Relation of Neutrophil/Lymphocyte Ratio to Coronary Flow to In-Hospital Major Adverse Cardiac Events in Patients With ST-Elevated Myocardial Infarction Undergoing Primary Coronary Intervention

With the growing understanding of the role of inflammation in patients with atherosclerotic disease, studies have focused on high-sensitivity C-reactive protein (hs-CRP) and other inflammatory markers in their association with outcomes in ST-segment elevation myocardial infarction. The goal of this study was to investigate the association of the neutrophil/lymphocyte (N/L) ratio and in-hospital major adverse cardiac events (MACEs) in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention (PCI). The association of hs-CRP and N/L ratio on admission with Thrombolysis In Myocardial Infarction (TIMI) flow grade after PCI was assessed in 418 consecutive primary patients with PCI. The N/L ratio was significantly higher in the no-reflow group (TIMI grade 0/1/2 flow, n = 158) compared to that of the normal-flow group (TIMI grade 3 flow, n = 260, 4.6 ± 1.7 vs 3.1 ± 1.9, p <0.001). In-hospital MACEs were significantly higher in patients with no reflow (23% vs 7%, p <0.001). There was a significant and positive correlation between hs-CRP and N/L ratio (r = 0.657, p <0.001). In receiver operating characteristic analysis, N/L ratio >3.3 predicted no reflow with 74% sensitivity and 83% specificity. In a multivariate regression model, N/L ratio remained an independent correlate of no reflow (odds ratio [OR] 1.54, 95% confidence interval [CI] 1.34 to 1.76, p <0.001) and in-hospital MACEs (OR 1.14, 95% CI 0.98 to 1.32, p = 0.043). The N/L ratio, an inexpensive and easily measurable laboratory variable, is independently associated with the development of no reflow and in-hospital MACEs in patients with ST-segment elevation myocardial infarction undergoing primary PCI.     

Increased carotid intima-media thickness is associated with higher SYNTAX score

The main purpose of this study was to investigate the relation between carotid intima-media thickness (CIMT) and coronary artery disease (CAD) complexity. Consecutive patients (n = 360) with CAD confirmed by coronary angiography were enrolled. Mean CIMT and the overall SYNTAX score (SXscore) were 0.87 ± 0.12 mm and 15 ± 9, respectively. In univariate analysis, there was a significant correlation between the overall SXscore and CIMT (r = .42, P < .001), age (r = .23, P < .001), hypertension (r = .27, P = 0.001), diabetes (r = 0.11, P = 0.02), smoking (r = .24, P = .01), dyslipidemia (r = .2, P = 0.03), and β-blocker use (r = .19, P < .001). In multivariate analysis, CIMT (β = .34, P < .001) and age (β = .11, P < .019) were independently associated with SXscore. We have demonstrated a significant relation between CIMT and SXscore. Although this study is correlative and no causative conclusions can be drawn, our findings suggest that increased CIMT could reflect complex coronary artery lesions.     

Epicardial mass causing cardiac compression: an unusual involvement in lymphomatoid granulomatosis

Lymphomatoid granulomatosis is a rare, diffuse, large B-cell lymphoma that is positive for Epstein-Barr virus. A multiorgan process, it manifests itself chiefly in the lungs but can also affect the skin, nervous system, and kidneys. Cardiac involvement and pericardial effusion are very unusual. We report the case of a 62-year-old man with lymphomatoid granulomatosis involving the heart and lungs. Diagnosis was confirmed with wedge biopsy at pericardiotomy, and the patient was treated with cyclophosphamide, prednisolone, and vincristine. Although the patient was still symptomatic at 6-month follow-up, he was in partial remission with improved functional capacity.     

Effects of montelukast on the healing of ischemic colon anastomoses

Background

The aim of this study was to examine whether treatment with montelukast, a selective leukotriene antagonist, would affect anastomotic healing in a reperfused colon rat model with remote ischemia/reperfusion injury.

Methods

Rats (n = 12 per group) were intraperitoneally administered normal saline or 10 mg/kg montelukast sodium 60 minutes before and for 5 days after surgery. Ischemia was induced for 45 minutes through superior mesenteric artery occlusion. A left colon anastomosis was made. Blood and perianastomotic tissue samples were obtained on postoperative day 5.

Results

Mean anastomotic bursting pressures of the control and montelukast groups were 159.17 ± 29.99 and 216.67 ± 26.40, respectively (P < .001). Compared with saline, montelukast treatment increased the mean tissue hydroxyproline level (2.46 ± .30 vs 3.61 ± .33 μmol/L) and decreased tissue caspase-3 activity (36.06 ± 5.72 vs 21.78 ± 3.87) and malondialdehyde levels (3.43 ± .34 vs 2.29 ± .34 nmol/g) (P < .001 for all). Other plasma markers of injury also showed differences.

Conclusions

Montelukast prevented ischemia/reperfusion-induced damage in a rat model of colonic anastomotic wound healing.     

Chylomediastinum Following Tracheal Surgery

Fever of unknown origin (FUO) is a diagnostic challenge for the practising physician. Detailed medical history, physical examination, non-invasive laboratory tests, and radiologic examinations compose the first level in the diagnostic approach to the FUO. When a diagnosis cannot be established with these procedures, some invasive diagnostic techniques and finally exploratory laparotomy are performed. Although advanced diagnostic measures and imag-ing-guided less invasive procedures have decreased the need, laparotomy remains as a final diagnostic method for FUO cases. In this study we evaluate the role and importance of laparotomy in the diagnosis of our FUO cases. In 17 out of 126 patients (8 male, 9 female, the median age 35.8 years) hospitalized in our clinic between 1982 and 2002 with the diagnosis of FUO, the diagnosis was established by laparotomy. The diagnosis was made directly in 13 patients, and indirectly (by excluding other diseases) in 2 patients. In several FUO series, the contribution of laparotomy to the diagnosis of FUO was reported as 27-100%. This rate was found to be 88% in the present study. During laparotomy on 17 cases, tissue samples were taken from spleen, liver, intra-abdominal and mesenteric lymph nodes. Pathologic examination of these tissue samples revealed miliary tuberculosis in 4; non-Hodgkin’s lymphoma in 3; Hodgkin’s lymphoma in 3; liver tumour in 1; hairy cell leukemia in 1; peritonitis carcinomatosis in 1. In the patients with miliary tuberculosis, the liver (3) and/or spleen (2), and/or lymph node (3) revealed caseating granulomas. Laparotomy diagnosed 3 of 5 cases whose abdominal ultrasonography and computerized tomography were normal. In conclusion, although advanced diagnostic methods decreased the need for laparotomy in FUO, if non-invasive and invasive diagnostic measures fail, laparotomy may contribute to the diagnosis. The selection of the patient and the timing are important for laparotomy.     

Cord blood nesfatin-1 and apelin-36 levels in gestational diabetes mellitus

To assess maternal serum and cord blood apelin-36 and nesfatin-1 concentrations in pregnant women with and without gestational diabetes mellitus (GDM). Thirty pregnant women with GDM and 30 gestational age matched healthy pregnant subjects participated to the study. Maternal serum and cord blood nesfatin-1 and apelin-36 levels were measured with ELISA, at the time of birth. The relationships between maternal serum and cord blood nesfatin-1 and apelin-36 levels, anthropometric and metabolic parameters were also assessed. Maternal serum apelin-36 levels were found higher (13.5?±?8.3 vs. 9.6?±?5.9?ng/ml, P?=?0.001) and nesfatin-1 levels were found lower (5.5?±?8.1 vs. 8.1?±?23.9?ng/ml, P?=?0.001) in patients with GDM compared with control pregnant women. However, the cord blood apelin-36 levels (8.8?±?4.3 and 8.2?±?1.9?ng/ml, P?=?0.618) and nesfatin-1 levels (5.4?±?4.0 and 6.2?±?10.3?ng/ml, P?=?0.688) were similar in the GDM and control groups, respectively. Maternal serum apelin-36 and nesfatin-1 levels correlated positively with their respective cord blood levels. Maternal serum and cord blood apelin-36 levels correlated negatively with the gestational age and birth weight. Similarly maternal serum and cord blood nesfatin-1 levels correlated negatively with the gestational age, but there was no correlation with the birth weight. We did not find a correlation between maternal serum apelin-36 and nesfatin-1 levels, maternal age, BMI, fasting glucose, fasting insulin, and HOMA-IR. Also cord blood apelin-36 and nesfatin-1 levels did not correlate with the maternal age, BMI, HOMA-IR, cord blood glucose, and cord blood insulin levels. Our results indicate that apelin-36 concentrations increase and nesfatin-1 concentrations decrease in maternal serum of women with GDM.