Variant angina is a form of angina pectoris that shows transient ST-segment elevation on electrocardiogram during an attack of chest pain. Ischemic episodes of variant angina show circadian variation and often occur at rest from midnight to early morning. Ischemic episodes also occur during mild exercise in the early morning. However, they are not usually induced by strenuous exercise in the afternoon. Other important clinical features of variant angina include the high frequency of asymptomatic ischemic episodes and the syncope that sometimes occur during the ischemic episodes. Syncope is due to severe arrhythmias, including ventricular tachycardia, ventricular fibrillation, and high-degree atrioventricular block. Coronary artery spasm is the mechanism of ischemic episodes in variant angina. The incidence of coronary artery spasm shows a racial difference and is higher in Japanese than in Caucasians. Coronary arteriograms are normal or near-normal in most Japanese patients with variant angina. Deficient basal release of nitric oxide (NO) due to endothelial dysfunction, and enhanced vascular smooth muscle contractility with the involvement of the Rho/Rho-kinase pathway are reported to play important roles in the pathogenesis of coronary artery spasm. Other precipitating factors of coronary artery spasm include imbalance in autonomic nervous activity, increased oxidative stress, chronic low-grade inflammation, magnesium deficiency, and genetic susceptibility. The genetic risk factors associated with coronary artery spasm include gene polymorphisms of endothelial NO synthase (NOS), paraoxonase, and other genes. Calcium channel blockers are extremely effective in preventing coronary spasm. The long-acting nitrate, nicorandil, and Rho-kinase inhibitor are also useful for inhibiting coronary artery spasm. Because variant angina can lead to acute myocardial infarction, fatal arrhythmias, and sudden death, early treatment is important. The prognosis of patients with variant angina is favorable, if early complications can be overcome. However, because coronary artery spasm cannot be suppressed in some patients, even with multiple medications, medications to suppress intractable coronary artery spasm must be developed.

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Somatic mutations of mitochondrial DNA (mtDNA) have been reported in different types of cancers and are suggested to play roles in metastasis, cancer development and response to anticancer agents. To predict potential roles of mtDNA alterations in colorectal cancer, we determined the entire mtDNA sequence of eleven human-derived colorectal cancer cell lines and compared with the revised Cambridge Reference Sequence to identify nucleotide alterations. Four homoplasmic and six heteroplasmic alterations were found to be novel. Among them, homoplasmic G6709A (MT-CO1) and G14804A (MT-CYB) alterations cause amino acid changes in the highly conserved residues. Heteroplasmic G1576A (MT-RNR1) and G2975A (MT-RNR2) alterations are expected to make the stem structure of mitochondrial ribosomal RNAs unstable. These nucleotide alterations are candidates that could play important roles in cancer.

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Background: 12-lead electrocardiograms (ECGs) provide insufficient information for the accurate diagnosis of posterior and/or right ventricular acute myocardial infarction (AMI) in patients with acute chest pain. Posterior chest leads (V7-V9) and/or right-sided precordial leads (V3R-V5R) provide important information from those specific areas, but these additional ECGs are not routinely recorded because of the time-consuming procedure involved. The purpose of the present study was to evaluate a newly developed system to synthesize these 6 additional lead ECGs non-invasively using standard 12-lead ECG information.
Patients and Methods: Thirty patients (25 men, 5 women; mean age: 65 ± 11 years) complaining of acute chest pain were enrolled. Standard 12-lead and V3R, V4R, V5R, V7, V8, V9 lead ECGs were successively recorded and compared with synthesized ECGs mathematically derived from standard 12-lead signals.
Results: The synthesized and actual ECG waveforms were almost identical, and there were significant correlations in ECG variables, including the P, QRS, and T waves (correlation coefficients about total 1-cycle signals: 0.97 in V3R; 0.93 in V4R; 0.88 in V5R; 0.98 in V7; 0.92 in V8; and 0.88 in V9, p<0.001). Both in patients with AMI (N=16) and in patients with ST elevation at the extended leads (N=8), significant correlations were also found (correlation coefficients were over 0.88 at all leads, p<0.001). The reproducibility of the ST segment was as good as that of the other ECG variables, even in patients with significant ST elevation due to posterior and/or right ventricular AMI.
Conclusion: Synthesized posterior and right-sided precordial lead ECGs appear to be highly reliable and useful in the rapid diagnosis of AMI, especially in the early detection of posterior and/or right ventricular involvement, thereby alleviating patient distress.

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We describe a 35-year-old man with hepatocellular carcinoma (HCC) that recurred in the diaphragm after right hepatic lobectomy. The patient had undergone right hepatic lobectomy for HCC with chronic hepatitis B virus infection 1 year previously. On pathological examination, the tumor measured 15 × 14.4 × 11 cm and was moderately well differentiated. The surgical margins were negative. After 1 year, computed tomography of the abdomen revealed a mass extending from the right side of the diaphragm to the retroperitoneal space. The mass was enhanced in the early phase and washed out in the late phase. Extrahepatic recurrence of HCC in the diaphragm was diagnosed. We performed tumor resection with partial resection of the right side of the diaphragm and wedge resection of the right lower lobe of the lung. The diaphragm was reconstructed with a sheet of artificial pericardium. The histopathological diagnosis was recurrence of HCC in the diaphragm with invasion of the right lung. The postoperative course was uneventful, and the patient was discharged on postoperative day 8. He underwent chemotherapy with cisplatin and 5-fluorouracil. After 9 months, the patient died of unresectable recurrence of HCC in the brain. No recurrence was detected in the right subphrenic area.

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We describe a patient with symptomatic giant hepatic hemangioma treated with hepatectomy. A 53-year-old woman presented with upper abdominal distension and appetite loss. The medical history included multiple hepatic hemangiomas that had been detected 2 years earlier but were left untreated. Initial laboratory tests revealed pancytopenia and mild coagulopathy. Computed tomography and magnetic resonance imaging demonstrated a giant hemangioma, 27 cm in diameter, in the enlarged right lobe of the liver. The inferior vena cava was compressed by tumor without thrombus in the infrahepatic vena cava. The portal venous phase of supramesenteric arteriography revealed compression of the portal vein. There were several hemangiomas in the left lobe. Gastric outlet obstruction due to giant hepatic hemangioma in the right lobe was diagnosed. Laparotomy was performed, and a markedly enlarged liver was detected. Right hepatectomy was performed with an anterior approach. The liver-hanging maneuver could not be performed because of tumor compression of the inferior vena cava. Right hepatectomy was performed with intermittent clamping (Pringle maneuver). Hepatic hemangiomas of the left lobe were not resected because the remnant liver would be reduced. The weight of the resected specimen was 2,100 g. Pathologic examination of the surgical specimen confirmed the presence of benign hepatic hemangiomas. The postoperative course was uneventful, and the patient's appetite improved. The patient was discharged 8 days after the operation. Abdominal distension decreased and laboratory data improved after the operation. Computed tomography revealed hypertrophy of the left lobe of the liver after the operation.

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We present here a case of isolated torsion of a left normal fallopian tube at 37 weeks' gestation. Although uncommon, especially on the left side, torsion of the fallopian tube should be included in the differential diagnosis of abdominal pain during pregnancy.

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Postnatal examination of fetal appendages is important because this information may help predict perinatal outcome. We present a case of a red streak along the entire umbilical vein after a cesarean section due to non-reassuring fetal status. The pathological findings revealed an umbilical cord with dilated vascular changes and mild funisitis. Because the dilated change was intense in the umbilical vein, the red streak of the umbilical cord was caused by venous congestion. Moreover, we considered that the umbilical venous congestion was due to increased resistance in the fetal intra-abdominal umbilical vein, which was associated with the non-reassuring fetal status.

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