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Health condition · Clinically reviewed

Atherosclerosis, the plaque behind most heart attacks and strokes.

Silent for decades, then sudden. Risk assessment, NICE lipid targets and modern lipid-lowering therapy change the story.

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Why trust this guide

  • 01

    Clinically reviewed

    Written by our editorial team and reviewed by a registered UK clinician before publication.

  • 02

    Sourced from guidance

    Checked against NICE, ESC, JBS3 and peer-reviewed sources you can see at the end.

  • 03

    Current for 2026

    Reflects modern UK guidance including NICE NG238 lipid targets, PCSK9 inhibitors, inclisiran and emerging Lp(a) therapies.

Key facts

Atherosclerosis at a glance.

The essentials, in plain English - what it is, how it forms, and how UK cardiology treats it today.

  • What it is

    Atheromatous plaque within the intima of arteries. The single biggest driver of cardiovascular death worldwide, and the process behind most heart attacks and ischaemic strokes.

  • How it starts

    Endothelial dysfunction lets LDL cross into the arterial wall, where it is oxidised and taken up by macrophages that become foam cells.

  • How it progresses

    Smooth muscle cells migrate over the lipid core, laying down a fibrous cap. Calcification, plaque enlargement and eventual rupture drive clinical events.

  • Key drivers

    LDL cholesterol, lipoprotein(a), high blood pressure, smoking, type 2 diabetes and chronic inflammation - most of them modifiable.

  • Foundation therapy

    High-intensity statins (atorvastatin, rosuvastatin) with ezetimibe added to hit NICE lipid targets.

  • Modern options

    PCSK9 inhibitors, inclisiran, bempedoic acid and icosapent ethyl for people who need more than statins alone.

Why this guide matters

Prevention is a plan, not a hope.

Atherosclerosis develops silently for decades. The three points below shape everything else on this page.

  • LDL is causal

    Every 1 mmol/L reduction in LDL cholesterol produces roughly a 22 percent fall in major vascular events. Lower for longer is better.

  • Statins are the foundation

    High-intensity statins with ezetimibe get most patients to NICE targets. PCSK9 inhibitors and inclisiran finish the job for the rest.

  • Lifestyle multiplies the medicine

    A Mediterranean pattern, 150 minutes of activity a week and stopping smoking add up to more than any single tablet.

How atherosclerosis is assessed

From risk score to a clear plan.

The steps a UK GP or cardiologist will normally follow, in order - so you know what to expect and why.

  1. 01

    Assessing

    Risk calculation

    A UK GP will run QRISK3 (or JBS3 for lifetime risk) to give you a 10-year cardiovascular risk figure and open the conversation about prevention.

  2. 02

    Assessing

    Lipid and metabolic bloods

    Full lipid profile, HbA1c, kidney and liver function. ApoB and lipoprotein(a) add depth where risk is unclear or family history is strong.

  3. 03

    Assessing

    Blood pressure and BMI

    Confirmed with home or ambulatory readings where relevant. BMI and waist circumference frame metabolic risk.

  4. 04

    Confirming

    hsCRP for inflammation

    High-sensitivity CRP flags residual inflammatory risk, especially after a cardiovascular event or when risk sits on the fence.

  5. 05

    Confirming

    Coronary calcium score (CTAC)

    A low-dose CT that quantifies calcified plaque. A useful tie-breaker for intermediate-risk patients deciding about statins.

  6. 06

    Confirming

    CT coronary angiography

    Non-invasive luminal and plaque imaging - the first-line test for stable chest pain in NICE guidance.

  7. 07

    Refining

    Carotid duplex and IMT

    Ultrasound of the neck arteries for plaque burden or stenosis, particularly after TIA, stroke or when a bruit is heard.

  8. 08

    Refining

    ABPI and AAA screening

    Ankle-brachial pressure index for peripheral arterial disease, and a one-off AAA ultrasound for men at 65.

  9. 09

    Refining

    Family history and polygenic risk

    A structured family history flags familial hypercholesterolaemia. Polygenic risk scores are entering specialist practice for early prevention.

Typical timeline: a first appointment to a settled prevention plan in a few weeks.

Symptoms

What atherosclerosis actually feels like.

Often nothing at all - until it isn’t. These are the patterns to know, and the moments to call for urgent help.

  • Angina on exertion

    Central chest tightness, jaw or arm ache that comes on with effort and eases with rest - the classic sign of coronary narrowing.

  • Breathlessness

    A drop in exercise tolerance can be the earliest whisper of ischaemic heart disease, especially in women and people with diabetes.

  • TIA or stroke symptoms

    Sudden weakness, speech change or vision loss - carotid plaque and cardioembolic disease are common causes.

  • Claudication

    Cramping calf, thigh or buttock pain on walking that eases with rest - a marker of peripheral arterial disease and system-wide atheroma.

  • Erectile dysfunction

    Often the first vascular symptom in men - small arteries clog before the big ones and it warrants full cardiovascular assessment.

  • Cold or pale feet

    Reduced pulses, hair loss on the shin and slow-healing foot wounds all point to peripheral disease.

  • Silent disease

    Most atherosclerosis is symptomless until a plaque ruptures. Risk assessment and imaging pick it up before that moment.

  • Red flag - acute chest pain

    New, severe or crushing chest pain, with sweating or breathlessness - call 999. Assume a heart attack until proven otherwise.

Treatment

How atherosclerosis is treated in the UK.

Lifestyle first, high-intensity statin plus ezetimibe next - and modern lipid-lowering, blood pressure and diabetes therapies to finish the job.

  • Mediterranean or DASH diet

    The most evidence-based dietary pattern for atherosclerosis - olive oil, oily fish, vegetables, legumes and whole grains, with less ultra-processed food.

  • Regular exercise

    At least 150 minutes a week of moderate activity plus two strength sessions. Improves lipids, blood pressure, insulin sensitivity and mortality.

  • Stop smoking

    Single biggest modifiable step. Combined behavioural support and pharmacotherapy (varenicline where available, NRT or bupropion) works best.

  • High-intensity statin

    Atorvastatin 20 to 80 mg or rosuvastatin 10 to 40 mg per NICE NG238. Target LDL under 1.4 mmol/L in very high risk, under 1.8 mmol/L in secondary prevention.

  • Ezetimibe

    Added when statin alone does not hit target, or as first-line where statins cannot be tolerated. Cheap, safe and additive to statin therapy.

  • PCSK9 inhibitors

    Alirocumab or evolocumab by fortnightly injection - powerful LDL reduction for familial hypercholesterolaemia and refractory secondary prevention.

  • Inclisiran

    Six-monthly RNAi injection that silences hepatic PCSK9. NICE-approved for secondary prevention when LDL remains above target on statin and ezetimibe.

  • Bempedoic acid

    An oral ACL inhibitor for people who cannot tolerate statins, often combined with ezetimibe.

  • Icosapent ethyl (Vazkepa)

    High-dose EPA for people with high triglycerides and established or high cardiovascular risk on optimal statin therapy.

  • Blood pressure control

    ACE inhibitor or ARB, amlodipine, indapamide and spironolactone where needed. Usual target under 130/80 mmHg.

  • Diabetes therapies with CV benefit

    SGLT2 inhibitors and GLP-1 receptor agonists reduce cardiovascular mortality in type 2 diabetes and are now core secondary prevention tools.

  • Antiplatelet therapy

    Aspirin 75 mg for secondary prevention only. Dual antiplatelet therapy after acute coronary syndrome or PCI, per specialist plan.

  • Revascularisation

    PCI with stenting, coronary artery bypass, carotid endarterectomy or peripheral bypass for symptomatic significant disease.

  • Emerging - Lp(a) and inflammation

    Olpasiran and pelacarsen (Lp(a)-targeted RNAi) and low-dose colchicine (LoDoCo2) point to the next generation of residual-risk therapy.

What this guide is based on

The sources behind every claim on this page.

UK national guidance and international cardiology standards, current at the time of last review.

Key references

Guidelines and standards we relied on.

A quiet reminder

This guide is for information, not medical advice.

Your GP or cardiologist knows your history and can tell you which parts apply to you. If in doubt, get seen.

  • NICE. Cardiovascular disease: risk assessment and reduction, including lipid modification (NG238).

  • NICE. Hypertension in adults: diagnosis and management (NG136).

  • NICE. Type 2 diabetes in adults: management (NG28).

  • ESC/EAS. Guidelines for the management of dyslipidaemias.

  • Joint British Societies (JBS3). Consensus recommendations for the prevention of cardiovascular disease.

  • MHRA. Guidance on inclisiran, PCSK9 inhibitors and icosapent ethyl.

Red flags

When atherosclerosis needs urgent attention.

Most atherosclerosis is managed in primary care with lifestyle change and lipid therapy. These are the situations that aren’t.

  • Acute chest pain

    Sudden crushing chest pain, sweating, breathlessness or radiation to the jaw or arm - call 999. Treat as a heart attack until proven otherwise.

  • Stroke or TIA symptoms

    Face droop, arm weakness, slurred speech - dial 999. Even a transient episode is a warning of impending stroke.

  • Cold, pale, painful leg

    Acute limb ischaemia needs vascular assessment within hours. Delay costs the limb.

  • Rapidly worsening angina

    Chest pain at rest or with minimal effort, more often or lasting longer - urgent cardiology assessment for unstable angina.

  • Familial hypercholesterolaemia

    Very high LDL, tendon xanthomata or a family history of early cardiovascular death deserves genetic testing and specialist review.

  • Very high lipoprotein(a)

    Lp(a) above 90 mg/dL (or 200 nmol/L) is a strong independent risk factor - triggers more aggressive LDL and BP targets.

  • Statin-resistant lipids

    Persistently high LDL on maximum tolerated statin plus ezetimibe - refer for PCSK9 inhibitors or inclisiran.

  • Suspected AAA

    Pulsatile abdominal mass or unexplained back pain in an older smoker - urgent ultrasound and vascular referral.

  • Renal artery disease

    Sudden resistant hypertension or an unexplained rise in creatinine after ACEi - consider renovascular atherosclerosis.

Living with it

A modifiable condition, with a clear ladder.

Four things that make the biggest difference day to day - a Mediterranean pattern, regular movement, taking the tablets, and knowing your numbers.

A quiet reminder

Consistency beats intensity, every time.

Small, steady habits kept up for years do more for your arteries than a heroic month that doesn’t last.

  1. 01 Diet

    Eat like the Mediterranean

    Olive oil, oily fish twice a week, nuts, legumes, plenty of vegetables and whole grains. Cut ultra-processed food and sugary drinks.

  2. 02 Move

    Aim for 150 minutes a week

    Any activity you enjoy and can keep up. Add two strength sessions - muscle drives insulin sensitivity as much as it moves you around.

  3. 03 Adhere

    Take the tablets

    Statins, blood pressure medicines and diabetes therapies work only if you take them - most side effects settle or can be worked around.

  4. 04 Monitor

    Know your numbers

    LDL, blood pressure, HbA1c and weight. Review annually, or sooner if anything changes - and celebrate progress.

Frequently asked

Everything we get asked about atherosclerosis.

Quick answers on LDL targets, statins, Lp(a), and whether plaque can be reversed.

  • What is atherosclerosis?

    Atherosclerosis is the build-up of cholesterol-rich atheromatous plaque within the inner lining (intima) of medium and large arteries. It starts with endothelial dysfunction that lets LDL cholesterol enter the arterial wall, where macrophages engulf it and become foam cells. Smooth muscle cells then lay down a fibrous cap that can rupture, causing heart attacks, strokes and peripheral arterial disease.

  • How is it different from arteriosclerosis?

    Arteriosclerosis is the umbrella term for hardening of the arteries and includes age-related medial calcification and arteriolosclerosis. Atherosclerosis is the specific, cholesterol-driven plaque form of arteriosclerosis and is the type behind most cardiovascular events. Our combined guide at /conditions/arteriosclerosis-atherosclerosis explains the family in more detail.

  • What LDL target should I aim for?

    NICE NG238 recommends an LDL under 1.8 mmol/L (non-HDL under 2.5 mmol/L) for secondary prevention and under 1.4 mmol/L (non-HDL under 2.2 mmol/L) for very high risk patients such as those with recurrent events or diabetes with target-organ damage. Primary prevention is individualised using QRISK3 or JBS3.

  • Are statins safe long-term?

    Yes. Large randomised trials and long-term follow-up show clear mortality benefit with a very low absolute risk of significant harm. Most muscle symptoms are not caused by the statin itself and resolve with a rechallenge or a switch to a different molecule or a lower dose.

  • What about lipoprotein(a)?

    Lp(a) is an inherited, independent risk factor. Levels are largely fixed for life and are not moved much by diet or statins. Very high values push you towards tighter LDL targets, PCSK9 inhibitors or inclisiran, and enrolment in trials of Lp(a)-targeted therapies such as olpasiran and pelacarsen.

  • Can atherosclerosis be reversed?

    Progression can be slowed and, with intensive lipid lowering and lifestyle change, imaging trials show modest plaque regression. The bigger prize is plaque stabilisation - a thicker fibrous cap and a smaller lipid core are much less likely to rupture, which is what prevents heart attacks and strokes.

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