MDCT-CA by prospective gating showed equivalent coronary assessability and diagnostic accuracy with decreased radiation dose in comparison with a retrospective ECG-gated helical scan with tube current modulation.

The clustering of risk factors including dyslipidemia, hyperglycemia, and hypertension is highly atherogenic along with the excess of remnants from triglyceride (TG)-rich lipoproteins. CD36 is involved in the uptake of long-chain fatty acids (LCFAs) in muscles and small intestines. Patients with CD36 deficiency (CD36-D) have postprandial hypertriglyceridemia, insulin resistance, and hypertension. To investigate the underlying mechanism of postprandial hypertriglyceridemia in CD36-D, we analyzed lipoprotein profiles of CD36-D patients and CD36-knockout (CD36-KO) mice after oral fat loading (OFL). In CD36-D patients, plasma triglycerides, apolipoprotein B-48 (apoB-48), free fatty acids (FFAs), and free glycerol levels were much higher after OFL than those of controls, along with increases in chylomicron (CM) remnants and small dense low-density lipoprotein (sdLDL) particles. In CD36-KO mice, lipoproteins smaller than CM in size in plasma and intestinal lymph were markedly increased after OFL and mRNA levels of genes involved in FFA biosynthesis, such as fatty acid binding protein (FABP)-1 and FAS, were significantly increased. These results suggest that CD36-D might increase atherosclerotic risk by enhancing plasma level of CM remnants due to the increased synthesis of lipoproteins smaller than CM in size in the intestine.-

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Background: Although statins vary in their effectiveness in lowering low-density lipoprotein cholesterol (LDL-C) and increasing high-density lipoprotein cholesterol (HDL-C) levels, there is little evidence that the degree of these changes can explain cardiac risk reduction in Japan. Our objective was to compare the efficacy of statins on serum lipid levels and to explore the association between those changes and cardiac events in patients after percutaneous coronary intervention (PCI). Methods and Results:The 743 consecutive patients who underwent PCI from 2001 to 2008 were retrospectively investigated. Treatment with either atorvastatin or pitavastatin significantly reduced LDL-C compared with pravastatin or no statin. In contrast, only pitavastatin treatment significantly increased HDL-C (13.4±22.9%, P=0.01 vs. no statin). Each statin significantly prevented major adverse cardiac events (MACE) compared with no statin, and pitavastatin was the most effective of all. Multivariate-adjusted analysis revealed that percent changes of both LDL-C and HDL-C independently predicted the incidence of MACE (hazard ratio [HR]: 1.015; 95% confidence interval [CI]: 1.010-1.020, HR: 0.988; 95%CI: 0.981-0.996, respectively). This relationship was preserved in patients with a baseline HDL-C level ≤45 mg/dl, but not HDL-C level >45 mg/ml. Conclusions:The extent of changes in LDL-C and HDL-C with statin treatment would independently alter the risk of cardiac events in Japanese patients for secondary prevention. Statins with varying lipid-modifying ability might provide differing prognosis in patients after PCI. (Circ J 2011; 75: 1951 - 1959 1952MARUYAMA T et al.and Welfare of Japan, and approved by the ethics committee of the hospital.

A 58-year-old female with a history of Wolff-Parkinson-White syndrome presented at our institution with palpitations and chest pain. Electrocardiography revealed paroxysmal supraventricular tachycardia with a heart rate of 188 beats/min. Antiarrhythmic drugs were ineffective, and tachycardia was resolved by electrical cardioversion. Transthoracic echocardiography revealed abnormal vessels around the right coronary artery (RCA) and pulmonary artery (PA); in addition, we suspected coronary arteriovenous fistula (CAVF). Coronary angiography and coronary computed tomography revealed dilated fistula vessels, with a 1 cm saccular aneurysm around the RCA, originating from the proximal RCA and left anterior descending artery into the main trunk of PA. Therefore, we confirmed the diagnosis of CAVF with an unruptured aneurysm. We surgically ligated and clipped the fistula vessels and resected the aneurysm. The resected aneurysm measured 1 × 1 cm in size. Pathological examination of the resected aneurysm revealed hypertrophic walls comprising proliferating fibroblasts cells thin elastic fibers. Very few atherosclerotic changes manifested in the aneurysm walls. We report the case of a patient with CAVF and an unruptured coronary artery aneurysm who was successfully treated by surgery.