The British Journal of Diabetes & Vascular Disease

Cardiovascular atherosclerosis is the commonest underlying cause of death in patients with diabetes mellitus. The development of atherosclerosis is often accelerated and the outcome is worse in diabetic than non-diabetic patients. This may relate to abnormalities of platelet function, coagulation, blood pressure and lipid metabolism that are characteristic of diabetes. Management of angina in diabetes should focus on reducing symptoms and prolonging life. In both of these areas there are issues specific to the diabetic patient. The role of percutaneous and surgical approaches to coronary disease in diabetic patients continues to evolve and optimal therapy remains unclear. Herein explores the clinical management of coronary artery disease in patients with diabetes. The pathophysiological basis of stable and unstable coronary syndromes is explained and the effect of diabetes on coronary disease and its subsequent management is discussed.

The vascular endothelium offers an attractive model for detecting functional abnormalities prior to structural changes in the vasculature. Demonstration of progression from endothelial dysfunction through to atherosclerosis is required. Measurements of forearm bloodflow, biochemical markers and biophysical assessments of the endothelium have been employed as research tools for investigating pre-symptomatic atherosclerosis.

However, studies examining endothelial function in type 1 diabetes have been sparse and conflicting. Differences in methodology and the study populations were potential confounding factors. Augmented vasodilatory prostanoids compensate for reduced nitric oxide bioavailability in determining endothelial function in type 1 diabetes. Hyperglycaemia appears to be the initiating event in type 1 diabetes which promotes a variety of biochemical events which are pathogenic to the endothelium.

Improved understanding of the endothelium may facilitate the development of novel diagnostic tools and interventions targeting the accelerated atherosclerosis associated with type 1 diabetes.

Although considerable research has addressed the potential role of inflammatory mediators in the pathogenesis of coronary heart disease, the relevance of this pathway to the pathogenesis of type 2 diabetes has only recently attracted interest. Circulating levels of inflammatory mediators correlate with insulin resistance and are significantly elevated in groups at risk of type 2 diabetes. Several prospective studies indicate that C-reactive protein and white cell count, together with other acute phase markers, predict incident diabetes independently of established predictors. Measures known to prevent diabetes (weight loss, exercise and metformin) and those more recently suggested (statins, ACE inhibitors and thiazolidinediones) have all been shown to exhibit anti-inflammatory actions. Mechanisms linking inflammation to diabetes development are beginning to be unravelled. Emerging knowledge of inflammatory mediators may help to predict those at risk of type 2 diabetes, and further work in this area may lead to novel means of prevention and treatment.

Obesity, diabetes and glycaemic control are inter-linked. Weight gain is associated with worsening diabetic control and can be exacerbated by therapies aimed at controlling hyperglycaemia. Auditing our practice in a district general hospital, we have examined our diabetic population with regards to age and weight, HbA1C and body mass index (BMI), and for weight gain following conversion to insulin.

Evidence of improvements in outcomes gained by aggressive treatment of hypertension, hyperglycaemia and Edyslipidaemia in type 2 diabetic patients has encouraged the setting of ambitious targets for risk factor control. The therapeutic regimens needed to achieve tight control results in polypharmacy for many patients. The recent DARTS Study demonstrated poor adherence to oral hypoglycaemic drug therapy, particularly in patients prescribed combination oral hypoglycaemic drug therapy, multiple daily dose regimens and co-medications. This suggests that simplifying drug regimens, minimising tablet-counts and the use of once-daily and modified-release preparations and of fixed-combination drug preparations may be important. With regard to taking medication an alliance is needed which allows greater mutual understanding and agreement between patient and doctor. This move towards `concordance' in care planning is also crucial to success.

A majority of type 2 diabetic patients now receive routine care from their General Practitioner. The biggest single cause of mortality amongst such patients is ischaemic heart disease; diabetes is now considered to be of equivalent risk to a previous myocardial infarction in non-diabetic individuals. Most type 2 diabetic patients have the insulin resistance syndrome, and accelerated atheromatous disease at the time of diagnosis. The current guidelines on lipid management fail to recognise the unique dyslipidaemia of diabetes, and tend to undertreat the disease. There is a powerful case for all type 2 diabetic patients to receive treatment with a statin at the time of diagnosis.

A prospective audit was undertaken to characterise Ametabolic control, risk-factor profiles and costs of pharmaceutical agents required to achieve quality target measures in 100 type 2 diabetic patients attending a diabetic clinic in UK general practice. Despite reasonable glycaemic control, the coronary risk of these patients was high due to age, diabetes and dyslipidaemia. It proved impossible to quantify coronary risk for many older patients exactly since existing scales do not apply to patients aged over 75 years. The extra cost of initiating new treatments to modify coronary heart disease (CHD) risk for an average patient with type 2 diabetes was estimated to be £400—£860 (average £633) per annum. The treatment costs of instituting treatment to achieve quality measures should be considered when new quality standards are introduced. Without this investment the long-term costs of managing the complications of diabetes will be much higher.

The modern general practitioner is able to examine and audit his practice diabetes population in great detail because of extensive computerisation and Read-coding. The ability to compare one practice statistics with another brings with it added pressures to be seen to achieve certain standards. Whilst this is a laudable concept, it results in some ethical issues that have hitherto not been explored. In this article, Dr Martin Cosgrove explores some ethical aspects of audit in general practice and outlines three pitfalls for general practitioners when undertaking audit in preparation for external assessment.