The rate of acetic acid formation in CO2 hydrogenation on Ag-Rh/SiO2 catalyst took two maxima at 463 K and 553 K. At 463 K, the rate was much faster than that of C2-oxygenates formation in CO hydrogenation. It was suggested that, at lower temperature, acetic acid is formed through the direct incorporation of adsorbed CO2.

and was admitted there. The day before admission, he was given a non-steroidal anti-inflammatory drug by his referring doctor to reduce his pain. He had been followed-up for atrial fibrillation and hypertension without any medication for 11 years.Physical examination on admission revealed fever elevation (38°C) and atrial fibrillation (heart rate, approximately 86 bpm) in addition to right abdominal tenderness. His blood pressure was 156/93 mmHg. Laboratory examination of blood showed a marked rise in lactate dehydrogenase (LDH: 2,161 IU/l) and slight rises in two transaminases, aspartate aminotransferase (AST: 340 IU/l) and alanine aminotransferase (ALT: 275 IU/l), while alkaline phosphatase (Al-Pase) was not elevated (Table 1). The serum creatinine concentration was normal (1.0 mg/dl). White blood cell counts (10,000/µl), C reactive protein (1.70 mg/dl) and D-D dimer (1.8 µg/ml) were slightly elevated, while eosinophilia (0.0%) was not recognized. Plasma renin activity (2.5 ng/ml/h) was slightly elevated, while plasma aldosterone concentration (67 pg/ml) remained normal. Initial urinalysis with a dipstick showed no hematuria, but proteinuria (2 ) was present. Microscopic examination of urinary sediment showed no casts

The patient was a 63-year-old man with drug-resistant atrial fibrillation who developed coronary spasm during cryoballoon ablation (CBA). CBA was started from the left inferior pulmonary vein. ST elevations in II, III, and aVf, with reciprocal ST depressions in V2-5, occurred in association with chest pain just after balloon rewarming and deflation, and the patient's blood pressure fell to 50 mmHg. Coronary angiography revealed 90% diffuse stenosis from the orifice of segment 1 to segment 4 in the right coronary artery. The stenosis and ST elevations improved after the intracoronary injection of nitroglycerine. Using continuous peripheral intravenous coronary vasodilation, we electrically isolated the other pulmonary veins with CBA without incident.

A 58-year-old man was referred to our hospital because of chest pain. The 12-lead electrocardiogram (ECG) revealed ST-segment elevation in II, III, and a Vf with advanced heart block. Transthoracic echocardiography demonstrated aortic root dilatation at the sinus of Valsalva, moderate aortic regurgitation, and decreased wall motion in the inferior part of the left ventricle. Non-ECG-gated enhanced computed tomography (CT) did not reveal an aortic dissection. The patient underwent emergent coronary angiography, which revealed a severely narrowed ostium of the right coronary artery (RCA). Percutaneous coronary intervention (PCI) was performed under intravascular ultrasound (IVUS) guidance. IVUS images demonstrated an intimal flap extending from the aortic wall to the proximal RCA, suggesting that a periaortic hematoma in the false lumen compressed the ostium of the RCA, leading to acute myocardial infarction. To recover hemodynamic stability, the RCA ostium was stented. Subsequent ECG-gated enhanced CT clearly depicted the entry point and extension of the dissection localized within the sinus of Valsalva. The dissection likely involved the left main coronary artery and an emergent Bentall procedure was performed. Intraoperative findings confirmed an intimal tear and extension of the dissection. Thus, ECG-gated CT can clearly depict the entry site and extension of a dissection occurring in the localized area that cannot be detected by conventional CT.

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