J Thorac Cardiovasc Surg 2002;124:841-843
© 2002 The American Association for Thoracic Surgery
Periannular abscess and aorta-left ventricular fistula after infection in the false lumen of an aortic dissection
Kazuhito Imanaka, MDa,
Shunei Kyo, MDa,
Shinichi Takamoto, MDb,
Masaaki Kato, MDa,
Hiroaki Tanabe, MDa,
Hiroshi Ohuchi, MDa,
Haruhiko Asano, MDa,
Yuji Yokote, MDa Saitama and Tokyo, Japan
From the Department of Cardiovascular Surgery, Saitama Medical School,a Saitama, and Department of Cardiothoracic Surgery, University of Tokyo,b Tokyo, Japan.
Received for publication Oct 24, 2001. Accepted for publication Nov 1, 2001.
Address for reprints: Kazuhito Imanaka, MD, Department of Cardiovascular Surgery, Saitama Medical School, 38 Morohongo, Moroyama-machi, Iruma-gun, Saitama 350-0495, Japan (E-mail: imanaka{at}saitama-med.ac.jp).
Aortic dissection and periannular abscess of the aortic valve are completely different entities. However, both lesions coexisted in a patient with a staphylococcal infection in the false lumen of the dissection. Because of persistent septicemia and aorta-left ventricular fistula, the patient's condition became critical; however, he was treated successfully with an allograft. This potentially fatal complication is described here.
A 72-year-old man had chest discomfort and dyspnea of acute onset and was admitted to another hospital. Moderate cardiomegaly was observed on chest radiography. Echocardiography revealed severe aortic valve stenosis and marked left ventricular hypertrophy with nearly normal contractility. Congestive heart failure was diagnosed. Clinical symptoms subsided within 2 days. Results of testing for serum C reactive protein (CRP) were negative on the day of admission. The leukocyte count was elevated but was decreasing (16,000 down to 11,000 cells/mm3), and the patient remained afebrile. Although some findings were inconsistent with pure heart failure, conservative treatment appeared to be successful. One week later, however, a spike fever developed. The leukocyte count increased to 22,000 cells/mm3, and the CRP level was 24.7 mg/dL. Blood culture yielded coagulase-negative Staphylococcus. Antibiotic therapy was started but was not terribly effective. A week later, rapidly progressive heart failure developed. Further examinations disclosed a DeBakey type II aortic dissection affecting the posterior third of the ascending aorta. Proximally, the false lumen reached as far as the aortic valve anulus. At its end were lobular cavities with abnormally edematous walls, and it had perforated into the left ventricle at the fibrous portion between the aortic valve and the mitral valve. This lesion was diagnosed as a periannular abscess (Figure 1). Aortic regurgitation had previously been trivial and originated only from the valve orifice. This time, however, severe regurgitation was observed through the fistula between the left ventricle and the false lumen of the ascending aorta. Because this communication was massive, blood flow across the intimal tear of the aorta, which was located 4 cm above the anulus, was detected only during diastole, and heart failure was refractory. Despite strenuous administration of antibiotics, moreover, septicemia was uncontrollable, and disseminated intravascular coagulopathy developed, which prompted an urgent operation. At surgery, the aortic valve found to be bicuspid and heavily calcified but appeared to be free of infection (Figure 2). The lobular periannular abscess had no continuity with the aortic valve leaflets, and there was no intimal tear at the level of the anulus, which strongly suggested that this abscess was a secondary lesion of the aortic dissection. Judging from the nature of the intimal flap, thrombi in the false lumen, and other structures, the dissection was of recent origin. Both the intimal tear and the orifice of the aorta-left ventricular fistula were about 5 mm in size. The tissues and structures affected by infection and dissection were resected in their entirety, and the aortic root and the ascending aorta were totally replaced with a cryopreserved allograft. The postoperative course of the patient was good.
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Fig. 1. A, DeBakey type II aortic dissection reached to aortic valve anulus, and proximal end of false lumen was lobular cavities with edematous wall. Communication with true lumen of aorta was absent at level of the aortic valve. B, P proximal end of false lumen perforated into left ventricle, which resulted in aorta-left ventricular fistula. Therefore periannular abscess after infection in false lumen of aortic dissection was diagnosed.
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Fig. 2. A, Aortic valve was bicuspid and was heavily calcified but appeared to be free of infection. There was no tear at level of anulus. B, Intimal flap was incised longitudinally, and periannular abscess was opened.
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Discussion
Aortic dissection is a relatively common disease. It can cause several types of aorta-cameral fistula, but it never overruns the aortic valve anulus. Infectious endocarditis may invade the periannular tissue to make an aorta-left ventricular fistula, but it rarely causes aortic dissection. The coexistence of both lesions was therefore strange. To our knowledge such a case has not been reported in the English-language literature. This patient did not undergo computed tomography or other imaging procedures at first. A few weeks after the onset, both lesions were already present. Their coexistence may have been incidental. However, the clinical course and the operative findings strongly suggest that acute aortic dissection was the precise cause of the initial symptoms but had been overlooked and that a periannular abscess had later developed at the proximal end of the false lumen and had perforated into the left ventricle, with the result that rapidly progressive refractory heart failure developed. Conversely, the aortic dissection was unlikely to have been secondary to the periannular abscess, because no infective valvular lesion or intimal tear was present at the level of the anulus and because results of CRP assay were at first negative.
The rarity of relevant articles on infections in the false lumen of an aortic dissection suggests that such infections are uncommon. Only a single case report has clearly demonstrated the evidence of an infection in the false lumen.
1 We often encounter patients with acute aortic dissection who show marked elevation of the leukocyte count and the CRP level with various grades of fever, 2 and these symptoms are thought to be caused by inflammatory substances released from the dissected aorta. 3 However, these phenomena are indistinguishable from bacterial infections, and infections in the false lumen can follow septicemia from other sources. 1 We therefore believe that prophylactic antibiotic therapy for such patients is justified. Physicians should keep this potentially fatal complication in mind when patients with aortic dissection show a marked elevation in CRP or a high fever, especially late after onset of the dissection. Cautious observation, appropriate examinations, and careful medical treatment are mandatory.
Once an infection in the false lumen is diagnosed, aggressive surgery should be considered early. We believe that lesions of this kind are best treated with allograft reconstruction. 4,5
References
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