Of an estimated 57 million deaths worldwide, more than 17 million (31%) are the consequence of cardiovascular disease (CVD). ¹ Of these CV deaths 43% are attributable to coronary artery disease (CAD) and 32% to stroke. It is often not appreciated that 78% of CV deaths occur in lower or middle income countries and not in the more prosperous countries. Furthermore, these deaths occur at a younger age in less developed countries thus impacting on their economic success. CVD accounts for up to 75% of the cases of overt heart failure in the general population under the age of 75 years. ² Over recent years the number of individuals with CAD has increased steadily and continues to do so. This is an almost inevitable consequence of more patients surviving MI, the ageing population and the increasing prevalence of diabetes, obesity and a lack of physical exercise. ³ The four great misconceptions of CHD are that it is a disease of old age, only occurs in men, is a pleasant way to die and is solely the responsibility of individuals. CHD matters.

Unlike the treatment of hypertension and heart failure (HF), there is a relative paucity of definitive information on the impact of drugs used to treat chronic angina pectoris on major clinical outcomes in patients with CHD. The medical management of patients with stable CAD developed initially, and logically, with the use of drugs that were effective in reducing or even abolishing the frequency of anginal symptoms. In contrast, lifestyle modification and other pharmacologic therapy (treatment of hypertension and high plasma cholesterol) may reduce the incidence of death and MI but there is little or no evidence to suggest these interventions provide immediate symptomatic benefit ⁴ i.e., the alleviation of angina pectoris. For example, smoking cessation reduces CV mortality and morbidity and improves a patient's ability to exercise, while moderation of excessive alcohol consumption and an increase in physical exercise may also be advantageous; ⁵ however, the major benefit in terms of the symptoms of angina is a consequence of specific medical therapy and/or revascularisation. ⁶

Targeting established risk factors in patients with chronic stable angina, and therefore CHD, is clearly of proven benefit. The efficacy of aspirin in unstable angina, and in acute and post-MI, is well established but the use of aspirin in chronic stable angina is largely founded on the Swedish Angina Pectoris Aspirin Trial (SAPAT). ⁷ In this study although there was a marked reduction of all vascular events, the reduction in allcause and CV mortality was not significant.

No specific trials with lipid-lowering agents have been conducted exclusively in patients with chronic stable angina. Nonetheless, the accumulated evidence from secondary prevention trials such as 4S, ⁸ Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) ⁹ and Cholesterol and Recurrent Events trial (CARE) ¹⁰ and studies performed in high-risk patients, many of whom had a history of chronic stable angina, such as the Heart Protection Study, ¹¹ and The Pravastatin or Atorvastatin Evaluation and Infection Therapy (PROVE-IT) trial ¹², provide compelling evidence of the benefit of statins in reducing CV mortality and morbidity. These data, along with relative benefits of aggressive lowering of low-density lipoprotein (LDL) cholesterol benefits in the AVERT Study ¹³ and more recently the TNT Study, provide an evidence base for the treatment of lipid abnormalities in chronic stable angina.