configurations were compatible with AAE, the pathologic findings of the aneurismal walls showed severe athero-sclerosis, with little sign of cystic medial necrosis. Both patients were successfully treated by emergency surgical repair and were discharged.
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References
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- Ellis P.R., Cooley D.A., DeBakey M.E. Clinical considerations and surgical treatment of annulo-aortic ectasia. J Thorac Cardiovasc Surg 1961;42:363-370.
- Shennan T. Dissecting aneurysms. Medical Research Council, special report series no 193. London: Her Majesty's Stationery Office; 1934
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Abstract
Introduction
