Post-ERCP pancreatitis: Pathophysiology, early identification and risk stratification.

Acute pancreatitis is the most common and feared complication of endoscopic retrograde cholangiopancreatography (ERCP). The aim of the study was to review the current knowledge on the nomenclature, etiology, pathophysiology, clinical presentation, diagnostic workup, and risk stratification of post-ERCP pancreatitis (PEP). A structured search in PubMed and Scopus databases was performed using search terms related to the subject of diagnosis, pathophysiology, risk stratification of post-ERCP pancreatitis, including full text articles and abstracts in the English language. Several causes, operating both at a local and systemic level, might play an important role in the pathogenesis of PEP. Different patient-related risk factors can help predict post-ERCP pancreatitis; diagnosis depends on clinical presentation, imaging and laboratory investigations. As an outpatient procedure, post-ERCP pancreatitis may be safe in a selected group of low-risk patients. Further investigation of the etio-pathogenesis of post-ERCP pancreatitis is required in order to improve diagnosis and treatment. Early identification and severity stratification of post-ERCP pancreatitis greatly affects the patient's outcome. There is still controversy concerning the risk factors related to PEP. More studies are needed to clarify early and definite diagnosis, risk and severity stratification, as well as treatment of post-ERCP pancreatitis.

B-type natriuretic peptide predicts postoperative cardiac events and mortality after elective open abdominal aortic aneurysm repair.

OBJECTIVE: The aim of this study was to determine if a single preoperative B-type natriuretic peptide (BNP) level correlated with perioperative cardiac events, cardiac death, and all-cause mortality in elective open abdominal aortic aneurysm (AAA) repair in the short term, intermediate term, and long term. METHODS: A prospective, 2-year multicenter observational cohort study in the three vascular units in Glasgow was performed. All patients who were admitted for elective open AAA repair were recruited. Preoperative BNP levels were performed and batch analyzed at the end of the study. Postoperative screening for cardiac events (nonfatal myocardial infarction and cardiac death) was performed at 2, 5, and 30 days. Follow-up for all-cause mortality was sustained to a minimum of 3 years, where possible. RESULTS: A total of 106 of 111 patients were recruited. Median BNP concentrations were higher in the 16 patients (15%) with immediate postoperative cardiac events (P = .001) and the five with cardiac death (P = .043). Area under the receiver-operating characteristic (AUC) curve analysis indicated BNP concentrations of 99.5 pg/mL best predicted cardiac events (AUC, 0.927), and 448 pg/mL predicted cardiac death (AUC, 0.963). BNP also predicted all-cause mortality in the short-term (P = .028), intermediate-term (P < .001), and long-term (P < .001) postoperative periods. CONCLUSIONS: Preoperative serum BNP concentration predicted postoperative cardiac events, cardiac death, and all-cause mortality in patients undergoing elective open AAA repair on short-term, intermediate-term, and long-term follow-up on an individual basis with greater accuracy than currently available risk prediction tools.

Reduced LDL-cholesterol levels in patients with coronary artery disease are paralleled by improved endothelial function: An observational study in patients from 2003 and 2007.

OBJECTIVE: Recent guidelines recommend more aggressive lipid-lowering in secondary prevention protocols. We examined whether this resulted in improved endothelial function. METHODS: We studied saphenous vein specimens of patients undergoing surgical coronary revascularisation in 2007 and compared results with those of patients examined in 2003. Endothelium-dependent vasodilation was assessed by relaxation to calcium ionophore A23187, and vascular superoxide production by lucigenin enhanced chemiluminescence. RESULTS: Statin dose increased from 26+/-16 mg/d in 2003 to 37+/-17 mg/d in 2007 (P<0.001), and total (4.0+/-0.9 mmol/L vs 4.8+/-1.0 mmol/L) and LDL-cholesterol levels (2.0+/-0.7 mmol/L vs 3.0+/-0.9 mmol/L) were lower in 2007 compared to 2003 (P<0.001; n=90 each). Endothelium-dependent vasodilation was greater in 2007 (44+/-15%) compared to 2003 (28+/-12%; n=36 each; P<0.001). Vascular superoxide derived from endothelial NO synthase (eNOS) was lower in 2007 than in 2003 (reduction by NG-nitro-L-arginine-methyl ester, 0.29+/-0.21 nmol/(mg min) vs 0.09+/-0.20 nmol/(mg min); P=0.002). In linear regression analysis, LDL-cholesterol levels have been shown to be the major determinant of endothelial function in the combined 2003 and 2007 cohort. CONCLUSION: Intensive lipid-lowering is associated with improved endothelial function and reduced superoxide production from eNOS. Further improvement in vascular function could be achieved by targeting other sources of superoxide including xanthine oxidase.