Stable angina pectoris is a common disorder; 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 coronary arteries and multiple non-obstructive lesions. Obstructive lesions limit the increase of blood flow that is required 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 (see Figure 1). Nonobstructive 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 (see Figure 1). The clinical presentation may remain silent or manifest as acute coronary syndrome (myocardial infarction (MI), unstable angina) or sudden ischaemic death.
Figure 1: Clinical Outcomes of Coronary Lesions in Patients with Stable Angina Pectoris
Source: U Thadani, ├óÔé¼┼øThe Pursuit of Optimum Outcomes in Stable Angina├óÔé¼┼Ñ, Am. J. Cardiovas. Drugs, 3 (2003), Suppl. 1, pp. 11├óÔé¼ÔÇ£20.
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. Treatment Goals 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 dyspnea due to transient elevation of left-ventricular systolic and diastolic pressure; and
- prevention or reduction of serious adverse outcomes (MI, unstable angina and ischaemic sudden death) due to plaque-endothelial surface disruption.
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