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Case Report

Prosthetic Aortic Valve Abscess Producing Left Main Coronary Artery Occlusion in a Patient with Type IV Dual Left Anterior Descending Coronary Artery

Ali Metin Esen, asc. PhD, Göksel Açar, MD, Elnur Alİzade, MD
January 2011
ABSTRACT: A 22-year-old female with a history of aortic and mitral valve replacement was admitted with a 4-week history of dyspnea and chest pain. Emergency coronary angiography revealed not only external compression of the left main coronary artery due to an aortic root abscess, but also the dual left anterior descending artery arising from the left and right coronary sinus. Although aortic root abscess is a well recognized complication of aortic valve endocarditis, coronary artery compression is an unusual mode of presentation. The binary distribution of the left anterior descending artery may limit the extent of ischemic insult to the anterior wall and thus led to a more insidious clinical course.
J INVASIVE CARDIOL 2011;23:E233–E235
Key words: infective endocarditis; aortic valve abscess; myocardial ischemia; coronary artery anomaly
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Prosthetic valve endocarditis remains a serious complication of aortic valve replacement. Mechanical compression of coronary arteries from perivalvular extension of aortic endocarditis is extremely rare. We report the clinical, echocardiographic and angiographic features of a patient with prosthetic aortic valve endocarditis and a perivalvular abscess who presented with dyspnea and chest pain. These features were confirmed at the time of emergency surgery. Case Report. A 22-year-old female was admitted to our institution with a 4-week history of dyspnea and chest pain. She had no risk factors for coronary disease. She had aortic valve replacement 5 years ago and subsequent mitral valve replacement 3 years later. Seven months before admission, she had a history of infective endocarditis that was successfully treated with intravenous teicoplanin. Transesophageal echocardiographic (TEE) evaluation at that time revealed mild paravalvular aortic and mitral valve regurgitation. When admitted to our hospital, the patient was aprexial with no peripheral signs of endocarditis. Head, eyes, ears, nose and throat examination results were unremarkable. There was a no jugular vein distention, and the cardiac apical impulse was not displaced. On auscultation, there was 3/6 apical systolic murmur with prosthetic valve sounds. Her pulse was 80 beats per minute and her blood pressure was 90/65 mmHg. Chest radiograph revealed evidence of a previous sternotomy with mild cardiomegaly and mild bilateral pleural effusion. Electrocardiography (ECG) showed normal sinus rhythm and nonspecific ST-T changes in the lateral leads. The patient’s hemoglobin concentration was 9 mg/dl, mean cell volume 81 fl, white cell count 12.2 x 109/l, platelet count 244 x 109/l, erythrocyte sedimentation rate 34 mm/hour and C-reactive protein 13.1 mg/dl. Three sets of blood cultures and serial cardiac enzymes were negative. Transthoracic echocardiography revealed normal left ventricular systolic function and mild-to-moderate paravalvular aortic and mitral regurgitation. TEE was planned to evaluate prosthetic aortic and mitral valve function, and the patient was given 1 unit of packed red blood cells and diuretic treatment. Five days after admission, the patient complained of worsening chest pain, and an ECG showed ST elevation at V1, V2, V3 and aVR with reciprocal changes in other leads (Figure 1). She was then transferred to the catheterization unit. Emergency coronary angiography revealed severe narrowing of the left main coronary artery with an unusual long, tapering contour, total occlusion of the proximal left circumflex coronary artery (LCX) and also a dual left anterior descending (LAD) coronary artery with normal origin only of one of its two branches (Figure 2A). Surprisingly, the other branch of the dual LAD originated from the right coronary sinus (Figure 2B). Both diagonals and septals originated from the first LAD, whereas only septal branches originated from the second LAD branch. The clinical and hemodynamic status of the patient deteriorated rapidly, progressing to acute left ventricular failure resulting in intubation and mechanical ventilation. The patient was then transferred to surgery.
Intraoperative TEE showed an echolucent mass within the area of the mitral-aortic intervalvular fibrosa (Figure 3). Emergency surgery revealed a large abscess cavity underneath the aortic valve. The abscess involved the entire left coronary and noncoronary cusp areas. Surgery consisted of obliteration of the abscess cavity, mechanical aortic valve replacement and annulus reconstruction using pericardium. Unfortunately, she died immediately after the operation because of the pump failure.
Discussion. Aortic root abscess is a relatively common and frequently fatal complication of aortic valve endocarditis that may occasionally present with coronary ischemia.1,2 Coronary ischemia in endocarditis is generally due to preexisting coronary disease or rarely as a result of embolism from vegetations. In the current case, coronary angiography revealed a severe long stenosis of the left main trunk and total occlusion of the proximal LCX. However, the mechanism of unstable angina in this patient was likely due to extrinsic compression of the left main coronary artery by the aortic root abscess. Total occlusion of the proximal LCX may be associated with antecedent endocarditis complicated by coronary emboli. Although our patient initially had chest pain and ECG abnormalities, there was no definitive evidence of myocardial ischemia or infarction. Ischemia was probably mild or absent in this case because the one branch of the dual LAD originating from the right coronary sinus supplied the mid and distal septum and the apex, and well-developed collaterals filled the LCX up to the first marginal branch. Dual connection of the LAD to the left and right coronary arteries is an extremely rare congenital coronary artery anomaly that was classified into four types by Spindola-Franco et al.3 In the present case, there were two coronary arteries supplying the anterior wall of the left ventricle. The first originated from the left main trunk and, after a short course, terminated in the proximal segment of the anterior interventricular groove, after first giving rise to septal and diagonal branches. The second one originated from the right coronary sinus and supplied the mid and distal septum and the apex. Our patient’s angiographic study is consistent with a type IV dual LAD. The clinical suspicion of endocarditis was not high at presentation because of the absence of fever and the patient’s chest pain. Extrinsic coronary compression may be overlooked as a mechanism of coronary ischemia and may represent a complication of a more insidious problem. In conclusion, coronary angiography can reveal coronary compression and still has a pivotal role in evaluating the patient with aortic valve endocarditis and evidence of myocardial ischemia. TEE remains an optimum imaging technique to define complications of aortic valve endocarditis, including formation of root abscess and fistulae. Additionally, the binary distribution of the LAD may limit the extent of ischemic insult to the anterior wall. The rarity of the extrinsic coronary artery compression as a cause of unstable angina, along with a very rare coronary anomaly, makes this case more interesting.

References

1. Cripps T, Guvendik L. Coronary artery compression caused by abscess formation in infective endocarditis. Int J Cardiol 1987;14:99–102. 2. Dean JW, Kuo J, Wood AJ. Myocardial infarction due to coronary artery compression by aortic root abscess. Int J Cardiol 1993;41:165–167. 3. Spindola-Franco H, Grose R, Solomon M. Dual left anterior descending coronary artery: Angiographic description of important variants and surgical implications. Am Heart J 1983;105:445–455.
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From Kartal Koşuyolu Heart and Research Hospital, Department of Cardiology, Istanbul, Turkey. The authors report no conflicts of interest regarding the content herein. Manuscript submitted March 1, 2010, provisional acceptance given March 9, 2010, final version accepted March 18, 2010. Address for correspondence: Göksel Açar, MD, Kartal Koşuyolu Heart and Research Hospital, Department of Cardiology, 34846, Denizer Cd, Cevizli Kavşağı, No:2, Kartal, Istanbul, Turkey. E-mail: doctorgokselacar@hotmail.com

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