6 In many of these patients with typical angina symptoms, exercise-induced myocardial ischaemia is caused by coronary microvascular dysfunction. It is important to note that as few as 38% of patients without previously known heart disease who undergo elective diagnostic coronary angiography are found to have obstructive CAD. ![]() Abnormal vasodilatory responses of the coronary microcirculation can cause effort-related angina (microvascular angina). The typical clinical characteristics of chronic stable angina are summarised in Box 1.Ĭoronary microvascular resistance is the main determinant of coronary flow reserve (the ratio of maximal induced myocardial flow to resting coronary blood flow). Patients with stable angina might or might not present with typical symptoms, and ‘silent’ myocardial ischaemia can be present in patients with diabetes mellitus and in the elderly. Transient myocardial ischaemia typically causes ‘constrictive’ chest discomfort, resulting from the activation of mechano- and chemo-sensitive myocardial receptors. Stable angina results from an imbalance between coronary blood supply and myocardial oxygen demand, which is often, but not always, associated with the presence of obstructive CAD. 4 The annual mortality rate resulting from coronary heart disease in patients with stable angina is 0.9–1.4% per year. 3 Its prevalence increases with age, rising from roughly 8% in men and 3% in women aged 55–64 years, to 14% in men and 8% in women aged 65–74 years, in England. Stable angina is the most common clinical manifestation of ischaemic heart disease, affecting 58% of patients with CAD. In this article, we use the term ‘angina’ in relation to the occurrence of typical central chest pain associated with myocardial ischaemia, irrespective of the presence or absence of flow-limiting organic coronary artery stenosis.Īngina is considered to be ‘chronic’ and ‘stable’ when symptoms are present for at least two months, without changes in severity, character or triggering circumstances. 1 There is currently no systematically agreed definition for angina pectoris and the term is used to define both the typical chest pain associated with myocardial ischaemia and the syndrome characterised by chest pain, myocardial ischaemia and obstructive atherosclerotic coronary artery disease. The term angina pectoris refers to William Heberden's classic description of the clinical symptoms of angina, as reported to the Royal College of Physicians in 1768. This article briefly reviews recent advances in the pharmacological management of chronic stable angina pectoris, highlighting how an understanding of the prevailing pathogenic mechanisms in the individual patient can aid appropriate selection of therapeutic strategies and improve clinical outcome. The combined use of traditional and novel treatments is likely to increase the proportion of patients who are managed successfully with medical therapy alone. These novel agents have specific mechanisms of action and fewer side effects compared to conventional drugs. Several new anti-anginal drugs have been introduced that might allow more effective symptom control. Despite modern therapies, many patients continue to suffer from angina. Rational treatment requires a multi-faceted approach combining lifestyle changes, aggressive management of modifiable coronary artery disease risk factors, pharmacological therapy and myocardial revascularisation when appropriate. An imbalance between myocardial oxygen supply and metabolic oxygen demand causes the symptoms of angina pectoris and represents a major therapeutic target. The coronary microcirculation can also play an important role. The pathogenesis of stable angina is complex and often, albeit not always, involves flow-limiting epicardial coronary artery stenoses (atheromatous plaques) that reduce the ability of the coronary circulation to deliver appropriate blood supply to the myocardium. ![]() Chronic stable angina is the most common manifestation of ischaemic heart disease in the developed world and is associated with impaired quality of life and increased mortality.
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