Does high thoracic epidural analgesia with levobupivacaine preserve myocardium? A prospective randomized study.

BACKGROUND: Our study aimed to compare HTEA and intravenous patient-controlled analgesia (PCA) in patients undergoing coronary bypass graft surgery (CABG), based on haemodynamic parameters and myocardial functions. MATERIALS AND METHODS: The study included 34 patients that were scheduled for elective CABG, who were randomly divided into 2 groups. Anesthesia was induced and maintained with total intravenous anesthesia in both groups while intravenous PCA with morphine was administered in Group 1 and infusion of levobupivacaine was administered from the beginning of the anesthesia in Group 2 by thoracic epidural catheter. Blood samples were obtained presurgically, at 6 and 24 hours after surgery for troponin I, creatinine kinase-MB (CK-MB), total antioxidant capacity, and malondialdehyde. Postoperative pain was evaluated every 4 hours until 24 hours via VAS. RESULTS: There were significant differences in troponin I or CK-MB values between the groups at postsurgery 6 h and 24 h. Heart rate and mean arterial pressure in Group 1 were significantly higher than in Group 2 at all measurements. Cardiac index in Group 2 was significantly higher than in Group 1 at all measurements. CONCLUSION: Patients that underwent CABG and received HTEA had better myocardial function and perioperative haemodynamic parameters than those who did not receive HTEA.

Experimental study on the effects of massive bowel resection on liver function and hepatocyte apoptosis.

BACKGROUND/AIMS: The effects of short-bowel syndrome on liver function and liver morphology independent of parenteral nutrition have not been thoroughly investigated. Our aim was to investigate the effects of massive bowel resection on hepatocyte apoptosis and liver function in rats. MATERIALS AND METHODS: A total of 37 female Sprague-Dawley rats were randomly assigned to five groups: Control (no procedure); Sham 1 [laparotomy (LT)/enterotomy (ET); evaluated on postoperative day (POD) 1]; Sham 2 (LT/ET; evaluated on POD7; Group 1 (80% bowel resection after LT/ET; POD1); and Group 2 (80% bowel resection; POD7). Blood samples were obtained for measuring aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase levels. For assessing hepatocyte apoptosis, liver tissue samples from the median lobe were obtained and used for a terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick-end labeling assay. RESULTS: Aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase levels showed statistically significant differences among the five groups. Apoptotic hepatocyte counts there were statistically significant differences among groups for counts made in 20 consecutive high-power fields. However, liver sinusoidal cell apoptosis rates among groups showed statistically significant differences for counts made in 20 consecutive high-power fields, particularly on POD7 in rats undergoing massive bowel resection. CONCLUSION: Parenteral nutrition is not the only factor involved in liver dysfunction after massive bowel resection. Massive bowel resection alone can cause liver abnormalities. Rats undergoing massive small intestinal resection show significant temporal increases in liver sinusoidal cell apoptosis rates.

Does on-pump normothermic beating-heart valve surgery with low tidal volume ventilation protect the lungs?

BACKGROUND: Postoperative pulmonary dysfunction following cardiopulmonary bypass (CPB) usually develops secondary to the inflammatory process with contact activation, hypothermia, operative trauma, general anesthesia, atelectasis, pain, and pulmonary ischemia/reperfusion due to cross-clamping. The aim of the present study was to evaluate the effects of an on-pump, normothermic, and beating-heart technique and of low-volume ventilation on lung injury. METHODS: We compared the results for 20 patients who underwent operations with an on-pump, normothermic, and beating-heart technique of mitral valve surgery with low-volume ventilation (group 1) with the results for 23 patients who underwent their operations with an on-pump, hypothermic cardiac-arrest technique (group 2). In both groups, blood samples were collected from the right superior pulmonary vein, and inflammation and oxidative stress markers (malondialdehyde, lactic acid, platelet-activating factor, and myeloperoxidase) were studied. RESULTS: Malondialdehyde, myeloperoxidase, and lactate values were significantly lower in group 1 than in group 2 just before the termination of CPB (P < .05). We observed no differences between the 2 groups with regard to values for platelet-activating factor. CONCLUSIONS: Inflammation and oxidative stress markers were lower in the group of patients who underwent beating-heart valve surgery with low-volume ventilation. These results reflect less of an ischemic insult and lower inflammation compared with the results for the patients who underwent conventional operations.

Decreased plasma concentrations of adiponectin in patients with slow coronary flow.

Adiponectin has multiple protective effects on vascular endothelium through anti-inflammatory and anti-atherogenic properties. Recent data suggested that endothelial activation and inflammation may contribute to the pathogenesis of slow coronary flow (SCF). Therefore, we investigated whether adiponectin plasma concentrations were decreased in patients with SCF compared to subjects with normal coronary flow. The study population consisted of 35 patients with angiographically documented SCF in all three coronary arteries and 35 sex- and age-matched cases with normal coronary flow. Coronary flow rates of all participants were determined by Thrombolysis in Myocardial Infarction (TIMI) frame count. Plasma adiponectin concentrations were measured by an enzyme-linked immunosorbent assay method using commercially available adiponectin kits. There were no statistically significant differences between the patients with SCF and the subjects with normal coronary flow in terms of demographic characteristics and cardiovascular risk factors (P>0.05). Plasma adiponectin concentrations of patients with SCF were found to be significantly lower than those with normal coronary flow (4.77+/-3.86 mg/ml vs 10.8+/-6.60 mg/ml, P=0.001, respectively). Plasma adiponectin levels were correlated significantly and inversely with mean TIMI frame count in patients with SCF (r= -0.441, P=0.008). Furthermore, the Receiver Operator Characteristics curve of adiponectin concentrations showed that an adiponectin <4.6 mg/ml is associated with SCF with a sensitivity of 68.6%, specificity of 82.9%, positive predictive value of 80.0%, and negative predictive value of 72.5%. Our findings suggest that endothelial inflammation may play a role in the pathogenesis of SCF phenomenon.

Impact of plasma adiponectin levels to the presence and severity of coronary artery disease in patients with metabolic syndrome.

OBJECTIVES: Adiponectin is thought to serve a protective function for the coronary endothelium by inhibiting many of the crucial steps in atherosclerotic process. Previous research has indicated an increased risk of coronary artery disease (CAD) in patients with metabolic syndrome (MetS). The objective of this study was to investigate whether plasma adiponectin concentrations were associated with the presence and severity of CAD in patients with MetS undergoing coronary angiography. METHODS: We measured plasma adiponectin levels in 167 consecutive patients with MetS undergoing coronary angiography. The severity of coronary atherosclerosis was defined by using Gensini score system. RESULTS: CAD was found in 70.1% of the patients. Patients with significant CAD had lower plasma adiponectin concentrations than those without CAD (4.14+/-3.83 vs. 8.94+/-6.63 microg/ml, P<0.001). Multiple regression analysis demonstrated that plasma adiponectin level was independently associated with CAD (odds ratio: 0.86; 95% confidence interval: 0.78-0.94; P=0.001). Plasma adiponectin levels were inversely related to the Gensini score (rho: -0.480, P<0.001) and predicted the severity of coronary atherosclerosis independent of other risk factors (beta: -0.054; 95% confidence interval: -0.074--0.034; P<0.001). CONCLUSIONS: These findings suggest that hypoadiponectinemia may play a role in the development of coronary atherosclerosis and the observation of adiponectin levels may be indicative of the presence of significant CAD in patients with MetS.

The effect of percutaneous balloon mitral valvuloplasty on N-terminal- pro B- type natriuretic peptide plasma levels in mitral stenosis.

The objectives of this study were to assess the effect of percutaneous mitral balloon valvuloplasty (PBMV) on the plasma levels of N-terminal-pro B-type natriuretic peptide (NT-proBNP) in patients with mitral stenosis (MS) and to investigate the relationship between the changes in hemodynamic variables and NT-proBNP levels after PBMV. Plasma NT-proBNP concentrations were obtained from 60 symptomatic patients with rheumatic MS who underwent PBMV, and in 35 age- and gender-matched healthy volunteers. Patients with MS were found to have significantly higher levels of plasma NT-proBNP compared to the control group (293 [77-1093] pg/mL versus 24 [12-67] pg/mL, respectively; [P < 0.001]). The mean preprocedural NT-proBNP level fell significantly from 293 (77-1093) pg/mL to 214 (69-1028) pg/mL (P < 0.001) following PBMV. The percentage decrease in plasma NT- proBNP levels was correlated only with the percentage decrease in systolic pulmonary artery pressure (r = 0.687, P < 0.001) and this correlation persisted in linear regression analysis (beta = -0.013; 95% CI [-0.018- -0.008] and P < 0.001). However, NT-proBNP levels did not correlate with the percentage of improvement in NYHA functional class, mitral valve gradients, or left atrial pressure (all P > 0.05). These findings indicate that NT-proBNP measurement following PBMV may be valuable for evaluating changes in pulmonary artery pressure and that elevated NT- proBNP levels in patients with MS may reflect the increased wall stress in the left atrium and right side of the heart.

Increased plasma soluble adhesion molecules; ICAM-1, VCAM-1, and E-selectin levels in patients with slow coronary flow.

BACKGROUND: Inflammation has been reported to be a major contributing factor to many cardiovascular events. In the present study, we aimed to evaluate plasma soluble adhesion molecules; intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin as possible indicators of endothelial activation or inflammation in patients with slow coronary flow. METHOD: Study population included 17 patients with angiographically proven normal coronary arteries and slow coronary flow in all three coronary vessels (group I, 11 male, 6 female, mean age=48+/-9 years), and 20 subjects with angiographically proven normal coronary arteries without associated slow coronary flow (group II, 11 male, 9 female, mean age=50+/-8 years). Coronary flow rates of all patients and control subjects were documented by Thrombolysis In Myocardial Infarction frame count (TIMI frame count). All patients in group I had TIMI frame counts greater than two standard deviation above those of control subjects (group II) and, therefore, were accepted as exhibiting slow coronary flow. Serum levels of ICAM-1, VCAM-1, and E-selectin were measured in all patients and control subjects using commercially available ELISA kits. RESULTS: Serum ICAM-1, VCAM-1, and E-selectin levels of patients with slow coronary flow were found to be significantly higher than those of control subjects with normal coronary flow (ICAM-1: 545+/-198 ng/ml vs. 242+/-113 ng/ml respectively, p<0.001, VCAM-1: 2040+/-634 ng/ml vs. 918+/-336 ng/ml respectively, p<0.001, E-selectin: 67+/-9 ng/ml vs. 52+/-8 ng/ml respectively, p<0.001). Average TIMI frame count was detected to be significantly correlated with plasma soluble ICAM-1 (r=0.550, p<0.001), VCAM-1 (r=0.569, p<0.001) and E-selectin (r=0.443, p=0.006). CONCLUSION: Increased levels of soluble adhesion molecules in patients with slow coronary flow may be an indicator of endothelial activation and inflammation and are likely to be in the causal pathway leading to slow coronary flow.