These results suggest that EAT may reflect the amount of visceral fat, which is associated with insulin resistance and inflammation. The echocardiographic measurement of EAT may provide additional information for assessing CAD risk and predicting the extent and activity of CAD.

Clinically important myocarditis is an unusual feature in systemic lupus erythematosus (SLE). We describe the clinical characteristics, management and outcomes of Wve SLE patients who developed severe left ventricular dysfunction. Four patients were female with mean age of 36.4 years. Three patients had both lupus myocarditis and lupus nephritis. Four patients had raised anti-dsDNA antibody titer and low complement level and two patients had positive IgG anticardiolipin antibody. Three patients were treated by high-dose corticosteroids, one patient by intravenous pulse methylprednisolone, and one patient by intravenous immunoglobulin and pulse cyclophosphamide with high dose corticosteroids. Left ventricular function improved markedly in four patients and all of them had no recurrence of lupus myocarditis up to follow-up of 33 months. However, one patient, who showed no improvement of left ventricular function, was expired due to sudden cardiac arrest. Lupus myocarditis should be treated by immunosuppressive therapy with high-dose corticosteroids and mostly the prognosis might be good with early treatment.

Systemic lupus erythematosus (SLE) is a typical autoimmune disease that's characterized by various autoantibodies to nuclear and cytoplasmic antigens. The presence of antinuclear antibodies (ANA) in serum is generally considered a decisive diagnostic sign of SLE. However, a small subset of SLE patients who had the typical clinical features of SLE was reported to show persistently negative ANA tests. Our report describes a 16-yr-old female who presented with the clinical manifestations of SLE such as malar rash, photosensitivity, arthritis, lymphopenia, pericarditis and proteinuria. The serum autoantibodies were all negative and renal biopsy showed that the histopathological changes of immune complex mediated the focal segmental necrotizing glomerulonephritis with crescent formation. She was treated with monthly pulse cyclophosphamide along with corticosteroids. During the 2-yr follow-up period, the proteinuria was markedly decreased and all of the ANA and anti-double stranded DNA antibody tests were negative. This case suggests that ANA may not be required in the pathogenesis of lupus nephritis.

Background and ObjectivesContrast-induced nephropathy (CIN) is associated with increased morbidity and mortality. This observational, non-randomized study evaluated the effect of rosuvastatin loading before percutaneous coronary intervention (PCI) on the incidence of CIN in patients with acute coronary syndrome (ACS).Subjects and MethodsA total of 824 patients who underwent PCI for ACS were studied (408 patients in the statin group=40 mg rosuvastatin loading before PCI; 416 patients of control group=no statin pretreatment). Serum creatinine concentrations were measured before and 24 and 48 hours after PCI. The primary endpoint was development of CIN defined as an increase in serum creatinine concentration of ≥0.5 mg/dL or ≥25% above baseline within 72 hours after PCI.ResultsThe incidence of CIN was significantly lower in the statin group than that in the control group (18.8% vs. 13.5%, p=0.040). The maximum percent changes in serum creatinine and estimated glomerular filtration rate in the statin group within 48 hours were significantly lower than those in the control group (5.84±22.59% vs. 2.43±24.49%, p=0.038; -11.44±14.00 vs. -9.51±13.89, p=0.048, respectively). The effect of rosuvastatin on preventing CIN was greater in the subgroups of patients with diabetes, high-dose contrast medium, multivessel stents, high baseline C-reactive protein, and myocardial infarction. A multivariate analysis revealed that rosuvastatin loading was independently associated with a decreased risk for CIN (odds ratio, 0.64; 95% confidence interval, 0.43-0.95, p=0.026).ConclusionHigh-dose rosuvastatin loading before PCI was associated with a significantly lower incidence of CIN in patients with ACS.

A 78-year-old man with a history of dilated cardiomyopathy diagnosed 5 years previously was admitted to our clinic with accelerating chest pain and dyspnea. The initial ECG showed sinus tachycardia and left bundle-branch block. Laboratory tests revealed elevated levels of troponin T (0.409 ng/mL), creatinine kinase (218 U/L), and creatinine kinase-MB isoenzyme (9.8 g/L). The peak level of creatinine kinase-MB isoenzyme was 41.9 g/L. Transthoracic echocardiography revealed a more progressed left ventricular remodeling in comparison with an echocardiography conducted 2 years previously. Compared with the previous study, the end-diastolic dimension of the left ventricle (LV) was increased from 68 mm to 76 mm and the LV end-diastolic volume was increased from 199 mL to 331 mL. Previously, the LV showed global hypokinesia with decreased global LV systolic function (ejection fractionϭ30%). The present study showed worsened regional wall motion abnormality at the territories of the left anterior descending coronary artery (LAD) with aggravated LV dysfunction (ejection fractionϭ23%; online-only Data Supplement Movies I and II).Coronary angiography revealed an unusual obstruction of the distal LAD (Figure 1). In the course of distal LAD, a filling defect, evident as a seeming loss of contrast, abruptly began and ended with sharp edges. The proximal and distal reference segments appeared normal. Intravascular ultrasonography (IVUS) and optical coherence tomography revealed that the distal LAD was deformed to a slitlike appearance, suggesting an extrinsic compression (Figure 2). To evaluate the cause of extrinsic compression of the distal LAD, cardiac multidetector computed tomography was performed. Cardiac multidetector computed tomography showed no evidence of mediastinal or intrathoracic masses, which could cause the extrinsic compression of LAD. Because the severely dilated LV contacted with the chest wall, the distal LAD was trapped between dilated LV and costochondral cartilage and was narrowed because of extrinsic compression by the costochondral cartilage (Figures 3 and 4). A diagnosis was made of extrinsic compression of the distal LAD secondary to LV remodeling resulting from dilated cardiomyopathy.