Left Main Coronary Thrombotic Occlusion Due to Secondary Polycythemia in a Normal Sinus of Valsalva

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Abstract: A case of acute myocardial infarction (AMI) due to thrombus in the left coronary cusp to the ascending aorta is described. There was no clinical evidence of coagulopathy, immunodisability, or local erosive lesion of the aortic and sinus of Valsalva wall macroscopically. Secondary polycythemia, induced by heavy smoking, was the likely cause of the myocardial infarction. Although this may be a rare case, intraaortic thrombus should be considered in the differential diagnosis of the causes of AMI.  

J INVASIVE CARDIOL 2013;25(8):421-422

Key words: intraaortic thrombus, acute myocardial infarction

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Case Report

A 65-year-old man was admitted to our hospital because of sudden chest pain with suspected acute coronary syndrome. He was transferred to our hospital 30 minutes after the onset. The patient’s risk factors included smoking 2 packs per day, diabetes mellitus, hyperlipidemia, and hyperuratemia. Previous medical history included pulmonary embolism 20 years prior.

On admission, the patient presented in cardiogenic shock, with a blood pressure of 63/49 mm Hg, and pulmonary congestion on chest x-ray. Electrocardiogram showed sinus rhythm with a pattern of acute myocardial infarction (AMI). Laboratory data showed no elevation of cardiac enzymes because of the very acute phase of myocardial infarction. However, his hemoglobin level was 19.8 mg/dL and hematocrit level was 57.1%, both being at a much higher level than normal.

Aspirin 200 mg and clopidogrel 300 mg were taken before emergent coronary angiogram was performed. Emergent coronary angiography (Figure 1) of the left coronary artery (LCA) showed a filling defect in the left main coronary artery (LMCA). Subsequent contrast injections revealed that the filling defect had disappeared from the LMCA and moved to the sinus of Valsalva, and the LCA had a smooth lumen with no significant stenosis. Angiography of the right coronary artery (RCA) revealed no significant stenosis either.

Aortography (Figure 2) showed a huge filling defect from left coronary cusp to the ascending aorta and no aortic regurgitation. There was no iatrogenic aortic or coronary dissection related to the catheter procedure. 

Multiplane transesophageal echocardiography (TEE) was performed immediately for further evaluation of the coronary cusp, where a mobile mass from the left coronary sinus of Valsalva to the ascending aorta was clearly seen (Figure 3). 

Although coronary flow was obtained and the patient’s vital signs were stable at that time, emergent surgery was performed to avoid further embolic complications. 

The mass size was 5 × 3 cm, and partially attached to the wall of the aorta 1 cm proximal to the LMCA and the soft part extended to the LMCA (Figure 4). Because the mass was loosely adhered to the left coronary cusp, it was removed without difficulty. No aortic and Valsalva wall injury or atheromatous lesions were noted during surgical exploration. Microscopically, the mass was determined to be thrombus without bacterial flora or inflammatory changes.

Laboratory data for platelet count, antithrombin III, protein C and protein S concentrations were normal. Anticardiolipin antibodies and lupus anticoagulant were negative. Though creatine kinase (CK) was 59 IU/L at admission, follow-up CK and CK-MB just before surgery were elevated to 10512 IU/L and 879 IU/L, respectively, indicating large myocardial infarction.

Follow-up cardiac CT revealed no filling defect in the left sinus of Valsalva and no organic coronary artery stenosis. 

The patient was transferred to respiratory rehabilitation hospital 8 weeks later with non-invasive positive-pressure ventilation (NPPV). One month later, the patient was discharged.

Discussion

Thrombosis in the ascending aorta^1-4 or in the sinus of Valsalva^5,6 associated with AMI is very rare.

Recently, eroded or disrupted atherosclerotic plaques have been recognized as a substrate for thrombus formation, leading to an ischemic coronary artery and cerebrovascular disease.⁵

The etiology of the thrombus was described as a local erosive lesion and age-generated degenerative change of the aortic wall. The exact mechanism for the formation of a giant thrombus in a high-flow environment, such as the sinus of Valsalva in the present case, is not fully known. In this case, the patient had no local aortic lesion or coagulopathy. However, the patient presented with secondary polycythemia due to smoking and lung injury causing a hyperthrombogenic state. Moreover, endothelial damage due to heavy smoking may have played a role in this case, although we could not investigate the wall of Valsalva or the aorta microscopically.

Conclusion

The patient was admitted with AMI due to thrombus in the left coronary cusp to the ascending aorta. However, there was no clinical macroscopic evidence of coagulopathy, immunodisability, or local erosive lesion of the aortic and sinus of Valsalva wall. He had secondary polycythemia induced by heavy smoking, which possibly caused the MI. Although this may be a rare case, intraaortic thrombus should be considered in the differential diagnosis of  AMI.

References

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