Objective-To review the literature on the benefits and disadvantages of clinical and medical audit, and to assess the main facilitators and barriers to conducting the audit process. Design-A comprehensive literature review was undertaken through a thorough review of Medline and CINAHL databases using the keywords of "audit", "audit of audits", and "evaluation of audits" and a handsearch of the indexes of relevant journals for key papers. Results-Findings from 93 publications were reviewed. These ranged from single case studies of individual audit projects through retrospective reviews of departmental audit programmes to studies of interface projects between primary and secondary care. The studies reviewed incorporated the experiences of a wide variety of clinicians, from medical consultants to professionals allied to medicine and from those involved in unidisciplinary and multidisciplinary ventures. Perceived benefits of audit included improved communication among colleagues and other professional groups, improved patient care, increased professional satisfaction, and better administration. Some disadvantages of audit were perceived as diminished clinical ownership, fear of litigation, hierarchical and territorial suspicions, and professional isolation. The main barriers to clinical audit can be classified under five main headings. These are lack of resources, lack of expertise or advice in project design and analysis, problems between groups and group members, lack of an overall plan for audit, and organisational impediments. Key facilitating factors to audit were also identified: they included modern medical records systems, eVective training, dedicated staV, protected time, structured programmes, and a shared dialogue between purchasers and providers. Conclusions-Clinical audit can be a valuable assistance to any programme which aims to improve the quality of health care and its delivery. Yet without a coherent strategy aimed at nurturing eVective audits, valuable opportunities will be lost. Paying careful attention to the professional attitudes highlighted in this review may help audit to deliver on some of its promise.

Decreased release of nitric oxide from damaged endothelium is responsible for the impaired endothelium-dependent vasodilator responses found in animal models of vascular disease. Dietary supplementation with fish oils has been shown to augment endothelium-dependent relaxations, principally by improving the release of nitric oxide from injured endothelium. Using forearm venous occlusion plethysmography we studied vascular responses to 60, 120, 180 and 240 nmol/min of acetylcholine (an endothelium-dependent vasodilator) and 3, 6 and 9 nmol/min of glyceryl trinitrate (an endothelium-independent vasodilator) infused into the brachial artery in 23 patients with Type 2 (non-insulin-dependent) diabetes mellitus. NG monomethyl-L-arginine was employed to inhibit stimulated and basal release of nitric oxide from the endothelium. On completion of the baseline studies patients randomly received either fish oil or matching olive oil capsules in a double-blind crossover fashion for 6 weeks followed by a 6-week washout period and a final 6-week treatment phase. Studies, identical to the initial baseline studies, were performed at the end of the active treatment periods at 6 and 18 weeks. Fish oil supplementation significantly improved forearm blood flow responses to each dose of acetylcholine when compared to the vasodilator responses recorded at baseline and after olive oil administration (p < 0.01). Neither fish oil nor olive oil supplementation produced any significant changes in forearm blood flow to the incremental infusions of glyceryl trinitrate when compared with responses recorded during the baseline studies.(ABSTRACT TRUNCATED AT 250 WORDS)

In a double-blind, placebo-controlled study we investigated the effects of dietary fish oil supplementation on arterial wall characteristics in 20 patients with non-insulin-dependent diabetes mellitus. Estimates reflecting compliance values in the large arteries and more peripheral vasculature, as measured by pulse-contour analysis, improved significantly after 6 weeks of fish oil therapy compared with values recorded at baseline and after 6 weeks' administration of olive oil. The large-artery compliance estimate increased from 1.50 (confidence interval [CI], 1.31 to 1.69) mL/mm Hg at baseline to 1.68 (CI, 1.52 to 1.84) mL/mm Hg after fish oil administration (P < .01). The oscillatory compliance value increased from 0.015 (CI, 0.011 to 0.019) mL/mm Hg at baseline to 0.022 (CI, 0.016 to 0.028) mL/mm Hg after fish oil ingestion (P < .05). No changes occurred in arterial blood pressure, cardiac output, stroke volume, or systemic vascular resistance with either intervention. The improved compliance estimates with fish oil ingestion occurred without altering fasting blood glucose and cholesterol concentrations. These results support the hypothesis that fish oils alter vascular reactivity and favorably influence arterial wall characteristics in patients with non-insulin-dependent diabetes mellitus. These direct vascular effects, expressed at the level of the vessel wall, may contribute to the cardioprotective actions of fish oil in humans.

Background-Impaired endothelium-mediated vasodilatation (EMVD) in congestive cardiac failure (CCF) has been linked to decreased nitric oxide (NO) bioavailability because of its interaction with vascular superoxide (O 2 ·Ϫ ), derived predominantly from NAD(P)H-dependent oxidases. When uncoupled from essential cofactors, endothelial nitric oxide synthase (eNOS) produces O 2 ·Ϫ . We studied the functional consequences of eNOS uncoupling in relation to EMVD in patients with CCF. Methods and Results-We employed the platelet as a compartmentalized ex-vivo model to examine O 2 ·Ϫ and NO production. When eNOS is functioning normally, incorporation of N -Nitro-L-Arginine methyl ester (L-NAME, 1 mmol/L), results in increased O 2 ·Ϫ detection, as inhibition of NO production prevents NO scavenging of O 2 ·Ϫ . This was observed in controls and 9 of the CCF patients, in whom O 2 ·Ϫ detection increased by 63% and 101%, respectively. In the remaining 9 CCF patients, incorporation of L-NAME reduced O 2 ·Ϫ production by 39%, indicating O 2 ·Ϫ production by eNOS uncoupling. Detection of platelet-derived NO was significantly greater in eNOS-coupled platelets compared with the uncoupled group (2.8Ϯ1.4 versus 0.9Ϯ0.4 pmol/10 8 platelets, Pϭ0.04). Endothelium-dependent and -independent vasodilator responses to acetylcholine and sodium nitroprusside recorded using venous occlusion plethysmography were significantly impaired in patients exhibiting eNOS uncoupling. Conclusions-This study provides first evidence that platelet eNOS can become uncoupled in human CCF. Impaired endothelium-dependent and -independent vasodilator responses and diminished platelet-derived NO production occurred in association with enzyme uncoupling.

Enalapril 20 mg should be prescribed as 10 mg twice daily and measures taken to improve patient compliance.