A cute pulmonary embolism (PE) is a potentially lifethreatening disease, spanning a wide spectrum of clinical outcomes.1 Hemodynamically stable patients with preserved right ventricular (RV) size and function are classified as lowrisk patients and have an excellent short-term prognosis once therapeutic levels of anticoagulation therapy are established. 2In contrast, hemodynamically unstable patients are at high risk of death from worsening RV failure and cardiogenic shock, with a hospital mortality rate >15%. 3,4 Approximately one quarter of hemodynamically stable patients with PE are at intermediate risk, with mortality rates ranging from 3% to 15% if imaging or biomarker evidence of RV dilatation or dysfunction is present. 5,6 Editorial see p 420 Clinical Perspective on p 486Systemic thrombolysis improves hemodynamic parameters 7 and reverses RV dilatation and dysfunction 8,9 but is associated with rates of major bleeding complications in up to 20% and intracranial hemorrhage in up to 3%.10,11 Systemic thrombolysis is standard treatment for high-risk PE 2,11 ; however, it is withheld in more than two thirds of such patients. 4,12 The use of systemicBackground-In patients with acute pulmonary embolism, systemic thrombolysis improves right ventricular (RV) dilatation, is associated with major bleeding, and is withheld in many patients at risk. This multicenter randomized, controlled trial investigated whether ultrasound-assisted catheter-directed thrombolysis (USAT) is superior to anticoagulation alone in the reversal of RV dilatation in intermediate-risk patients. Methods and Results-Fifty-nine patients (63±14 years) with acute main or lower lobe pulmonary embolism and echocardiographic RV to left ventricular dimension (RV/LV) ratio ≥1.0 were randomized to receive unfractionated heparin and an USAT regimen of 10 to 20 mg recombinant tissue plasminogen activator over 15 hours (n=30; USAT group) or unfractionated heparin alone (n=29; heparin group). Primary outcome was the difference in the RV/LV ratio from baseline to 24 hours. Safety outcomes included death, major and minor bleeding, and recurrent venous thromboembolism at 90 days. In the USAT group, the mean RV/LV ratio was reduced from 1.28±0.19 at baseline to 0.99±0.17 at 24 hours (P<0.001); in the heparin group, mean RV/LV ratios were 1.20±0.14 and 1.17±0.20, respectively (P=0.31). The mean decrease in RV/LV ratio from baseline to 24 hours was 0.30±0.20 versus 0.03±0.16 (P<0.001), respectively. At 90 days, there was 1 death (in the heparin group), no major bleeding, 4 minor bleeding episodes (3 in the USAT group and 1 in the heparin group; P=0.61), and no recurrent venous thromboembolism. Conclusions-In

Objectives-Pericardial fat as a visceral fat depot may be involved in the pathogenesis of coronary atherosclerosis. To gain evidence for that concept we sought to investigate the relation of pericardial fat volumes to risk factors, serum adiponectin levels, inflammatory biomarkers, and the quantity and morphology of coronary atherosclerosis. PϾ0.001). No association was found between BMI and coronary atherosclerosis. PAT volumes Ͼ300 cm 3 were the strongest independent risk factor for coronary atherosclerosis (odds ratio 4.1; CI 3.63 to 4.33) also significantly stronger compared to the Framingham score. We furthermore demonstrated that elevated PAT volumes are significantly associated with low adiponectin levels, low HDL levels, elevated TNF-␣ levels, and hsCRP. Conclusion-In the present study we demonstrated that elevated PAT volumes are associated with coronary atherosclerosis, hypoadiponectinemia, and inflammation and represent the strongest risk factor for the presence of atherosclerosis and may be important for risk stratification and monitoring. Key Words: cardiac CT Ⅲ pericardial fat Ⅲ obesity Ⅲ adiponectin Ⅲ plaque imaging T here is growing evidence that regional visceral fat distribution may contribute to an unfavorable metabolic and cardiovascular risk profile. 1,2 In patients with obesity, insulin resistance, diabetes, and hyperlipidemia visceral fat hypertrophies and transforms into a multifunctional organ that produces and secretes multiple endocrine and paracrine factors promoting inflammation, neovascularization, and oxidative stress, features that also characterize atherosclerosis. 3 Pericardial fat as a local visceral fat depot with close proximity to coronary arteries may serve as a source of inflammatory cytokines and cells that may locally enhance systemic proatherogenic effects via outside to inside signaling. 4,5 Thus it may be a specific parameter indicating an unfavorable cardio-metabolic state and may be used for risk stratification. To date, however, only little attention has focused on this regional fat depot located around the heart and its relation to cardiovascular risk factors, and the quantity and composition of coronary atherosclerosis is not well studied yet. Methods and Results-UsingMulti-slice CT is a noninvasive tool that allows to reliably assess both obstructive and nonobstructive subclinical coronary artery disease in an earlier stage than invasive angiography. 6 -9 Based on density measurements, plaques can be further characterized in noncalcified, mixed, and calcified plaques. 7 By using the same scan data this tool furthermore allows to quantify the exact pericardial fat volume. 9 We thus sought to assess the relation of pericardial fat volume to cardiovascular risk factors, levels of inflammatory cytokines, adiponectin, and to the extent and the phenotype of coronary atherosclerosis.