Angina Pectoris

Angina pectoris (AP) is the main symptom of coronary heart disease (CHD). The name comes from Latin and means “chest tightness.” Medically, angina pectoris is also referred to as “stenocardia.”

Angina pectoris corresponds to the typical pain caused by insufficient blood flow to the heart. In most cases, acute insufficient blood supply is triggered by exertion or stress and indicates coronary heart disease. Angina pectoris is therefore the name of the symptom and not the disease itself. A basic distinction is made between stable and unstable angina pectoris. This distinction refers to the severity and frequency of the symptoms. Stable angina pectoris signifies when the symptoms happen consistently when you're exerting yourself. Unstable AP is when it happens for the first time or is especially severe. An AP attack can be a sign of a heart attack that is actually happening or can warn of a heart attack (pre-infarction angina). Men and older people are more likely to suffer from AP.

Stable angina pectoris is when the symptoms occur repeatedly and under similar conditions. Depending on the severity of the AP, an attack may occur during moderate or greater exertion (exertional angina), but not during physical or mental rest. In the majority of cases, the attacks resolve spontaneously within a matter of seconds or minutes.

The cause of the pain is reduced blood flow (ischemia) to the heart. This is often triggered by a narrowing of the coronary arteries (arteriosclerosis). This condition is known as coronary heart disease. If the symptoms are due to cramp-like contractions, i.e., spasms of the coronary arteries, this is referred to as Prinzmetal angina.

Unstable angina pectoris (UAP) refers to the first occurrence (de novo angina) of symptoms on the one hand, and a change in symptoms on the other. The probability of a heart attack occurring or already occurring is high in the case of UAP. UAP is present when pain is more severe than usual, occurs more frequently, or occurs with less exertion (crescendo angina). The occurrence of symptoms at rest (rest angina) is also classified as UAP.

Angina pectoris manifesting within two weeks following myocardial infarction (post-infarction angina) is categorized as a form of unstable angina. Episodes precipitated by recumbency are designated as angina decubitus (from the Latin decubitus, ‘lying down’) or angina nocturna (‘night angina’), both of which are likewise considered clinical variants of unstable angina pectoris.

The chest pain of angina pectoris is caused by a narrowing of the coronary arteries. When this narrowing results from atherosclerosis—plaque deposits made up of fats and other substances on the inner vessel walls—the condition is known as coronary artery disease. If these plaques restrict blood flow enough to reduce the oxygen supply to the heart muscle (ischemia), angina pectoris occurs as a symptom. Physical exertion or emotional stress, which raise blood pressure and heart rate, increase the heart’s demand for oxygen and can trigger an attack. If a coronary artery becomes completely blocked, a heart attack develops, and heart tissue deprived of blood begins to die within 20 to 60 minutes.

The risk of developing CHD is higher for men and increases overall with age. High blood pressure, diabetes mellitus, and high cholesterol levels contribute to the disease. The risk can also be genetically increased. Modifiable risk factors include unhealthy diet, obesity, and smoking.

Diseases other than CHD can also cause temporary narrowing of the blood vessels and lead to angina pectoris.

Spasms of the coronary arteries can also cause reduced blood flow to the heart. Prinzmetal angina is triggered by such coronary spasms. It occurs independently of physical exertion, and the risk of developing the condition is not influenced by age or gender. Microvascular dysfunction, i.e., a disturbance in the function of the small heart vessels, can also trigger angina pectoris. On the one hand, stress increases the risk of heart attack in CHD patients due to increased blood pressure and increased oxygen demand of the heart. On the other hand, the physical effects of a stressful situation can also be responsible for angina pectoris attacks and heart attacks in people who are otherwise healthy. In addition, there are various symptoms that resemble angina pectoris but are not caused by coronary artery disease. For example, diseases of the lungs or digestive tract can lead to symptoms similar to those of AP.

The clinical presentation of angina pectoris encompasses both physical and psychological dimensions. Depending on severity, symptoms may arise during strenuous exertion, moderate physical activity, or even at rest. Episodes can also be precipitated by psychological stress. The hallmark feature is the characteristic sensation of chest tightness, accompanied by thoracic pain and a feeling of pressure or pulling localized retrosternally. Patients may additionally report a burning discomfort in the chest or upper abdomen. The pain is often described as pulling, dull, or numb, and may radiate to the shoulders, arms, neck, or jaw, with the left side of the body most commonly affected. In some cases, discomfort extends to the upper back. Rarely, the pain may be mistaken for toothache, which can complicate diagnosis, particularly when concurrent dental pathology is present. These symptoms are frequently accompanied by diaphoresis, dyspnea, and pronounced anxiety, the latter sometimes described as a ‘fear of impending death.’

Angina pectoris represents the cardinal symptom of coronary artery disease, yet it does not always manifest in its classic form. Women often present with atypical symptoms such as dyspnea, gastrointestinal discomfort, and fatigue. Similar non-specific complaints, including reduced physical performance, are frequently observed in elderly patients. In individuals with diabetes mellitus, neuropathic changes may attenuate symptom intensity, leading to mild presentations or even asymptomatic ischemia.

If you experience angina pectoris symptoms for the first time or if they are particularly severe, you must call an emergency doctor. This is because the risk of a heart attack is high, especially when symptoms occur for the first time or change.

Depending on whether it is an acute attack or the symptoms occurred some time ago, the doctor will first conduct a detailed medical history interview or use emergency medical diagnostic procedures. During the medical history interview, questions will be asked about previous illnesses, family history, the specific triggers for the AP attacks, frequency, duration, and severity of the symptoms. A stress ECG and stress ultrasound can be used to determine whether the symptoms recur during physical exertion and whether there is a temporary narrowing of the coronary arteries.

The severity of angina pectoris is an important consideration in both diagnosis and prognosis. Stable angina generally carries a more favorable prognosis than unstable angina, although outcomes worsen as disease severity increases. Notably, reduced coronary blood flow may occur even in the absence of overt symptoms.

Unstable angina is indicated when there is a change in disease stage or when anginal attacks occur at rest. The classification of angina severity is typically described in four stages:

• Stage 1: Symptoms appear only during sudden or prolonged exertion, with no limitation during ordinary physical activity.
• Stage 2: Angina occurs with activities such as eating, climbing stairs, or walking uphill. Episodes may also be triggered by stress or cold. There is mild restriction of normal physical activity.
• Stage 3: Even minimal exertion, such as short walks or slow stair climbing, induces symptoms. The individual experiences significant limitation during routine activity.
• Stage 4: Anginal attacks occur during any physical exertion and may also be present at rest.

Unstable angina pectoris—manifesting as initial, atypical, particularly severe, or prolonged symptoms—is considered a medical emergency and requires immediate clinical attention.

In acute episodes, administration of glycerol trinitrate (nitroglycerin spray) induces coronary vasodilation. In cases of stable angina, symptoms typically resolve rapidly. Pharmacological management may also include antihypertensive and heart rate–lowering medications, which reduce vascular strain and myocardial oxygen demand.

As angina pectoris is a symptom rather than a standalone disease, further diagnostic and therapeutic measures are guided by the underlying clinical context. Initial evaluation should confirm whether the presenting symptoms are indeed attributable to angina pectoris. In patients with confirmed coronary artery disease, interventional procedures such as stent implantation or coronary artery bypass grafting may be indicated, depending on the extent and severity of atherosclerotic obstruction.

Prevention of atherosclerosis, and consequently the development of angina pectoris, involves the management of predisposing factors such as smoking and other substance dependencies, obesity, dyslipidemia, hypertension, diabetes mellitus, depression, gout, sleep apnea, and hormonal disorders. Routine medical examinations play a key role in early detection; in many healthcare systems, these preventive services are covered by health insurance from the age of 35. Lifestyle measures—including a balanced diet, regular physical activity, adequate sleep, and effective stress management—contribute to cardiovascular health and are integral to the prevention of coronary artery disease.