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Propaedeutics · Cardiovascular system

Coronary artery disease

Morbus ischaemicus cordis

Coronary artery disease (CAD) is a condition caused by an imbalance between myocardial oxygen demand and its actual delivery. The main morphological substrate is stenosing atherosclerosis of the coronary arteries.

Main symptomEpisodes of typical retrosternal pain (anginal syndrome)
High mortalitySudden cardiac death accounts for 50% of all fatalities from myocardial infarction
Gold standardAngiocardiography precisely determines the localization and degree of vascular stenosis
Diagnostic markerNitroglycerin relieves a typical episode of stable angina within 1–2 minutes
5 min readFor medical studentsUpdated 09/24/2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Etiology and latent course

Atherosclerotic lesions of the coronary vessels begin long before the first symptoms appear. For example, autopsy data from soldiers killed in the Korean War revealed coronary atherosclerosis in 40% of young individuals without signs of the disease. Clinically significant ischemia develops when the vascular lumen is obstructed by more than 50%. At this point, an anginal episode occurs when cardiac workload increases.

Triggers include physical exertion, emotional stress, transitioning from a warm environment to the cold, or a heavy meal. The disease is more common in men. Key risk factors include arterial hypertension, hyperlipidemia, diabetes mellitus, obesity, and smoking. A prior history of myocardial infarction makes a diagnosis of CAD indisputable.

Stable angina and its classification

The most typical manifestation of CAD is effort angina, historically described as «angina pectoris». The patient complains of a pressing or squeezing pain behind the sternum at the peak of physical activity. The pain lasts for 1–3 minutes and subsides at rest or after taking nitroglycerin. The pain frequently radiates to the left shoulder and arm, and less commonly to the lower jaw, back, or epigastrium.

The severity of the condition is assessed using the Canadian Cardiovascular Society (CCS, 1976) classification, based on exercise tolerance:

  • Class I: Symptoms appear only with extreme, prolonged exertion.
  • Class II: Slight limitation; attacks are triggered by walking (more than 200–500 m) or climbing more than one flight of stairs.
  • Class III: Marked limitation; pain occurs with mild walking or climbing just one flight of stairs.
  • Class IV: Discomfort during any activity; attacks may occur even at rest.
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Unstable and vasospastic forms

While the stable form is associated with predictable exertion, unstable angina is characterized by an unpredictable course. It includes new-onset attacks (within the past month), progression of previous symptoms (increased frequency, decreased exercise tolerance), or the onset of pain at rest. The underlying mechanism is the rupture of an atherosclerotic plaque cap and the formation of a thrombus that partially occludes the artery. This condition requires mandatory hospitalization due to the high risk of myocardial infarction and sudden cardiac death.

A separate category is vasospastic (Prinzmetal) angina, which involves an isolated spasm of a major coronary artery. The attacks are severe and often occur at night. Exercise tolerance during the day may remain high, as significant atherosclerosis is frequently absent.

Instrumental and laboratory diagnostics

The primary diagnostic method is ECG. The electrocardiogram is normal in half of cases outside an attack, but during pain, ischemic shift of the ST segment or changes in the T wave amplitude are recorded.

To detect latent ischemia, the following are used:

  1. Stress tests: Treadmill test, bicycle ergometry, or transesophageal atrial pacing (TEAP) to artificially induce tachycardia.
  2. Echocardiography: Identifies myocardial segments with impaired contractility (akinesia, hypokinesia), including during dobutamine stress testing.
  3. Isotope scintigraphy: Administration of radioactive thallium ($^{201}\text{Tl}$) reveals «cold spots» — areas of poor blood supply.

The definitive invasive method is angiocardiography. Laboratory evaluation assesses the lipid profile: total cholesterol > 5.2 mmol/L, LDL > 3.1 mmol/L, and triglycerides > 2 mmol/L against the background of reduced HDL are considered alarming markers.

Treatment strategy

Therapy includes lifestyle modification, pharmacotherapy, and surgery. For stable disease, graded medical exercise therapy is indicated.

Pharmacotherapy is based on:

  • Nitrates: Sublingually for acute relief (they reduce preload and afterload) and long-acting forms for prophylaxis.
  • Beta-blockers: Reduce myocardial oxygen demand by lowering heart rate (atenolol, metoprolol).
  • Antiplatelet agents: Acetylsalicylic acid for the prevention of thrombosis.

If significant stenosis is proven, surgical revascularization is indicated: balloon dilation (angioplasty) or coronary artery bypass grafting (CABG).

Briefly: answers to topical questions

Which pharmacological drug classes are used for the basic treatment and prevention of stable CAD?

Three main drug classes are used for the basic medical treatment and prevention of stable coronary artery disease attacks.

  • Nitrates — used for acute attack relief (sublingually) and prophylaxis (long-acting forms: tablets, ointments, patches).
  • $eta$-Blockers — reduce myocardial oxygen demand by decreasing heart rate and myocardial contractility (e.g., propranolol, atenolol).
  • Antiplatelet agents — prescribed to reduce the risk of thrombosis (acetylsalicylic acid).

Which laboratory biomarkers of myocardial necrosis should be investigated when myocardial infarction is suspected?

When myocardial infarction is suspected, key biomarkers of myocardial necrosis are investigated dynamically:

  • Creatine kinase MB fraction (CK-MB).
  • Cardiac troponins T and I.

Diagnostic significance lies in the increasing titer of these markers within the first few hours after the pain attack.

In which ECG leads are ischemic changes recorded during anterior left ventricular wall involvement?

Ischemic changes during anterior left ventricular wall involvement are recorded predominantly in the chest leads.

  • Leads V1–V6 — reflect ischemia and injury in this area.

These leads may record characteristic signs, such as downsloping ST-segment depression transitioning into a tall, positive, symmetrical T wave (e.g., during occlusion of the proximal segment of the left anterior descending artery).

How to memorize

To assess the efficacy of nitroglycerin, remember the «1–2 minute» rule. If the pain takes longer to resolve or the effect is absent, the typical diagnosis of effort angina is called into question.

Class and exam questions

How to differentiate anginal pain from other chest pains?

Anginal pain is clearly related to physical or emotional exertion, is localized behind the sternum, has a pressing character, and rapidly resolves after cessation of activity or administration of nitroglycerin.

Why is unstable angina considered a life-threatening condition?

It is caused by plaque rupture and the formation of a floating thrombus. This is an intermediate stage that can lead to complete vessel occlusion and acute myocardial infarction at any moment.

What ECG pattern is typical for Prinzmetal's angina?

During a pain attack caused by vascular spasm, the ECG records a pronounced ST-segment elevation, reflecting ischemia of the subepicardial layers.

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What else to study on this topic

  • Pathogenesis of atherosclerotic plaque formation and rupture
  • Detailed ECG interpretation in myocardial ischemia (lead localization)
  • Methodology and evaluation criteria for functional stress tests (TEAP, treadmill)
  • Surgical revascularization methods: choosing between dilation and CABG
  • Differential diagnosis of retrosternal pain syndrome

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