Excerpt
Angina is pain or constricting discomfort that typically occurs in the front of the chest (but may radiate to the neck, shoulders, jaw or arms) and is brought on by physical exertion or emotional stress. It is the main symptomatic manifestation of myocardial ischaemia and is usually caused by obstructive coronary artery disease restricting oxygen delivery to the cardiac myocytes. Other factors may exacerbate angina either by further restricting oxygen delivery (for example severe anaemia) or by increasing oxygen demand (for example left ventricular hypertrophy). Angina symptoms are associated with other cardiac disease such as aortic stenosis but the management of angina associated with non-coronary artery disease is outside the scope of this guideline.
Stable angina is a chronic medical condition. The aim of management is to abolish or minimise symptoms, and to improve quality of life and long-term morbidity and mortality. Medical management includes pharmacological strategies or a combination of pharmacological and revascularisation strategies and lifestyle interventions. Revascularisation may be performed using percutaneous techniques or by surgery.
Completed in 2003, the Euro Heart Survey on Stable Angina Pectoris included 3,779 ambulatory patients from 36 countries, presenting to a cardiologist as an outpatient, with new-onset stable angina. The survey revealed considerable variation between participating countries in the use of non-invasive and invasive investigations, the prescription of anti-anginal drugs and rates of revascularisation. Guideline compliant therapy was associated with reduced rates of myocardial infarction and death.
The variation in practice documented within the Euro Heart Survey likely reflects continuing uncertainty about appropriate management strategies in key clinical areas where the evidence base is incomplete or contradictory. This applies particularly to the role of revascularisation, for which some consensus has emerged around symptomatic indications, but prognostic indications are less well defined. Indeed, the only trials to report prognostic benefit for revascularisation were randomised comparisons of bypass surgery and medical treatment that are now more than 25 years old. It is noteworthy that these trials antedated introduction of statins and other secondary prevention treatments and the relevance of their findings to contemporary practice is unclear. More recent trials of percutaneous and surgical revascularisation strategies (COURAGE, BARI-2D, MASS II) have not demonstrated prognostic benefit, but these trials generally excluded patients with high risk coronary anatomy for whom bypass surgery might be expected to improve outcome.
Uncertainty about the effectiveness of revascularisation for delivering prognostic benefit in people with stable coronary artery disease is heightened by some recent analyses that have reported excessive incremental cost-effectiveness ratios for percutaneous revascularisation strategies compared with medical therapy. These areas of uncertainty surrounding the relative roles of medical therapy and revascularisation in managing people with stable angina have received special attention from the guideline group in making its recommendations.