'This morning I will present to you an extraordinary case: a patient with coronary thrombosis.' These were the words of the Professor of Internal Medicine at the Karolinska Institutet (Stockholm, Sweden), Nanna Svartz, when she opened the morning session for medical students in the Karolinska Hospital auditorium, in the autumn of 1949. The diagnosis was determined only by examining the patient's symptoms and electrocardiographs (ECG). No diagnostic tests for measuring the levels of transaminases or troponins were available at the time. Treatment of the patient was with morphine for pain, digitalis and venesection for heart failure and three weeks of absolute bed rest in hospital. Treatments such as thrombolysis and revascularisation procedures were unknown, and as distant and strange as the idea of putting a man on the moon. Nobody had heard of risk factors and cholesterol was only measured to confirm the diagnosis of hypothyroidism by finding a high value (thyroid-stimulating hormone [TSH] had not yet been discovered).

Now, 50 years later, the time is ripe, due to the enormous progress of medical research, to introduce you to the Lectures in Clinical Atherosclerosis and Dyslipidaemia. This series will:

• take you beyond the simple concept of cholesterol as a risk factor into the world of lipoproteins and dyslipidaemia as causal risk factors;
• take you beyond bed rest as treatment for myocardial infarction;
• take you into both primary and secondary prevention of clinical atherosclerosis; and
• bring you up-to-date on, and perhaps also take you into the future of, evidence-based clinical knowledge on dyslipidaemia as one major, easily modifiable risk factor.

One of the main aims of the series is to give a comprehensive view of the management of dyslipidaemia, for the prevention of clinical atherosclerosis, using both simple, cost-effective therapeutic lifestyle changes and the more demanding method of using lipid-lowering drugs for reaching established therapeutic goals.

'Clinical atherosclerosis' is a manifestation of atherosclerosis, which occurs when the silent, progressive process in the arterial walls reaches a clinical horizon by causing either severe ischaemia and/or thrombotic or embolic complications. The spectrum of manifestations of clinical atherosclerosis covers a wide range from sudden death, other forms of coronary heart disease (CHD; including myocardial infarction, stable and unstable angina), via carotid stroke to intermittent claudication.

Cardiovascular disease causes more than 235,000 deaths in the UK each year and raised cholesterol levels have been linked to cardiovascular risk. Extensive research has shown that if lower low-density lipoprotein (LDL) is lowered and high-density lipoprotein (HDL) raised then the risk of developing CHD and having a secondary CHD event is reduced. Target levels for total blood cholesterol set by the government state that for patients with, or at risk of, CHD, the level must be reduced to either less than 5 mmol/L (190 mg/dL) or by 20-25%, whichever is greater. This places significant burden on primary care teams (in terms of time, resource and cost) in order to get at-risk CHD patients to their cholesterol target as effectively and efficiently as possible. The series gives an understanding of the current thinking and data for the disease area. It highlights that, although this is a well researched area, there still remain many unanswered questions and many remaining requirements for optimal treatment.

The overall aim of Lectures in Clinical Atherosclerosis and Dyslipidaemia is to describe how to achieve health-effectiveness and cost-effectiveness in the management of dyslipidaemia for the prevention of clinical atherosclerosis. It is my belief, and hope, that we together have reached this goal.

Lars A Carlson
Karolinska Institutet, Stockholm, February 2002.