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Angina Pectoris

Q: What is the clinical presentation (nature and localization of pain) during a stable angina attack?

The clinical presentation of a stable angina attack (angina pectoris) manifests as typical ischemic chest pain. Characteristics of this attack include: Type of pain — squeezing, pressing.Localization — retrosternal.Radiation — typical referral of pain to the left scapula and left arm. Pain occurs due to a mismatch between myocardial oxygen demand and supply. In stable angina (effort angina), attacks are provoked by increased heart rate during physical or emotional stress, because atherosclerosis-diseased vessels cannot adequately dilate.

Angina pectoris

For medical students2 min readUpdated 2026-10-10

Angina pectoris is the leading clinical manifestation of transient (reversible) coronary insufficiency. The condition develops when the myocardial oxygen demand exceeds coronary blood flow capacity, causing temporary cardiomyocyte ischemia without immediate total cell death, while triggering structural myocardial remodeling.

Pathology coreA clinical manifestation of transient (reversible) coronary insufficiency.

Unstable formAttacks progressively increase in severity, frequency, and duration, frequently occurring at rest.

Time factorIschemia lasting up to 40–60 minutes leads to irreversible damage of many cardiomyocytes.

Main outcomesRepeated attacks lead to cardiosclerosis, whereas prolonged ischemia leads to myocardial infarction.

Main Types of Coronary Insufficiency

In pathophysiology, myocardial blood supply disorders are divided into two fundamental types that determine patient prognosis:

Irreversible coronary insufficiency. Characterized by permanent cessation of blood flow, inevitably leading to tissue death. The predictable outcome in this case is myocardial infarction.
Reversible (transient) coronary insufficiency. Underlies all forms of angina pectoris. Furthermore, it occurs following the onset of reperfusion (restoration of blood flow or revascularization) of a previously ischemic myocardial area. The primary classification criterion within this group is the duration of oxygen deprivation until the moment of reperfusion.

Clinical Variants of Angina Pectoris

Depending on the clinical course and underlying causes, several variants of the disease are distinguished:

Stable (typical) angina. The most common type of pathology. It is based on a prolonged decrease in coronary blood flow volume to a critical level, a significant increase in cardiac workload, or a combination of both factors.
Unstable angina. Known by synonyms such as "progressive" or "pre-infarction" angina, as it carries a high risk of myocardial infarction. Ischemic episodes progressively increase in frequency, duration, and severity, frequently occurring even at rest. The primary causes include prolonged coronary artery spasm or systemic forms of vasculitis (e.g., in systemic lupus erythematosus).
Variant angina (Prinzmetal's angina). A specific form associated with more prolonged periods of transient ischemia.

The Role of the Time Factor: From Ischemia to Reperfusion

The pathogenesis of injury and the clinical presentation strictly depend on the time interval during which the myocardium remains deprived of oxygen:

Brief ischemia. Cardiomyocyte injury in the reperfusion zone remains reversible. Clinically, this corresponds to stable angina.
Ischemia lasting up to 40–60 minutes. Injury becomes irreversible for many myocardial cells. Clinically, this interval manifests as unstable or variant angina.
Ischemia lasting more than 60–120 minutes. Leads to irreversible injury of the vast majority of cardiomyocytes. This situation is typical following myocardial revascularization in patients with ischemic heart disease (IHD).

Morphological Outcomes of the Disease

Any form of coronary insufficiency leaves a structural footprint in cardiac tissue. Two main morphological outcomes are distinguished:

Cardiosclerosis. A predictable result of repeated episodes of stable angina, as well as a consequence of prior unstable and variant angina.
Myocardial infarction. The outcome of initially irreversible coronary insufficiency or prolonged transient ischemia lasting more than 60–120 minutes.

Mnemonic

To remember the outcomes of transient ischemia, use the "Time Rule": Brief — cells survive (stable angina; outcome: cardiosclerosis upon recurrence). Up to 60 minutes — many cells die (unstable form; outcome: cardiosclerosis). More than 60–120 minutes — the majority of cells die (outcome: myocardial infarction).

Frequently asked questions

What is the clinical presentation (nature and localization of pain) during a stable angina attack?

The clinical presentation of a stable angina attack (angina pectoris) manifests as typical ischemic chest pain. Characteristics of this attack include:

Type of pain — squeezing, pressing.
Localization — retrosternal.
Radiation — typical referral of pain to the left scapula and left arm.

Pain occurs due to a mismatch between myocardial oxygen demand and supply. In stable angina (effort angina), attacks are provoked by increased heart rate during physical or emotional stress, because atherosclerosis-diseased vessels cannot adequately dilate.

What is the precise mechanism of vasospasm development in variant angina?

An attack of variant angina (Prinzmetal's angina) is driven by the spasm of a large epicardial coronary artery.

Proposed mechanisms and factors of coronary vasospasm include:

an imbalance between vasoconstricting and vasodilating factors;
a likely reduction in the synthesis of endothelium-derived relaxing factor;
an additional contributing factor of intravascular platelet aggregation.

The consequence of this spasm is subepicardial myocardial ischemia. Attacks occur spontaneously, frequently at rest or during sleep, without obvious provoking factors.

Through which pathophysiological processes does post-ischemic cardiosclerosis develop?

Post-ischemic cardiosclerosis is described as the morphological outcome of repeated transient episodes of coronary insufficiency in stable, unstable, or variant angina.

Processes involved include:

repeated myocardial ischemia with cardiomyocyte injury in the reperfusion zone;
ischemia lasting up to 40–60 minutes resulting in irreversible damage to many cardiomyocytes in the reperfusion zone;
development of myocardial sclerosis/fibrosis;
compensatory cardiomyocyte hypertrophy;
relative hypoxia of hypertrophied cardiomyocytes due to a mismatch between capillary network growth and muscle mass enlargement;
the cascade: "hypertrophy → hypoxia → dystrophy → additional sclerosis".

In post-infarction/diffuse cardiosclerosis, the combination of myocardial hypertrophy, myocardial fibrosis, and leukocyte infiltration leads to elevated left ventricular end-diastolic pressure and the development of heart failure.

What is the primary danger of unstable angina?

This form carries a high risk of progressing to myocardial infarction. Ischemic episodes progressively increase in frequency, duration, and severity, and attacks may occur even at complete rest.

What factors provoke the development of stable angina?

The main causes include a prolonged reduction in coronary blood flow to a critical level, a significant increase in mechanical cardiac work, or a combination of both factors.

What do repeated attacks of reversible ischemia lead to?

Even with reversible transient insufficiency, repeated episodes of stable, unstable, or variant angina eventually lead to the development of cardiosclerosis.

What happens to the myocardium during ischemia lasting longer than 60–120 minutes?

With such prolonged transient ischemia, injury becomes irreversible for the vast majority of cells. The morphological outcome in this situation is myocardial infarction.

Go deeper

Pathogenesis of systemic vasculitis (e.g., systemic lupus erythematosus) as a cause of unstable angina.
Mechanisms underlying prolonged coronary artery spasm.
Specific features of cardiomyocyte injury within the reperfusion zone.
Differences between variant (Prinzmetal's) angina and typical angina pectoris.
Morphological stages of cardiosclerosis development following repeated ischemic episodes.