Chronic stable angina pectoris: Overview

A 47-year-old man reports a six-month history of intermittent chest discomfort while playing squash. He describes lower substernal tightness with numbness of the left upper arm only during exertion. He does not smoke. His father died suddenly at the age of 49 years. His blood pressure is 138/84 mm Hg. The level of total cholesterol is 261 mg per deciliter (6.7 mmol per liter), of low-density lipoprotein cholesterol 172 mg per deciliter (4.4 mmol per liter), and of high-density lipoprotein cholesterol 50 mg per deciliter (1.3 mmol per liter), and the triglyceride level is 113 mg per deciliter (2.9 mmol per liter). The result of an exercise test is positive, with pain and 1.5 mm of horizontal ST-segment depression at stage 4 of the Bruce protocol. How should the patient’s case be managed?

The Clinical Problem
The diagnosis of chronic stable angina pectoris includes predictable and reproducible left anterior chest discomfort after physical activity, emotional   stress, or both; symptoms are typically worse in cold weather or after meals and are relieved by rest or sublingual nitroglycerin. The presence of one or more obstructions in major coronary arteries is likely; the severity of stenosis is usually greater than 70 percent.


Angina occurs when there is regional myocardial ischemia caused by inadequate coronary perfusion and is usually but not always induced by increases in myocardial oxygen requirements. Cardinal features of chronic stable angina include complete reversibility of the symptoms and repetitiveness of the anginal attacks over time, typically months to years. New, prolonged, or recent-onset symptoms are characteristic of unstable angina. Coexisting conditions, such as poorly controlled hypertension, anemia, or Thyrotoxicosis, can precipitate or accentuate angina.

As coronary atherosclerosis progresses, there is deposition of plaque external to the lumen of the artery; the plaque may extend eccentrically and outward without compromising the lumen. Thus,  stress testing or angiography may not suggest coronary disease, even in the presence of significant Atherosclerosis. As Atherosclerosis worsens, encroachment of the plaque mass into the lumen can result in hemodynamic obstruction and angina1. Disordered endothelial vasomotor function of the coronary arteries is common in patients with angina and results in diminished vasodilatation or even vasoconstriction in response to various stimuli, including exercise. Occasionally, patients with severe aortic-valve disease or hypertrophic cardiomyopathy have angina-like chest pain in the absence of overt coronary disease.

Typical Progression of Coronary Atherosclerosis.
As the plaque burden increases, the atherosclerotic mass tends to stay external to the lumen, which allows the diameter of the lumen to be maintained; this is known as the Glagov effect, or positive remodeling. As plaque encroaches into the lumen, the coronary artery diameter decreases. Myocardial ischemia results from a discordant ratio of coronary blood supply to myocardial oxygen consumption. Luminal narrowing of more than 65 to 75 percent may result in transient ischemia and angina. In acute coronary syndromes, vulnerable plaque is a more important factor than is the degree of stenosis; acute coronary events result from ulceration or erosion of the fibrous cap, with subsequent intraluminal thrombosis. Vulnerable plaque within the vessel wall may not be obstructive and thus may remain clinically silent until it causes rupture and associated consequences.

Classification of Angina Pectoris
Chest pain is characterized as classic, or typical, angina; as atypical angina, which includes symptoms that have some but not all the features of angina; and as nonanginal Chest pain , which has none of the features of angina. Chest pain that occurs during rest or at night is well described in persons with chronic stable angina, particularly women.

Atypical presentations of angina are more common in women than in men. Women with ischemia are more likely than men to report variable pain thresholds, inframammary pain, palpitations, or sharp, stabbing pain. Overall, Chest pain in women is quite common and usually is not due to coronary artery disease. Data from the Women’s Ischemia Syndrome Evaluation initiative of the National Heart, Lung, and Blood Institute indicate that many women with anginal symptoms have inducible ischemia and a reduced coronary flow reserve yet no significant obstruction on coronary angiography. Atypical presentations of angina are also more frequent in older patients (who often have exertional dyspnea, weakness, or sweating) than in younger patients and in patients with Diabetes (who often have atypical or even silent ischemic episodes) than in those without Diabetes; a high level of suspicion for coronary disease is needed in these groups. The severity of angina should be assessed to aid in management decisions. However, there is no direct correlation between the class of angina and the severity of coronary artery disease as determined on angiography.

Provided by ArmMed Media
Revision date: June 14, 2011
Last revised: by Janet A. Staessen, MD, PhD