Ann Thorac Surg 1997;63:1162-1163
© 1997 The Society of Thoracic Surgeons
Case Report
Calcified Embolus of the Left Coronary Ostia After Aortic Valve Replacement
Thierry A. Folliguet, MD,
Marie-Christine Malergue, MD,
Jacques Temkine, MD,
Alain Dibie, MD,
Jean Petrie, MD,
François Laborde, MD
Department of Cardiac Surgery, Institut Mutualiste Montsouris, Paris, France
Accepted for publication November 7, 1996.
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Abstract
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A patient with a left coronary calcified embolus causing acute myocardial dysfunction immediately after aortic valve replacement is described. Prompt diagnosis by transesophageal echocardiogram was made, which led to removal of the embolus and a subsequent satisfactory course.
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Introduction
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Embolization of calcified material to the left main coronary artery after aortic valve replacement is extremely rare and usually fatal [1]. We describe a patient who sustained embolization of a calcified fragment blocking the left main coronary artery immediately after aortic valve replacement.
A 69-year-old man was admitted for a history of recurring syncope and dyspnea on exertion. Prior medical history revealed a history of hypertension and transient ischemic attack.
On admission the patient was in sinus rhythm with a left bundle-branch block. Auscultation revealed a harsh systolic murmur radiating to the neck. Chest roentgenography revealed a mildly enlarged heart. Echocardiography revealed severe aortic stenosis with extensive calcification of the leaflet and the aortic ring. The valve area was estimated at 0.5 to 0.6 cm2. A mild mitral insufficiency was noted, with calcification present on the mitral valve. Catheterization results were normal except for a 70% stenosis of a small diagonal branch and 1+ aortic insufficiency. The ventricular aortic gradient could not be measured.
Doppler ultrasound of the cervical vessels revealed an occlusion of the right vertebral artery, with no significant lesion of the carotid arteries. Computed tomographic scan of the head did not show any lesion.
Operation was performed through a median sternotomy, with cardiopulmonary bypass with moderate hypothermia, aortic cannulation, and a single venous cannula. A single dose of crystalloid solution was delivered through the aortic root.
Aortotomy revealed a severely calcified aortic valve with calcification on the annulus and extending onto the anterior leaflet of the mitral valve. Removal of the valve and of the calcified area was performed, and a 23-mm bileaflet valve was placed with pledgeted sutures. Total cross-clamp time was 42 minutes, and cardiopulmonary bypass time was 55 minutes. After aortic unclamping, normal sinus rhythm resumed and the patient was easily weaned from cardiopulmonary bypass.
After sternal closure as the patient was being prepared for transfer to the intensive care unit, sudden bradycardia and hypotension occurred. An electrocardiogram showed sinus bradycardia with a left-bundle branch block. Cardiopulmonary bypass was immediately resumed. The left ventricle appeared stunned and dilated, whereas the right heart was contracting normally. An intraoperative multiplane transesophageal echocardiogram (Hewlett Packard 1500) showed akinesis of the anterior, lateral, and septal wall, with normal right ventricular function. The prosthesis was normally placed in an annular position, with normal leaflet movement and no paravalvular insufficiency. However, the left main coronary artery bifurcating in the left anterior descending and circumflex artery was clearly seen, as well as an image blocking the left main coronary trunk (Fig 1
). Retrograde cardioplegia was performed, and aortotomy revealed a calcified embolus lodged in the ostia of the left main coronary artery (Fig 2).
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Fig 1. . Intraoperative transesophageal echocardiogram showing the calcified embolus blocking the left main coronary trunk. (AO = aorta; LA = left atrium.)
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Examination of the prosthesis revealed no malfunction. After removal of the embolus, closure of the aortotomy, and aortic unclamping, the heart resumed a normal sinus rhythm. Transesophageal echocardiography showed a normal left ventricle without evidence of dysfunction. The patient was easily weaned from cardiopulmonary bypass. Postoperative analysis of myocardial enzymes showed an elevation of the creatine kinase-MB level (>448 U/L). Echocardiography performed on the 8th postoperative day revealed normal left ventricular function, and the patient made an uneventful recovery.
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Comment
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Embolus to the left main coronary artery has been reported in the literature, but it remains a rare entity [2]. The diagnosis is most often made retrospectively after anatomic review, as it is usually fatal. The consequences and clinical symptoms will depend on the size of the embolus and the size of the lumen artery in which it becomes impacted. The larger the embolus the greater the likelihood of myocardial necrosis or fatal arrythmia. Causes are variable: it has been reported during left cardiac catheterization, or secondary to a paradoxical embolus resulting from peripheral venous thrombi [2]. Other sources can be cardiac, most often secondary to migration of a cardiac thrombus (left ventricle, left atrium), or from a vegetation or a thrombus located on a valve or the annulus [3], or from embolism of a mitral papillary muscle to the left main coronary artery [4]. It has also been seen in the left anterior descending artery, right coronary artery, and circumflex artery [3].
A case has also been reported of myocardial infarction secondary to calcific embolization from a bioprosthetic valve [1]. Autopsy revealed a calcified embolus lodged in the circumflex artery, responsible for a posterior myocardial infarction. Other reports have described acute myocardial infarction complicating percutaneous aortic valvuloplasty [5] or after balloon angioplasty or thrombolytic therapy [6].
In this case the cause was probably secondary to migration of an embolus from the aortic annulus or the anterior aspect of the mitral valve, which was calcified. It is important in case of sudden left ventricular failure to eliminate a myocardial ischemia, which is usually seen on the electrocardiogram. Other differential diagnosis includes a malposition or malfunction of the prosthesis, and finally an embolic event. Both of these diagnoses can be made with transesophageal echocardiography. Only rapid diagnosis and treatment can save the patient and allow a smooth recovery.
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Footnotes
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Address reprint requests to Dr Folliguet, Department of Cardiac Surgery, Institut Mutualiste Montsouris, 6 place de Port au Prince, 75013, Paris, France.
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References
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- Johnson D, Gonzalez-Lavin L. Myocardial infarction secondary to calcific embolization: an unusual complication of bioprosthetic valve degeneration. Ann Thorac Surg 1986;42:102–3.[Abstract/Free Full Text]
- Waller BF, Dixon DS, Kim RW, Roberts WC. Embolus to the left main coronary artery. Am J Cardiol 1982;50:658–60.[Medline]
- Loire R, Tabib A. Coronary embolism: a review of 61 autopsy cases. Arch Mal Coeur 1984;78:823–6.
- Loisance D, Aubry P, Heulin A, Di Matteo J. Embolism of a fragment of the mitral papillary muscle to the left main coronary artery. A rare complication of valve replacement. Arch Mal Coeur 1979;72:1029–33.[Medline]
- Romanello PP, Moses FW, Wilentz JR, Schiffer MB, DePasquale NP. Acute myocardial infarction complicating percutaneous aortic valvuloplasty successfully treated by percutaneous coronary angioplasty. Am Heart J 1990;119:4:953–5.[Medline]
- Saber RS, Edwards WD, Bailey KR, McGovern TW, Schwartz RS, Holmes DR. Coronary embolization after balloon angioplasty or thrombolytic therapy: an autopsy study of 32 cases. J Am Coll Cardiol 1993;22:1238–8.
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Abstract
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