t is widely recognized that accumulation of abdominal visceral fat is strongly related to the development of coronary artery disease (CAD). [1][2][3][4][5][6] Epicardial adipose tissue (EAT) is the actual visceral fat of the heart deposited under the visceral layer of the pericardium and has the same origin as abdominal visceral fat. Pathological investigations revealed EAT and the adventitia of coronary arteries or myocardium to be contiguous, with no intervening structures. 7 The accumulation of EAT shows a good correlation with the volume of abdominal visceral fat and EAT is also known to be a rich source of free fatty acids and a number of bioactive molecules and inflammatory cytokines. [8][9][10][11] Some reports have suggested a crucial role of EAT in the development of CAD through changes in adipokine expressions in EAT, which promote pro-inflammatory characteristics, thereby possibly facilitating the progression of coronary atherosclerosis. [9][10][11] In fact, de Vos et al have reported that peri-coronary EAT thickness is strongly related to vascular risk factors and coronary calcification in post-menopausal women. 12 A recent study demonstrated that 64-slice multidetectorrow computed tomography (MDCT) is suitable for volumetric quantification of EAT with higher reproducibility than measurements of EAT thickness by echocardiography, and that excessive accumulation of EAT was associated with obesity and metabolic syndrome. 13 MDCT provides noteworthy information about coronary arteries including not only the presence and degree of stenotic lesions but also of subclinical atherosclerotic plaques. 14-19 MDCT can identify atherosclerotic plaques, in vessels with only minimal angiographic disease, with high sensitivity and moderate specificity as compared with intravascular ultrasound (IVUS). Moreover, MDCT can detect significant atherosclerotic plaques in vessels with signs of positive remodeling, which tend to be underestimated by conventional coronary angiography (CAG). 20,21 We sought to determine the relationship between the epicardial fat volume and the severity and extent of atherosclerosis of the whole coronary tree using CAG and MDCT in patients presenting with a possible diagnosis of stable effort angina. The relationship between the epicardial fat volume measured by 64-slice multidetector computed tomography (MDCT) and the extension and severity of coronary atherosclerosis was investigated. Methods and Results: Both MDCT and conventional coronary angiography (CAG) were performed in 71 consecutive patients who presented with effort angina. The volume of epicardial adipose tissue (EAT) was measured by MDCT. The severity of coronary atherosclerosis was assessed by evaluating the extension of coronary plaques in 790 segments using MDCT data, and the percentage diameter stenosis in 995 segments using CAG data. The estimated volume of EAT indexed by body surface area was defined as VEAT. Increased VEAT was associated with advanced age, male sex, degree of metabolic alterations, a history of acute corona...

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D-dimer measurement is a useful complementary initial diagnostic marker in patients with acute aortic dissection (AAD). However, it has not been clarified whether serial measurements of D-dimer are useful during in-hospital management of Stanford type B AAD. We studied 30 patients who were admitted with diagnosis of Stanford type B AAD and treated conservatively. D-dimer was serially measured on admission and then every 5 days during hospitalization. Patients were divided into two groups according to the presence or absence of re-elevation of D-dimer during hospitalization, in which D-dimer transition were biphasic and latter peak >10.0 μg/ml. Re-elevation of D-dimer was observed in 17 patients. There were no differences in atherosclerotic risk factors, blood pressure on admission, D-dimer level on admission, extent of AAD, and false lumen patency. Patients with re-elevation of D-dimer showed higher incidence of re-dissection and/or venous thromboembolism (VTE). Peak D-dimer level in patients with re-dissection and/or VTE was significantly higher than that without these complications (p = 0.005). In conclusion, serial measurements of D-dimer are useful for early detection of re-dissection or VTE in patients with Stanford type B AAD, which may contribute to the prevention of disastrous consequences such as pulmonary embolism and extension of AAD.

We have reported that serum C-reactive protein (CRP) elevation is an independent predictor of lung oxygenation impairment (LOI) after distal type acute aortic dissection (AAD). Systemic activation of the inflammatory system after aortic injury may play a role in the development of LOI. The aim of this study is to clarify the effect of beta-blockers on systemic inflammation and the development of LOI after distal type AAD. A total of 49 patients, who were admitted with distal type AAD and treated conservatively, were examined. White blood cell (WBC) count, serum CRP level, and arterial blood gases were measured serially. Forty patients received beta-blocker treatment within 24 h of the onset, while 9 patients received no beta-blocker treatment. Maximum WBC count, maximum CRP level, lowest PaO(2)/FiO(2) (P/F) ratio, and patient background were compared between the two groups. There was no difference between the groups according to age, sex, coronary risk factors, blood pressure, serum level of CRP, WBC count, and oxygenation index on admission. Beta-blocker treatment was associated with lower maximum WBC count (P = 0.0028) and lower maximum serum CRP level (P = 0.0004). The minimum P/F ratio was higher in patients with beta-blocker treatment than in those without (P = 0.0076). Multivariate analysis revealed that administration of a beta-blocker was an independent negative determinant of LOI (P/F ratio < or = 200 mmHg). In conclusion, early use of beta-blockers prevented excessive inflammation and LOI after distal type AAD, suggesting a pleiotropic effect of beta-blockers on the inflammatory response after AAD.

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