Stable angina pectoris is a common disorder, and its prevalence increases with age. Patients with stable angina pectoris experience a pressure or a choking sensation in the chest and adjacent areas, or shortness of breath (angina equivalent), associated with physical or emotional stress. Most patients with stable angina pectoris have severe obstructive atherosclerotic lesions of complex morphology in one or more than one coronary artery and multiple non-obstructive lesions.
Obstructive lesions limit the increase of blood flow needed during periods of increased myocardial oxygen demand, such as exercise. The endothelium overlying the lesions is dysfunctional and is responsible for paradoxical constriction of the stenotic site during exercise resulting in further reduction of blood flow distal to the lesion. The resultant imbalance between myocardial oxygen supply and demand produces reversible myocardial ischaemia and its clinical consequences, such as anginal pain and/or shortness of breath.
Non-obstructive lesions are lipid-rich and soft in consistency and the endothelium overlying these lesions is prone to fissuring and disruption. The exact mechanism of plaque-endothelial surface disruption remains elusive. Several mechanisms, including an active inflammatory process, have been implicated. The fissured endothelium exposes the atheromatous material inside the vessel wall to the circulating blood. This results in platelet aggregation and deposition, which may be followed by additional intraluminal thrombosis. The clinical presentation may remain silent or manifest as acute coronary syndrome (myocardial infarction, unstable angina) or sudden ischaemic death.
The annual death rate of patients with stable angina is 1.6% to 3.2%. The most important determinant of prognosis is underlying left ventricular systolic function at rest, co-morbid conditions, and the severity and extent of coronary artery disease (CAD). Treatment goals are:
- abolition or reduction of the frequency of angina attacks;
- prolongation of angina-free walking duration;
- abolition or reduction of other consequences of reversible myocardial ischaemia, such as dyspnoea; and
- prevention or reduction of serious adverse outcomes (myocardial infarction, unstable angina and ischaemic sudden death) due to plaqueendothelial surface disruption.
The treatment must be applicable to a large segment of the population with stable angina. Pharmacological therapy should be devoid of intolerable adverse effects and drug interactions. Newer therapy should be either superior to, or as effective as, already proven therapy and should show additional beneficial effects when used in addition to currently proven and effective treatment of stable angina pectoris.
Currently available anti-anginal drugs (long-acting nitrates, beta blockers and calcium channel blockers) and revascularisation procedures alleviate or prevent anginal symptoms but have not been shown to improve survival or reduce the incidence of myocardial infarction in patients with stable angina pectoris. On the other hand, the strategies that reduce the incidence of adverse outcomes have few anti-anginal effects. Therefore, treatment of stable angina must include the use of anti-anginal drugs and/or revascularisation procedures plus strategies that reduce adverse clinical outcomes.
Treatment Aimed at Decreasing the Frequency and Severity of Anginal Symptoms and Myocardial Ischaemia
Several strategies are available to achieve this goal. Anti-anginal drugs (nitrates, beta-blockers and calcium channel blockers) are usually the first option. Revascularisation procedures, percutaneous balloon dilation of the coronary artery (PTCA), with or without stent placement, are being increasingly used, especially in the US, and coronary bypass surgery is now being offered only to selected patients with stable angina pectoris. />/>