Coronary Artery Disease: Causes, Diagnosis and Treatment

Coronary Artery Disease: Causes, Diagnosis and Treatment

Coronary artery disease (CAD) is a major cause of illness and death worldwide. It results from the progressive narrowing of the arteries that supply blood to the heart muscle — a process driven primarily by the accumulation of cholesterol-laden plaques in the artery walls.

What Are the Coronary Arteries?

The heart muscle works continuously, beating around 100,000 times a day. Like any organ, it requires a constant supply of oxygen-rich blood. This is delivered by the coronary arteries, which branch off from the aorta immediately above the heart.

• The left main coronary artery divides into two major branches: the left anterior descending (LAD) artery (supplying the front and septum of the heart) and the left circumflex artery (supplying the lateral wall)
• The right coronary artery (RCA) supplies the right ventricle and, in most people, the posterior wall

Disease in any of these arteries — particularly the LAD, sometimes called the "widow maker" — reduces blood flow to the corresponding region of heart muscle.

How Coronary Artery Disease Develops

Atherosclerosis

The underlying process is atherosclerosis — the gradual build-up of plaques within artery walls. A plaque consists of cholesterol, inflammatory cells, calcium deposits and fibrous tissue. Over years to decades, plaques enlarge, harden, and protrude into the artery lumen, restricting blood flow.

Atherosclerosis is not unique to the coronary arteries — it affects vessels throughout the body, including the carotid arteries (raising stroke risk) and peripheral arteries (causing leg pain on walking).

Plaque Rupture and Heart Attack

A stable plaque that narrows an artery by 50–70% may cause angina (chest pain on exertion) but not complete blockage. However, even a smaller plaque can rupture suddenly, exposing its interior to the blood and triggering an immediate clot. This clot can completely block the artery within minutes, cutting off blood supply to a region of heart muscle — a heart attack (myocardial infarction). The affected muscle dies if blood flow is not restored urgently.

Risk Factors

Non-Modifiable

• Age — risk increases progressively; men above 45, women above 55
• Sex — men develop CAD earlier than women; the gap narrows after menopause
• Family history — a first-degree male relative with CAD before age 55, or female relative before 65, substantially raises risk
• Genetic cholesterol disorders — familial hypercholesterolaemia causes very high LDL from birth

Modifiable

Risk Factor	Mechanism
High LDL cholesterol	Drives plaque formation
Low HDL cholesterol	Reduces plaque clearance
High blood pressure	Damages the artery lining; promotes plaque growth
Smoking	Damages endothelium; promotes clotting; raises LDL, lowers HDL
Type 2 diabetes	Promotes inflammation and plaque formation
Obesity	Raises blood pressure, cholesterol, and blood glucose
Physical inactivity	Reduces HDL; promotes obesity and insulin resistance
Chronic psychological stress	Activates hormones that raise blood pressure and promote inflammation

Symptoms

Stable Angina

Stable angina is chest pain or pressure that occurs predictably with physical exertion or emotional stress, and resolves with rest within a few minutes. It results from temporarily inadequate blood flow to the heart muscle (ischaemia) when demand exceeds what the narrowed artery can supply.

Typical features:

• Location: central or left-sided chest, often described as tightening, heaviness or pressure
• Radiation: may spread to the left arm, jaw, neck, or shoulder
• Duration: 2–10 minutes; resolves with rest or sublingual nitrate
• Triggers: walking uphill, cold weather, large meals, emotional upset

Atypical presentations — particularly in women, older adults and diabetic patients — may involve breathlessness, nausea, jaw pain or fatigue without chest pain.

Unstable Angina and Heart Attack

Unstable angina occurs at rest, with minimal exertion, or in a new, severe, or worsening pattern — signs that a plaque has become unstable. It requires urgent medical assessment.

A heart attack (myocardial infarction) can present with:

• Severe, crushing chest pain lasting more than 20 minutes
• Pain may persist or fluctuate; improvement after rest or nitrates does not rule out a heart attack
• Sweating, nausea, shortness of breath
• In some cases (particularly women and diabetics), atypical symptoms: jaw pain, back pain, extreme fatigue, epigastric discomfort

A heart attack is a medical emergency. Prompt assessment and treatment can limit heart muscle damage. Call emergency services immediately; do not wait for a time threshold.

Silent Ischaemia

In some people — particularly those with diabetes or older adults — significant coronary artery disease causes no symptoms at all. The condition may be discovered only during routine testing or after a silent heart attack detected on an ECG.

Diagnosis

Non-Invasive Testing

• Resting ECG — may show signs of prior infarction or current ischaemia; normal in many patients with stable CAD
• Exercise stress test (ECG) — monitors the heart's electrical activity and symptoms during graded physical exercise; low cost and widely available
• Stress echocardiogram — detects regional wall motion abnormalities during stress, indicating reduced blood flow
• CT coronary angiogram (CTCA) — non-invasive visualisation of coronary artery anatomy; excellent sensitivity for ruling out CAD; can quantify stenosis and detect plaque before symptoms develop
• Cardiac MRI — assesses viability of heart muscle (alive vs. scarred) and detects ischaemia

Invasive Coronary Angiogram

Gold standard for diagnosis. A thin catheter is passed through the wrist or groin to inject contrast dye into the coronary arteries under X-ray guidance. This precisely maps the location and severity of narrowings and is performed when coronary intervention (stenting or surgery) is being considered. It can be combined with fractional flow reserve (FFR) measurement — a pressure-wire assessment performed during maximal hyperaemia, usually induced with medication, to assess the functional significance of a narrowing. Resting indices such as iFR are different measurements.

Treatment

Medications

Medicines used for coronary artery disease include the following; the combination depends on the clinical indication and contraindications:

• High-intensity statin (e.g. atorvastatin 40–80 mg, rosuvastatin 20–40 mg) — reduces LDL cholesterol and stabilises plaques; independently reduces cardiovascular events beyond cholesterol-lowering
• Antiplatelet therapy — aspirin (low-dose), plus a second agent (clopidogrel, ticagrelor, prasugrel) after stenting or heart attack
• Beta-blocker — may be used for angina, reduced ventricular function or other specific indications; long-term treatment is not required for every patient with coronary disease
• ACE inhibitor or ARB — particularly beneficial in patients with diabetes, reduced ejection fraction or kidney disease
• Sublingual nitrates — for rapid relief of acute angina

Coronary Intervention (PCI — Stenting)

Percutaneous coronary intervention (PCI), commonly called angioplasty, involves inflating a small balloon inside the narrowed artery to restore blood flow, followed by placement of a drug-eluting stent (DES) to hold the artery open. PCI is performed through the radial artery (wrist), using local anaesthetic and mild sedation. The procedure typically takes 30–60 minutes and most patients are discharged within 24–48 hours.

For eligible patients with ST-elevation myocardial infarction (STEMI), primary PCI is an emergency treatment. A common system target is treatment within 90 minutes of first medical contact when taken directly to a PCI-capable hospital; transfer pathways have different targets. Call emergency services immediately for a suspected heart attack.

Coronary Artery Bypass Grafting (CABG)

CABG may be favoured in selected patients with the following patterns, but these labels alone do not determine treatment. A Heart Team assesses coronary anatomy and complexity, heart function, surgical risk, other conditions and patient preferences when comparing surgery, PCI and medical treatment:

• Disease in three major coronary arteries (triple vessel disease)
• Disease in the left main artery
• Severe narrowings in multiple vessels alongside poor heart function
• Diabetic patients with multivessel disease

In CABG, blood vessels taken from the chest (internal mammary artery — the gold standard) or leg (saphenous vein) are sewn in to bypass the blocked segments. It is a major operation requiring general anaesthesia, typically a 5–7 day hospital stay, and 6–12 weeks recovery — but it offers excellent long-term results and can restore normal life expectancy in appropriate patients.

Cardiac Rehabilitation

A structured programme of supervised exercise, dietary guidance and cardiovascular risk education dramatically reduces subsequent heart attacks and improves long-term quality of life. Enrolment is recommended after any coronary event.

Coronary Artery Disease Treatment in China

For planned coronary care in China, confirm the receiving hospital’s services, team experience and proposed pathway before travel:

• CT coronary angiography: confirm availability and whether it is indicated for the planned assessment
• Emergency care: suspected heart attack requires immediate local emergency assessment; do not delay care to arrange overseas treatment
• Complex multivessel PCI and left main stenting: confirm clinical suitability, the receiving team’s experience and available support
• CABG options: discuss whether on-pump or off-pump surgery is appropriate and the expected benefits and risks for the individual case
• Cost: request a written, itemised hospital quote for the proposed care and clarify separately charged coordination services; this guide does not establish comparative savings
• Full English coordination including pre-procedure consultation, in-hospital translation and post-procedure follow-up planning

Contact a PriumCare care navigator to arrange a coronary artery assessment or surgical consultation.

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Sources and editorial correction

• Clinical source.
• Clinical source.
• Clinical source.

Editorial source correction: 25 October 2026. This targeted correction addresses the specific claims documented above; it is not a clinical review of the whole article. No named medical reviewer is claimed. Original publication date is retained.

Additional editorial source clarification

Editorial clarification: 25 October 2026. This targeted update addresses the specific diagnostic, treatment-selection or service claims identified in the sources below. It is not a clinical review of the whole article; the original publication date is retained.

• Source 1

Additional targeted source clarification

Editorial source check: 25 October 2026. These corrections address the specific assessment and treatment-selection statements above; this is not a whole-article medical review.

• Source 1