oronary arteriovenous fistula (CAVF) is an abnormal communication between a coronary artery and a cardiac chamber, great vessel, or other vascular structure. Most of them are found incidentally during coronary angiography (CAG), and are identified as a cause of a continuous murmur, myocardial ischemia, congestive heart failure or, rarely, bacterial endocarditis. [1][2][3] However, cases with pericardial effusion (PE) caused by rupture of the aneurysmal coronary artery are quite rare; only 3 cases of cardiac tamponade caused by rupture of the CAVF have been previously reported. [4][5][6] We report a case of chronic PE caused by a CAVF. The PE was observed for 6 months, and finally developed into cardiac tamponade.
Case ReportA 75-year-old woman was referred to hospital for investigation of recurrent PE. She had a history of pulmonary tuberculosis 50 years ago. In August 1998, she had been admitted to another hospital for further investigation of cardiomegaly (cardiothoracic ratio (CTR) 63%) and was the PE was diagnosed for the first time. However, she was free of symptoms and the laboratory examinations were normal, including thyroid function and tuberculin reaction. Chest computed tomography (CT) did not show any abnormal findings except for the PE and a scar from the pulmonary tuberculosis. She was treated with diuretics and the PE disappeared within 6 months. The CTR decreased
Circulation Journal Vol.66, August 2002from 63% to 54% on the chest X-ray. In February 1999, she developed shortness of breath and general fatigue, and echocardiographic examination revealed that the PE had recurred.On the admission to hospital in February 1999, her vital signs were: blood pressure 148/70 mmHg, heart rate 92 beats/min, respiratory rate 20 breaths/min, and body temperature 36.5°C. Pulsus paradoxus was not detected. Chest auscultation revealed bilaterally normal respiratory sounds and a soft continuous murmur at the left sternal border of the 4th intercostal space. She had hepatomegaly, bilateral leg edema and a markedly expanded external jugular vein.Laboratory tests were as follows: leukocytes 7.2×10 3 / l; C-reactive protein 0.5 mg/dl; erythrocyte sedimentation rate of 24 mm/h; TSH 1.86 IU/ml; free T3 1.77 pg/ml; free T4 0.83 ng/ml; tuberculin reaction 10×10 mm. A chest Xray revealed cardiomegaly (CTR = 67%) without pulmonary infiltration. The electrocardiogram (ECG) on admission was normal except for flat T waves in leads V4-6 (Fig 1A). An enhanced CT scan revealed a dilated right coronary artery (RCA) and a dilated coronary sinus (CS) vein, an expanded inferior vena cava and a large, circumferential PE (Fig 2). However, leakage of contrast media into the pericardial space was not seen. A diagnostic pericardiocentesis yielded 20 ml of bloody fluid (Hct = 22%) that contained 5.7 mg/dl of protein, 56 mg/dl of glucose and 23.2 IU/L of adenosine deaminase. The culture for bacteria in the pericardial fluid was negative, and a polymerase chain reaction for the tuberculosis bacillus was not detected. There was no evidence of ...