Prophylactic amiodarone versus lidocaine for prevention of reperfusion ventricular fibrillation after release of aortic cross-clamp.

BACKGROUND AND OBJECTIVE: Ventricular fibrillation is common after aortic cross-clamp release in patients undergoing open-heart surgeries. The aim of the study was to evaluate the efficacy of the prophylactic administration of 150 mg amiodarone by way of the pump 2 min before release of aortic cross-clamp in preventing ventricular fibrillation. METHODS: The present study is a prospective, randomized, controlled and blinded study performed at a teaching university hospital where 120 patients undergoing coronary bypass graft surgery were randomly assigned to three groups. Each group received either 150 mg of amiodarone or 100 mg lidocaine or isotonic saline by way of pump 2 min before release of the aortic cross-clamp. The frequency of occurrence of ventricular fibrillation and the subsequent required defibrillation counter shocks were determined in all groups. RESULTS: The frequency of occurrence of ventricular fibrillation was significantly higher in both the amiodarone (48%) and the control group (45%) as compared with the lidocaine group (20%) with no statistically significant difference between the amiodarone and the control groups. Furthermore, when ventricular fibrillation occurred, the percentage of patients requiring defibrillation counter shocks was significantly higher in both the amiodarone (58%) and control (61%) groups as compared with the lidocaine group (13%) with no difference between the amiodarone and the control groups, despite a significant decrease in the defibrillation counter shocks energy requirements in the amiodarone group. CONCLUSION: The present study showed no difference between amiodarone (150 mg) and placebo in preventing ventricular fibrillation after release of aortic cross-clamp. In addition, the use of lidocaine was able to reduce the incidence of ventricular fibrillation as compared with both amiodarone and placebo.

Does ondansetron or granisetron prevent subarachnoid morphine-induced pruritus after cesarean delivery?

BACKGROUND: We compared the efficacy of granisetron and ondansetron for the prevention of subarachnoid morphine-induced pruritus after cesarean delivery. METHODS: The incidence of pruritus was assessed in parturients who were randomly allocated into Group G (granisetron 3 mg IV, n = 45), Group O (ondansetron 8 mg IV, n = 42), and Group S (saline IV, n = 42). RESULTS: The incidence of pruritus was not significantly different among the 3 groups (86.6% in Group S, 83.3% in Group O, and 88% in the Group G). CONCLUSION: Neither prophylactic ondansetron nor granisetron reduced the incidence of subarachnoid morphine-induced pruritus when compared with the saline group.

[Management of diabetes mellitus]. / Diabète sucré: actualités de la prise en charge et objectifs thérapeutiques.

Diabetes mellitus is a chronic disease characterized by carbohydrate metabolic derangement and the onset, over years, of micro- and macrovasculopathies in association with high cardiovascular mortality. The management of diabetics evolved over the years due to a better understanding of the pathophysiology and onset mechanisms of complications of diabetes. It is a multidisciplinary task revolving round the patient and should address, in addition to diabetes mellitus, other cardiovascular risk factors. Therapeutic objectives have improved and set stricter glycemic criteria; it is proven nowadays that a good glycemic control protects against the onset or progression of diabetic complications. This article reviews in details the principles of an efficient management and the latest therapeutic recommendations.

Pravastatin does not affect insulin sensitivity and adipocytokines levels in healthy nondiabetic patients.

BACKGROUND: The effect of statins on insulin resistance is controversial and poorly studied in nondiabetic subjects. In addition, the effect of statins on leptin and adiponectin has never been studied. METHODS: Forty healthy nondiabetic volunteers (22 men and 18 women) aged 28 to 72 were randomized either to placebo or pravastatin 40 mg daily for a 12-week period. Insulin resistance, assessed using the Quantitative Insulin Sensitivity Check Index (QUICKI), as well as serum leptin and adiponectin levels, was measured at baseline and at the end of therapy. RESULTS: Pravastatin treatment decreased total cholesterol, low-density lipoprotein cholesterol, and triglycerides levels by 24%, 32%, and 14%, respectively ( P < .05 for all), but did not affect glucose and insulin levels, the (QUICKI) index, and adiponectin and leptin levels. When stratification was performed according to QUICKI index or sex, no significant differences were observed in the prevalues and postvalues of leptin, adiponectin, or QUICKI index in the pravastatin group. Adiponectin, leptin, and QUICKI index were statistically higher in women than in men ( P < .001 for both variables). Adiponectin was negatively correlated with body mass index (BMI; r = -0.39, P < .05) and positively correlated with the QUICKI index ( r = 0.54, P < .001) and with high-density lipoprotein cholesterol ( r = 0.50, P < .01). The relation between adiponectin and QUICKI index remained significant after adjustment for sex and BMI ( P = .005 and P = .007, respectively). Leptin was only related to BMI ( r = 0.57, P < .001) and to sex ( P < .001) with no significant correlations with lipid parameters or QUICKI index. Both sex and BMI are independent predictors of leptin ( P < .001 and P < .001). CONCLUSION: A 12-week treatment with pravastatin 40 mg/d does not change the QUICKI index and leptin and adiponectin levels in healthy volunteers. In addition, our results emphasize the importance of sex and BMI in the determination of both adiponectin and leptin. Adiponectin was also related to QUICKI index, whereas this relation was not found with leptin.

Intraperitoneal and intravenous routes for pain relief in laparoscopic cholecystectomy.

BACKGROUND: Postoperative abdominal and shoulder pain are the most common complaints after elective laparoscopic cholecystectomy. Postoperative pain is multifactorial in origin, and therefore multimodal therapy may be needed to optimize pain relief. METHODS: We conducted a double-blind study where patients were randomly allocated to 1 of 5 groups of 20 patients each. Statistical significance was considered P<0.05. Group 1 received 40 mL bupivacaine 0.25% intraperitoneal spray. Group 2 received 40 mL bupivacaine 0.25% intraperitoneal spray mixed with 200 mg ketoprofen. Group 3 received 40 mL bupivacaine 0.25% intraperitoneal spray and intravenous 200 mg ketoprofen. Group 4 received 200 mg ketoprofen intravenously. Group 5 was the control group. RESULTS: Demographic data were similar in the 5 groups. As compared with the control group, group 1 had significantly lower abdominal pain scores at 6 hours; group 2 at 0, 1, 2, and 6 hours; group 3 at 0, 1, 2, 6, 12, and 24 hours; and group 4 at 2 hours. Group 1 had significantly lower shoulder pain scores at 1 and 6 hours; group 2 at 0 and 6 hours; and groups 3 and 4 at 0, 1, and 6 hours. The number of patients requiring postoperative rescue analgesics and the incidence of postoperative vomiting were significantly lower in group 3 only. CONCLUSIONS: A multimodal approach to pain management following elective laparoscopic cholecystectomy is best achieved with a combination of 40 mL bupivacaine 0.25% intraperitoneal spray and 200 mg intravenous ketoprofen, achieving the least incidence of postoperative vomiting.

Muallem endo-tracheal tube introducer: (METTI)--an aid for the difficult airway.

This is a brief report evaluating a new single use endotracheal tube introducer (METTI) which has a soft curved atraumatic tip. The introducer was tried in 44 patients, whose direct laryngoscopic view was simulated to Cormack IIIb score, and in six patients with real Cormack III score. The overall success rate of railroading of the tracheal tube over the introducer was 94% from the first attempt.

Allergic myocardial ischemia causing reversible hemodynamic collapse during gastroscopy.

This case report details the development of an acute heart dysfunction during gastroscopy under sedation in a patient with normal coronary arteries. The early diagnosis by echocardiography and aggressive management allowed us to prevent a serious and fatal outcome. We spot on the diagnosis of allergic cardiogenic shock based on our clinical and laboratory finding.

Comparison of the effects of combination atorvastatin (40 mg) + ezetimibe (10 mg) versus atorvastatin (40 mg) alone on secretory phospholipase A2 activity in patients with stable coronary artery disease or coronary artery disease equivalent.

Secretory phospholipase A2 (sPLA2) is an enzyme that plays an important role in the pathogenesis of atherosclerosis and of adverse cardiovascular events. It is currently the target of emerging therapeutic agents. Our study was designed to investigate the effect of aggressive lowering of low-density lipoprotein (LDL) cholesterol with ezetimibe and atorvastatin on sPLA2 activity. We randomized 100 patients with stable coronary artery disease (CAD) or CAD equivalent (diabetes, stroke, or peripheral vascular disease) to receive ezetimibe 10 mg/day in association with atorvastatin 40 mg/day (combination therapy group) versus atorvastatin 40 mg/day and placebo (monotherapy group). Patients on statin therapy before inclusion were allowed to enter the study as long as the potency of the statin was lower than atorvastatin 40 mg/day. Lipid profile, high-sensitivity C-reactive protein (hs-CRP), and sPLA activity were measured at baseline and after 8 weeks of therapy. The decrease in LDL cholesterol was more significant in the combination therapy group, but the decrease in hs-CRP was similar. sPLA2 activity significantly decreased in the ezetimibe/atorvastatin group from 29 U/ml (interquartile range 23 to 35) to 26 U/ml (23 to 29, p = 0.001) but remained similar in the placebo/atorvastatin group (23 U/ml, 19 to 32, vs 22 U/ml, 19 to 28, p = NS). In a multivariate stepwise linear regression model, change in sPLA2 correlated with change in hs-CRP (p <0.001), baseline LDL cholesterol level (p = 0.001), body mass index (p = 0.003), diabetes mellitus (p = 0.04) and combination therapy with ezetimibe/atorvastatin (p = 0.05). In conclusion, this study demonstrates that coadministration of ezetimibe and atorvastatin decreases sPLA2 activity.

Effect of ezetimibe/atorvastatin combination on oxidized low density lipoprotein cholesterol in patients with coronary artery disease or coronary artery disease equivalent.

Ezetimibe is effective in providing additional low-density lipoprotein (LDL) cholesterol lowering when coadministered with statins, but its effect beyond LDL cholesterol lowering is unknown. Oxidized LDL (ox-LDL) is a better predictor of adverse cardiovascular events than standard lipid parameters. The objective of this study was to investigate the effect of ezetimibe on ox-LDL. A total of 100 patients with coronary artery disease or coronary artery disease equivalent were randomized to atorvastatin 40 mg/day and ezetimibe 10 mg/day or to atorvastatin 40 mg/day and placebo. LDL cholesterol, LDL cholesterol subfractions, and ox-LDL were measured at baseline and after 8 weeks of therapy. The ezetimibe group had a larger reduction in total LDL cholesterol compared to placebo. This was due mainly to a larger reduction in large buoyant LDL (24% vs 10%, p = 0.008). Ox-LDL level did not change in the placebo group (50 +/- 13 vs 51 +/- 13 U/L), while it decreased in the ezetimibe group, from 51 +/- 13 to 46 +/- 10 U/L (p = 0.01 vs baseline and p = 0.02 vs final level in placebo). The change in ox-LDL correlated significantly with those in total LDL and in large buoyant LDL (r = 0.6 and r = 0.5, respectively, p <0.01 for both), but not with that of small dense LDL, high-density lipoprotein, or very low density lipoprotein. In conclusion, this study demonstrates that ezetimibe decreases ox-LDL cholesterol through reductions in total LDL cholesterol and in large buoyant LDL cholesterol.

Percutaneous coronary intervention increases leptin and decreases adiponectin levels.

OBJECTIVE: The study was designed to examine the effect of percutaneous coronary intervention (PCI) on adiponectin and leptin levels. We have previously demonstrated that PCI triggers a systemic inflammatory response. We hypothesized that inflammation participates in the pathogenesis of diabetes mellitus and the metabolic syndrome by modulating levels of adiponectin and leptin. DESIGN: Prospective study in which inflammation was induced by PCI. PATIENTS: Forty-eight patients with stable coronary artery disease and without diabetes mellitus. MEASUREMENTS: High-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), leptin and adiponectin were measured at baseline and 48 h after the procedure. RESULTS: Following PCI, hs-CRP increased by 211%, IL-6 by 87% and leptin by 19%, while adiponectin decreased by 14% (P < 0.001 for all). The change in IL-6 correlated with that in hs-CRP (rho = 0.32; P = 0.027), as did the changes in IL-6 and leptin (rho = 0.31; P = 0.03). The change in adiponectin, however, did not correlate with the change in any of the other markers. CONCLUSION: This study demonstrates that PCI affects the levels of adiponectin and leptin within 48 h. These effects may be secondary to the inflammatory response triggered by PCI.