No abstract

n acute occlusion of coronary artery fails into acute myocardial infarction (AMI) and it is thought that rupture of vulnerable fibrous caps of atherosclerotic plaque is involved. 1,2 Several cytokines, including interleukin-1 (IL-1 ), IL-6 and tumor necrosis factor-(TNF-), may be released from vulnerable plaques, [3][4][5][6] which then activates macrophages. [7][8][9][10] Most studies have investigated the atherosclerotic plaques of experimental animals [8][9][10][11] and there are only a few clinical reports of mild elevation of cytokines in the systemic circulation after rupture of atherosclerotic plaque. [12][13][14][15][16] Only one study has reported the regional changes in cytokines in the occluded coronary artery, 17 but the recent development of a coronary artery intervention technique now enables us to find any local alteration in the infarct-related coronary artery. 18 In the present study we determined regional changes in cytokines and proteolytic enzymes in the infarct-related coronary artery in patients with AMI in order to elucidate the pathological role of inflammation in acute occlusion of a coronary artery. Circulation Journal Vol.68, May 2004 Methods SubjectsThirty-six patients with AMI were admitted to the Emergency Units of Jichi Medical School Omiya Medical Center between March 2001 and July 2002 (28 males, 8 females; age range, 37-84 years (62.6±11.9 years, mean ± SD)). The diagnosis of AMI was determined by the findings of continuous chest pain lasting more than 30 min, ST-segment elevation greater than 2.0 mm on at least 2 successive ECG leads, and a more than 2-fold increase in serum creatine kinase (CK) concentrations. Most of the patients had one or more coronary risk factors; that is, 19 patients had diabetes mellitus, 11 had hyperlipidemia, 26 had hypertension, 14 were obese and 25 smoked. Only one patient did not have any coronary risk. Anterior myocardial infarction was found in 26 patients, lateral myocardial infarction in 1 and inferior myocardial infarction in 9. Maximal serum concentrations of CK ranged from 379 to 8,270 mU/ml (3,048.8±1,651.6 mU/ml, mean ± SD). Cardiac catheterization was carried out within 24 h of the onset of myocardial infarction in all the patients. We excluded those with cardiogenic shock, chronic renal failure on hemodialysis, apparent infectious disease, bypass failure, history of prior use of thrombolytic therapy and those in whom it was not possible to cross the target lesion with a thrombectomy catheter because of excessive proximal vessel tortuosity. Study ProtocolBlood samples were collected in chilled tubes containing EDTA-Na2 (1 mg/ml blood) from a peripheral vein, and Background To elucidate the involvement of inflammation in coronary artery occlusion, the regional changes in cytokines and matrix metalloproteinases (MMPs) in the infarct-related coronary artery were determined in patients with acute myocardial infarction. Methods and ResultsCardiac catheterization was carried out within 24 h of the onset of infarction in 36 patients. Blood sampl...

Postprandial hyperglycemia is a risk factor for cardiovascular disease and mortality. Serum 1,5-anhydroglucitol (1,5-AG) level is an useful clinical marker of glucose metabolism which reflects postprandial hyperglycemia more robustly compared to hemoglobin A1c (HbA1c). Relationship between serum 1,5-AG level and cardiovascular disease has been reported; however, comparison between HbA1c and 1,5-AG as markers of cardiovascular disease was not performed. We included 227 consecutive patients who underwent coronary angiography meeting the following inclusion criteria: (1) patients who had no history of coronary artery disease (CAD); (2) patients without acute coronary syndrome; (3) patients without poorly controlled diabetes mellitus; (4) patients without anemia, liver dysfunction, acute, and chronic renal failure and malnutrition; and (5) patients without adhibition of acarbose or Chinese herbal medicine. We measured HbA1c, glycoalbumin, and 1,5-AG. Serum 1,5-AG was significantly lower in patients with CAD (16.6 ± 8.50 vs. 21.1 ± 7.97 μg/ml, P < 0.001). Multivariable logistic regression analysis showed decrease in serum 1,5-AG was independently associated with the presence of denovo CAD (0.93, 95% CI 0.88-0.98, P = 0.006). Serum 1,5-AG was also independently associated with the presence of denovo CAD in patients without diabetes mellitus (0.94, 95% CI 0.88-0.99, P = 0.046). In conclusion, lower serum 1,5-AG was associated with the presence of denovo CAD. Serum 1,5-AG may identify high cardiovascular risk patients for denovo CAD in both diabetic and non-diabetic patients.

Introduction: Aberrant expression of T-cell markers is occasionally observed in B-cell lymphomas. We conducted a retrospective study to establish its incidence and to determine its relationship with clinical features of patients with diffuse large B-cell lymphoma (DLBCL). Patients and Methods: We reviewed DLBCL patients diagnosed between January 2002 and April 2009. Patients fulfilled the following criteria: (1) age >18 years, (2) HIV negative, (3) B-cell lymphoma confirmed by restricted expression of surface immunoglobulin light chains by flow cytometry (FCM). Aberrant T-cell marker expression (ATCME) was defined as positivity for CD2, CD3, CD4, CD7, and/or CD8 on DLBCL cells by FCM. Phenotyping was also performed by immunohistochemistry (IHC). Patients were grouped according to positive or negative ATCME and their clinical features including survival were compared. Results: Of 150 patients, 11 (7.3%) showed ATCME; CD2 and CD7 were most often expressed. ATCME was less often detected and the signal was weaker using IHC. There were no statistically significant differences in clinical features between the two groups. Conclusions: FCM may be useful to detect ATCME in a small amount of lymphoma cells. The mechanism responsible for ATCME, and whether it contributes in any way to the pathogenesis of B-cell neoplastic transformation, requires clarification.

Increased LV wall thickness and decreased hemoglobin concentration might contribute to LA enlargement in patients with normal LV systolic function irrespective of gender.