A 72 years old male patient was hospitalized after a month of heart palpitations. One month previously, the patient complained of slight chest discomfort and palpitations while climbing stairs. The patient received medications at that time, but they did not help relieve the symptoms. The patient had been previously diagnosed with atrial fibrillation 15 years ago, and he had not been treated for it with any medication, including anticoagulants.
On admission to the hospital, a mid-diastolic rumbling murmur was heard (Grade III/VI) at the apex of the chest on the physical examination. A standard chest PA showed an increase of the pulmonary vascular markings and enlargement of the left atrium. The echocardiography showed a mitral valve orifice of 0.83 cm2, a mean diastolic pressure gradient of 10 mmHg and a left atrial volume index of 96 mm3/m2. In addition, there were trivial amounts of mitral regurgitation and multiple variably sized thrombi, including an 8 × 5 cm thrombus, in the septum, posterior wall and entrance of the left auricle.
Surgery was performed under general anesthesia with superior and inferior vena cava and aortic cannulation. After the procedure, antegrade and retrograde cold blood cardioplegia was used for myocardial protection. The left atrium was opened through the Waterston's groove to remove the multiple thrombi; however, the atrial surface was very rough even after removing the thrombi (Figure 1). Resection of the left atrial auricle, mitral valvuloplasty and partial left atrial volume reduction were performed. During the cardiopulmonary bypass, the ACT remained greater than 450 seconds and there was no problem during weaning from the cardiopulmonary bypass. After protamine was injected, the ACT was 130 seconds. The platelet count was 45,000/mm3 during sternal closure; five units of platelets were then transfused. After this, no mitral regurgitation was observed by trans-esophageal echocardiogram, but a new thrombus was detected at the left atrium (Figure 2). Injection of 0.5 mg of heparin/kg was done to maintain the ACT at greater than 250 seconds and to block the formation of new thrombi. The developing thrombus did not affect the blood flow through the mitral valve; the sternum was closed and the surgery completed.
On that day, the patient received constant doses of heparin until postoperative day 1, and then the medication was changed to Coumadin for further anticoagulation. To determine the cause of thrombus formation, coagulation studies such as hyperhomocysteinemia and heparin-induced thrombocytopenia were performed using a blood sample from surgery. Yet we could not find a definite cause of the new thrombus formation on the hematologic studies. The patient gradually recovered with no special problems. The postoperative echocardiogram on day 10 showed a mitral valve area of 1.77 cm2 and a mean diastolic pressure gradient of 5.1 mmHg. While some signs of thrombus formation at the left atrium were noted during early follow-up, by three months post-surgery none were detected on the follow up echocardiogram (Figure 2).