[Acute abdominal aortic occlusion in a patient with a giant thrombus in the left atrium and mitral stenosis; report of a case].

The patient was a 69-year-old male who had had percutaneous transvenous mitral commissurotomy (PTMC) 15 years ago, and had stopped taking warfarin after PTMC. He was transferred to our emergency room( ER) because of sudden severe pain in his both lower legs. We recognized pulselessness in his both femoral arteries, and pallor, paresthesia and poikilothermia in his lower extremities. Electorocardiogram(ECG) showed arterial fibrillation, and computed tomography( CT) showed occlusion of the abdominal aorta just below inferior mesenteric artery( IMA) and both common iliac arteries. By echocardiography, a giant thrombus was detected in the left atrium with severe mitral stenosis. Thrombectomy and angioplasty were performed at about 5 hours after the onset of occlusion, and revascularization was successful. Three days after the operation, we excised the giant thrombus in the left atrium and performed mitral valve replacement because we considered that myonephropathic metabolic syndrome (MNMS) had been prevented. The postoperative course was uneventful and he was discharged on the 27th postoperative day.

[Cardiac failure caused by intrapericardial chronic expanding hematoma 18 years after CABG].

Chronic expanding hematoma(CEH)was first recognized by Reid in 1980. It begins to expand chronically more than 1 month after surgery or trauma, which is considered the possible cause of bleeding. It resembles chronic subdural hematoma. Most of the reports on CEH are those in the thoracic cavity or muscles, and few are in the pericardial cavity after open heart surgery. Our case was a 64-year-old male, who had undergone coronary artery bypass grafting (CABG) 18 years before. He presented with symptoms of heart failure such as exertional dyspnea, general fatigue and appetite loss. Computed tomography( CT) scan showed severe compression of the left ventricle by a large mass, and he was diagnosed with intrapericardial CEH. Resection of the severely calcified epicardium as well as removal of the hematoma in the pericardial cavity was performed, and the symptoms of heart failure improved. No recurrence has been noted for 1 year since the operation. A long-term follow-up will be necessary.

Melatonin prevents the increase in hydroxyl radical-spin trap adduct formation caused by the addition of cisplatin in vitro.

We studied the generation of reactive oxygen species (ROS) caused by cisplatin administration and the preventive effect of melatonin, the main secretory product of the pineal gland, on the reaction in vitro using electron spin resonance spectroscopy. Cisplatin induced generation of the hydroxyl radical (OH*) in phosphate buffer in pH 7.4 as a dose-dependent manner. However, OH* was not generated in phosphate buffer containing chloride ions at concentration exceeding 120 mM. The induction of OH. production by cisplatin was completely inhibited by the addition of melatonin, but not by the addition of 6-hydroxymelatonin, which is a hepatic metabolite of melatonin. Furthermore, melatonin was the most effective agent for preventing of OH* formation among various well-known antioxidants including mannitol and reduced glutathione. These results indicate that melatonin may scavenge OH. directly and thereby prevent renal tissue damage caused by OH* produced in response to cisplatin treatment.