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Ann Thorac Surg 2007;83:1170-1171
© 2007 The Society of Thoracic Surgeons

Case Reports

Myocardial Infarction Secondary to a Coronary Ostial Thrombus in Antiphospholipid Syndrome

Ibrahim S. Abu Romeh, MD, Adnan K. Chhatriwalla, MD, Fernando A. Atik, MD, Deepak L. Bhatt, MD, Jose L. Navia, MD*

The Cleveland Clinic, Cleveland, Ohio

Accepted for publication September 6, 2006.

* Address correspondence to Dr Navia, 9500 Euclid Ave, F25, Cleveland, OH 44195 (Email: naviaj{at}ccf.org).


   Abstract
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 Abstract
Introduction
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 References
 
A 44-year-old woman presented with an acute inferior ST elevation myocardial infarction, followed by a stroke in the right hemisphere. To search for a cardiac source of embolism, a transesophageal echocardiogram was performed, which showed a mass obstructing the origin of the right coronary artery. The mass was surgically excised and a histologic examination confirmed its thrombotic origin. The diagnosis of antiphospholipid antibody syndrome was confirmed by positive lupus anticoagulant antibodies.


   Introduction
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 Abstract
 Introduction
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 References
 
Acute myocardial infarction is usually caused by rupture of an atheromatous plaque, which can evolve to a completely occlusive thrombus. The presence of a thrombus occluding a coronary artery ostium leading to acute myocardial infarction is rare. We report a case of a large thrombus in the ascending aorta extending into the right coronary ostium causing acute myocardial infarction in a young patient with antiphospholipid antibody syndrome (APS).

The patient is a 44-year-old previously healthy woman who experienced acute chest pain while on a cruise. There was no history or symptoms suggestive of previous thromboembolism or systemic lupus erythematosus. There was no family history of premature coronary artery disease or connective tissue diseases.

She presented to a local hospital and was transferred 2 days later to a community hospital in Cleveland where she was treated with heparin and aspirin. During her hospitalization, she developed quadriparesis and gaze palsy and was transferred to The Cleveland Clinic for further management. Her medical history was significant only for idiopathic thrombocytopenic purpura, which was treated with splenectomy during childhood.

On admission, the patient was intubated and sedated. Blood pressure was 150/100, heart rate was 80 beats/min, and oxygen saturation was 98%. Her chest was clear to auscultation bilaterally. A cardiac examination revealed normal S1 and S2, and no murmurs or gallops. The abdomen was soft. A neurologic examination showed left hemiplegia.

Results of a laboratory evaluation showed positive cardiac enzymes: creatine kinase, 649 U/L and creatine kinase-MB, 21%; troponin T, 2.44 µg/L; normal prothrombin time and partial thromboplastin time, positive lupus anticoagulant antibodies, and negative anticardiolipin antibodies.

A chest roentgenogram revealed bilateral hilar infiltrates. An electrocardiogram revealed normal sinus rhythm and Q waves in lead III and aVF. Brain magnetic resonance imaging showed a large pontine infarct.

The patient underwent cerebral angiography on admission. Basilar artery occlusion was diagnosed, and basilar artery revascularization was achieved with intravascular catheter-based thrombus extraction. No further neurologic complications occurred thereafter.

A transesophageal echocardiogram showed an ejection fraction of 0.40 and a 1.1-cm x 1.0-cm mass in the ostium of the right coronary artery and protruding into the aorta (Fig 1). In addition, there was 2+ mitral regurgitation. No patent foramen ovale was seen. Open heart surgery with excision of the right coronary ostial mass and mitral valve repair was performed. The mass was firmly attached to the aorta, with propagation into the right coronary artery. Histologic examination confirmed that the mass was entirely thrombotic (Fig 2).


Figure 1
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  		Fig 1. A transesophageal echocardiogram shows a mass in the right coronary artery ostium (circle) extending into the aorta.

 

Figure 2
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  		Fig 2. Surgical findings. Intraoperative photograph shows a large mass obstructing the origin of the right coronary artery.

 
On the first postoperative day, an acute deep venous thrombosis developed in her lower extremities. An inferior vena cava filter was placed. Although the patient had no further embolic phenomena, her hospitalization was complicated by femoral artery pseudoaneurysm after a cerebral angiography and an episode of gastrointestinal bleeding on postoperative day 18 (2 days after starting warfarin), treated by injecting the bleeding site in the stomach. Anticoagulation was held for 2 days. She was discharged with Coumadin therapy (5 mg/d) with a target international normalized ratio (INR) of 2.5 to 3.5.


   Comment
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References
 
APS is characterized by antibodies against phospholipid-binding proteins in plasma, leading to a hypercoagulable state. Serologic markers for APS include anticardiolipin antibodies or lupus anticoagulant, or both.

Numerous mechanisms have been proposed to explain thrombus formation by antiphospholipid antibodies, such as direct endothelial damage, enhanced platelet aggregation, and inhibition of endogenous anticoagulants. The endocardial surface may be an important site for thrombus formation in patients with circulating antiphospholipid antibodies. These antibodies, in the presence of other hemostatic defects, may affect surface factors and promote clot formation.

A wide spectrum of cardiac involvement has been recently described in patients with APS, including valvular lesions, intracardiac thrombosis, cardiomyopathy, pulmonary hypertension, and myocardial infarction. Patients with APS and systemic lupus erythematosus tend to have more thrombotic complications than patients with primary APS [1].

There is an increased risk of myocardial infarction in patients with APS [2] caused by coronary thrombosis rather than by premature atherosclerosis. The usual pathophysiology of acute myocardial infarction is rupture of an atheromatous plaque, which can evolve to a completely occlusive thrombus. The presence of a thrombus occluding a coronary artery ostium and leading to an acute myocardial infarction is rare [3].

Patients have previously treated with long-term anticoagulation and excision of the thrombus, if appropriate. In a recent study, high-intensity warfarin therapy (INR 3 to 4) was not superior to moderate-intensity warfarin for thromboprophylaxis in patients with APS and previous thrombosis [4].

Thrombosis in the ascending aorta or the sinus of Valsalva associated with acute myocardial infarction is a very rare condition. Dik and colleagues [5] reported a patient with inferior myocardial infarction secondary to an ascending aortic thrombus with extension into the right coronary artery. The diagnosis was made by coronary angiogram and treatment was surgical excision. The patient, a 46-year-old woman, was a smoker who was taking oral contraceptives.

Nader and colleagues [6] were the first to describe a 49-year-old patient with a massive myocardial infarction leading to death, in whom the diagnosis of coronary embolism from an aortic thrombus was made at autopsy. In their report, the cause of the aortic thrombus was thought to be a complication of age-related degenerative changes in the aorta. Schlatmann and Becker [7] described the occurrence of a dissecting aneurysm incipiens, especially in the first part of the ascending aorta, which could be easily missed macroscopically. Our patient had no evidence of aortic dissection, however.

Three embolic events (two strokes and a myocardial infarction) occurred in our patient within 1 week. The goal should be early identification of thrombus origin, with urgent surgery to prevent further emboli. The role of intravenous thrombolysis [8] in this case is not clear, as it can potentially lead to more embolic events. In this case, the patient presented 3 days after the onset of chest pain, and was therefore felt not to be a good candidate for thrombolysis.


   References
Top
 Abstract
 Introduction
 Comment
 References
 

  1. Nihoyannopoulos P, Gomez PM, Joshi J, Loizou S, Walport MJ, Oakley CM. Cardiac abnormalities in systemic lupus erythematosus, association with raised antiocardiolipin antibodies Circulation 1990;82:369-375.[Abstract/Free Full Text]
  2. Petri M. The lupus anticoagulant is a risk factor for myocardial infarction (but not atherosclerosis): Hopkins Lupus Cohort Thromb Res 2004;114:593-595.[Medline]
  3. Shahin GM, Bosker HA, Knaepen PJ, Morshuis WJ, Lindeboom JE. Organized thrombus in the ascending aorta originating from the ostium of the right coronary artery Cardiovasc Surg 2002;10:62-64.[Medline]
  4. Crowther MA, Ginsberg JS, Julian J, et al. A comparison of two intensities of warfarin for the prevention of recurrent thrombosis in patients with the antiphospholipid antibody syndrome New Engl J Med 2003;349:1133-1138.[Abstract/Free Full Text]
  5. Dik H, Hellemans I. An unusual cause of myocardial infarction? Eur Heart J 1993;14:428-430.[Abstract/Free Full Text]
  6. Nader RG, Barr F, Rubin R, Hirscfeld JW, Eisen HJ, Laposata E. Aortic degenerative changes and thrombus formation: an unusual cause of massive myocardial infarction with normal coronary arteries Am J Med 1989;86:718-722.[Medline]
  7. Schlatmann TJ, Becker AE. Histologic changes in the normal aging aorta: implications for dissecting aortic aneurysm Am J Cardiol 1977;39:13-20.[Medline]
  8. Ito H, Takahashi K, Sasaki H, et al. Large thrombus in the ascending aorta successfully treated by thrombolysis Jpn Circ J 2001;65:572-574.[Medline]




This Article
Right arrow Abstract Freely available
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Right arrow Author home page(s):
Fernando A. Atik
Jose L. Navia
Right arrow Permission Requests
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Right arrow Articles by Abu Romeh, I. S.
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Right arrow Articles by Abu Romeh, I. S.
Right arrow Articles by Navia, J. L.
Related Collections
Right arrow Myocardial infarction

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