Skip to main content
M
Doctor-Reviewed Content Verified Hospital Data Updated Medical Information Patient-First Guidance Not for Emergencies — Call 911

Coronary Artery Disease — Causes, Symptoms, Diagnosis & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Updated: 2026-07-06
Ad — after-intro

Quick Facts

Type
Ischaemic Heart Disease / Atherosclerotic Vascular Disease
Specialist
Cardiologist / Interventional Cardiologist / Cardiothoracic Surgeon
Key Treatment
Statins; antiplatelets; PCI (stenting); CABG surgery; lifestyle modification
Prevalence
Affects 200 million people globally; leading cause of death worldwide — 9 million deaths annually

About Coronary Artery Disease

Coronary artery disease (CAD), also called ischaemic heart disease (IHD), is the most common form of heart disease and the leading cause of death globally, accounting for approximately 9 million deaths annually. It is caused by atherosclerosis — accumulation of cholesterol-rich plaques within the walls of the coronary arteries that supply oxygenated blood to the heart muscle. As plaques grow, they narrow the arterial lumen (stenosis), reducing coronary blood flow. Stable plaques cause chronic stable angina (chest pain on exertion). Plaque rupture triggers acute coronary syndromes (ACS): unstable angina, non-ST elevation myocardial infarction (NSTEMI), and ST elevation myocardial infarction (STEMI) — medical emergencies requiring immediate treatment. Approximately 200 million people worldwide have CAD, with prevalence rising due to ageing populations, obesity, diabetes, and physical inactivity.

Causes & Risk Factors

CAD develops through progressive atherosclerosis over decades, beginning with endothelial dysfunction and progressing to fatty streak formation, fibrous plaque development, and complex vulnerable plaques. Major modifiable risk factors: hypertension (the single most important — doubles CAD risk), dyslipidaemia (elevated LDL cholesterol, low HDL, elevated triglycerides), type 2 diabetes (2-4x increased CAD risk — diabetes is considered a CAD risk equivalent), smoking (increases risk 2-4x — even passive smoking increases risk), physical inactivity, obesity (particularly central adiposity), and unhealthy diet (high saturated fat, low fibre, excess sodium). Non-modifiable risk factors: age (men over 45, women over 55), male sex (women are protected by oestrogen before menopause but catch up with men postmenopausally), family history of premature CAD (first-degree relative: male below 55, female below 65), and ethnicity (South Asians have 50% higher CAD risk than White Europeans). Chronic kidney disease, inflammatory diseases (rheumatoid arthritis, psoriasis, lupus), and HIV also substantially increase CAD risk.

Symptoms & Warning Signs

Stable angina: central chest tightness, pressure, heaviness, or squeezing on exertion (Canadian Cardiovascular Society grade I-IV) — typically precipitated by a predictable level of activity, relieved within 5 minutes of rest or sublingual GTN (glyceryl trinitrate). May radiate to the jaw, left arm, shoulder, or back. Unstable angina: angina occurring at rest, with increasing frequency, or with decreasing exercise threshold — requires urgent hospital assessment. Myocardial infarction (heart attack): sudden severe central chest pain (often crushing, not relieved by GTN), radiating to the arm or jaw, associated with sweating (diaphoresis), nausea, breathlessness, and a sense of impending doom — lasts more than 20 minutes. Silent ischaemia (no symptoms) is common in diabetics. Acute heart failure, syncope, or sudden cardiac arrest may be the first presentation. Women and elderly patients may have atypical symptoms: fatigue, epigastric pain, breathlessness, or jaw pain without chest pain.

Diagnosis & Cardiac Investigations

12-lead ECG: ST elevation (STEMI — immediate PCI indication), ST depression, T-wave inversion, bundle branch block, or new Q waves. Serum troponin (I or T — high-sensitivity): rises within 1-3 hours of myocardial infarction — used in serial measurements at 0 and 1-3 hours for NSTEMI diagnosis. Echocardiogram: assesses left ventricular function, wall motion abnormalities (ischaemia/infarction), and valve disease. Non-invasive functional testing: exercise ECG (treadmill stress test), stress echocardiography (dobutamine or exercise), nuclear myocardial perfusion imaging (SPECT/PET), and cardiac MRI perfusion imaging. CT coronary angiography (CTCA): non-invasive high-resolution imaging of coronary arteries — recommended first-line investigation for stable chest pain (NICE 2021); high negative predictive value; also quantifies coronary calcium score (CAC) as a risk stratification tool. Invasive coronary angiography (catheter angiography): gold standard for visualising coronary anatomy, severity of stenoses, and guiding PCI or CABG planning — fractional flow reserve (FFR) and iFR measure the functional significance of a stenosis.

Treatment Options

Medical therapy for all CAD patients: antiplatelet therapy (aspirin 75 mg lifelong; ticagrelor or clopidogrel for 12 months post-ACS or PCI); high-intensity statin (atorvastatin 80 mg — target LDL below 1.4 mmol/L for secondary prevention); ACE inhibitor or ARB (for reduced EF, hypertension, or diabetes); beta-blocker (post-MI, heart failure with reduced EF); GTN spray for acute angina relief. For chronic stable angina: add long-acting nitrates, calcium channel blockers, or ivabradine if beta-blockers inadequate. Percutaneous Coronary Intervention (PCI): coronary angioplasty with drug-eluting stent (DES) implantation — first-line revascularisation for STEMI (primary PCI within 90 minutes of first medical contact) and for stable multivessel CAD with significant ischaemia. Coronary Artery Bypass Grafting (CABG): superior to PCI for left main stem disease, three-vessel disease with complex anatomy (SYNTAX score above 33), or diabetes with multivessel disease — using internal mammary artery grafts which remain patent for over 90% of patients at 10 years.

Complications

Acute myocardial infarction (heart attack) — caused by plaque rupture and coronary thrombosis — is the most serious acute complication, causing permanent heart muscle death and potentially fatal arrhythmias (ventricular fibrillation). Post-MI complications include left ventricular failure, cardiogenic shock, mechanical complications (papillary muscle rupture causing acute mitral regurgitation, ventricular septal defect, free wall rupture — all rare but life-threatening), and Dressler's syndrome (pericarditis at 1–6 weeks post-MI). Chronic complications include heart failure (ischaemic cardiomyopathy — EF below 40%), ventricular arrhythmias (VT, VF — highest risk in first 48 hours post-MI and with low EF), and sudden cardiac death. Stable CAD causes significant exertional limitation from angina, impairing quality of life and exercise capacity. In-stent restenosis (ISR) occurs in approximately 5–10% of drug-eluting stents and requires repeat revascularisation.

Prevention & Cardiovascular Risk Reduction

Primary prevention: cardiovascular risk scoring (QRISK3 in UK, Framingham, PCE in USA) guides statin initiation in those with 10-year MACE risk above 10%. Lifestyle: quit smoking (halves CAD risk within 1 year), Mediterranean diet (reduces cardiovascular events by 30% — Lyon Diet Heart Study), 150 minutes moderate intensity exercise weekly, achieve and maintain healthy weight (BMI 20-25), limit alcohol. Control cardiovascular risk factors: blood pressure target below 130/80 mmHg, LDL cholesterol below 2.6 mmol/L (primary prevention) or below 1.4 mmol/L (secondary prevention), HbA1c below 7% in diabetes. Secondary prevention (post-MI, established CAD): dual antiplatelet therapy for 12 months, lifelong statin and aspirin, ACE inhibitor, and beta-blocker as indicated. Cardiac rehabilitation after myocardial infarction significantly reduces mortality and recurrence. PCSK9 inhibitors (evolocumab, alirocumab) for statin-intolerant or very high-risk patients achieve LDL reductions of 50-60%.

When to Seek Emergency Care

Call emergency services (999/911) immediately for: sudden severe chest pain lasting more than 15-20 minutes not relieved by rest or GTN spray, pain radiating to the arm or jaw with sweating or nausea, sudden breathlessness with chest discomfort, collapse or loss of consciousness — these are signs of a heart attack requiring immediate medical intervention. Do not drive yourself to hospital — call an ambulance. For GTN-responsive chest pain on exertion that is new, worsening, or occurring at rest, seek same-day urgent GP or hospital assessment — this is unstable angina. Anyone with unexplained severe breathlessness, palpitations, or presyncope should have same-day cardiac evaluation. People with established risk factors (diabetes, hypertension, hypercholesterolaemia, family history) should discuss formal cardiovascular risk assessment with their GP.

Frequently Asked Questions

Angina is temporary chest pain from reduced blood flow to the heart during exertion or stress — the heart muscle becomes ischaemic but does not die. It is relieved within 5 minutes by rest or GTN spray and leaves no permanent damage. A heart attack (myocardial infarction) occurs when a coronary artery is completely blocked (usually by plaque rupture and thrombus formation), causing permanent death of heart muscle — it is not relieved by GTN, lasts more than 20 minutes, and is associated with rising troponin levels. A heart attack is a medical emergency requiring immediate hospital treatment.
Both PCI (stenting) and CABG (bypass surgery) are effective revascularisation strategies, but their optimal use depends on coronary anatomy. For single or two-vessel disease, PCI with drug-eluting stents provides equivalent long-term outcomes to CABG with faster recovery. For three-vessel disease and/or left main stem disease — particularly with complex anatomy (high SYNTAX score) or diabetes — CABG provides superior long-term survival and lower repeat revascularisation rates. The SYNTAX, NOBLE, and EXCEL trials have refined these indications, and decisions are made by a multidisciplinary Heart Team.
Significant plaque regression is achievable with very intensive lifestyle modification and pharmacological lipid-lowering. The REVERSAL and ASTEROID trials demonstrated measurable plaque regression with high-intensity statins. Intensive lifestyle programmes (Ornish programme — very low-fat vegan diet, exercise, stress management) have shown angiographic regression. However, established CAD cannot be fully reversed to normal — the goal of treatment is halting progression, reducing plaque vulnerability, and preventing events through optimal medical therapy.
A coronary stent is a small metal mesh tube deployed inside a blocked or narrowed coronary artery during PCI to restore blood flow. Drug-eluting stents (DES) are coated with antiproliferative drugs (everolimus, zotarolimus) that are slowly released to prevent scar tissue from growing inside the stent (in-stent restenosis). After DES implantation, dual antiplatelet therapy (aspirin plus ticagrelor or clopidogrel) is required for at least 12 months to prevent stent thrombosis. Modern DES have less than 1% annual in-stent thrombosis rates and produce excellent long-term outcomes.

References

  1. ESC Guidelines on Chronic Coronary Syndromes, European Heart Journal, 2019
  2. ESC Guidelines on Acute Coronary Syndromes — NSTEMI, 2020
  3. ESC/EACTS Guidelines on Myocardial Revascularisation, European Heart Journal, 2018
Ad — after-content

Medically Reviewed

Our medical content follows strict editorial guidelines to ensure accuracy and reliability.

Up to Date

Last updated: 2026-07-06

Important: This information is for educational purposes only and does not constitute medical advice. Always consult a qualified healthcare provider for diagnosis and treatment.

Ready to take the next step?

Connect with top hospitals and specialists. Get personalized guidance for your medical journey.

Latest from our blog and forum

Latest from Our Blog

View All →

Latest Forum Discussions

View All →
Compare Costs Get Free Help

Medical Disclaimer: The information on MyMedicPlus is for educational and informational purposes only. It is not a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay seeking it because of something you have read on this site.