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Health condition

Arteriosclerosis and atherosclerosis, lipids, blood pressure and the modern toolkit that changes outcomes.

The leading cause of cardiovascular mortality, and one of the most treatable. A structured plan across lifestyle, lipids, blood pressure and diabetes cuts events for life.

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Why trust this guide

  • 01

    Editorial team

    Written by our editorial team from the UK sources listed on each page.

  • 02

    Sourced from guidance

    Checked against NICE NG238, JBS3, ESC and peer-reviewed cardiology sources you can see at the end.

  • 03

    Current for 2026

    Reflects modern UK guidance including high-intensity statins, PCSK9 inhibitors, inclisiran and emerging Lp(a) therapies.

Key facts

Arteriosclerosis and atherosclerosis at a glance.

The essentials, in plain English. What each term means, why the distinction matters and how modern UK cardiology treats it.

  • What it is

    Arteriosclerosis is a general term for arterial wall thickening and stiffness. Atherosclerosis is the specific form driven by lipid-rich intimal plaque.

  • Why it matters

    Atherosclerosis is the leading cause of cardiovascular mortality worldwide, underlying most heart attacks, ischaemic strokes and peripheral arterial disease.

  • Subtypes

    Atherosclerosis, Monckeberg medial calcification (diabetes, CKD) and arteriolosclerosis (hypertensive and diabetic small vessel disease) all sit under the umbrella.

  • Foundation therapy

    High-intensity statins remain the backbone. NICE NG238 sets an LDL target under 1.4 mmol/L in very high-risk patients.

  • Second-line lipid

    Ezetimibe, PCSK9 inhibitors (alirocumab, evolocumab), inclisiran and bempedoic acid extend LDL lowering when statins are not enough.

  • Antiplatelet rule

    Aspirin 75 mg is for secondary prevention only. It is no longer recommended for routine primary prevention because bleeding risk outweighs benefit.

Why this guide matters

Small daily changes, big lifetime effect.

Atherosclerosis develops silently over decades. The three ideas below reshape how it should be assessed and treated in the UK today.

  • Lower LDL, earlier, for longer

    Cumulative LDL exposure drives plaque. Starting statins earlier, at higher intensity and reaching a lower target changes lifetime risk, not just short-term numbers.

  • Blood pressure and diabetes matter equally

    A stepped BP plan targeting under 130/80 for most patients, plus SGLT2 inhibitors or GLP-1 agonists in type 2 diabetes, cut cardiovascular events beyond glucose control.

  • Antiplatelets have narrowed indications

    Aspirin 75 mg is now recommended for secondary prevention only. Dual antiplatelet therapy after ACS or PCI is duration-limited.

How the diagnosis is made

From risk score to a shared plan.

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

  1. 01

    Assessing

    Cardiovascular risk score

    A structured QRISK3 (or JBS3, ASCVD) 10-year risk calculation using age, sex, BP, smoking, lipids, diabetes and comorbidities.

  2. 02

    Assessing

    Lipid panel with ApoB and Lp(a)

    Total cholesterol, LDL, HDL, non-HDL, triglycerides plus ApoB where available and a one-off Lp(a) to unmask hidden inherited risk.

  3. 03

    Assessing

    Metabolic and inflammatory bloods

    HbA1c, fasting glucose and hsCRP place the patient on the diabetes and inflammation spectrum that drives plaque.

  4. 04

    Confirming

    BP, BMI, smoking and lifestyle

    Confirmed blood pressure (ideally home or ambulatory), BMI, waist, smoking status, alcohol, diet and activity all reshape the plan.

  5. 05

    Confirming

    Imaging where it changes decisions

    Coronary calcium score, coronary CTA, carotid duplex with IMT, ankle-brachial pressure index and AAA screening in eligible men.

  6. 06

    Planning

    Family history and inherited risk

    Premature CV disease in first-degree relatives, familial hypercholesterolaemia screening and, selectively, a polygenic risk score.

  7. 07

    Planning

    Shared decision on treatment

    Absolute risk, lifetime benefit, tablet burden and patient preference decide who starts statins, adds ezetimibe or steps up to PCSK9 or inclisiran.

Typical timeline: a first review to a settled treatment plan in weeks, not months.

Symptoms

What atherosclerosis actually looks like.

Silent for decades, then vessel-specific. The picture depends on which artery is narrowed and whether a plaque ruptures acutely.

  • Silent for years

    Atherosclerosis is asymptomatic until a plaque narrows a vessel enough to cause ischaemia or ruptures acutely.

  • Angina on exertion

    Central chest tightness with exercise or emotion, relieved by rest or GTN, suggests significant coronary narrowing.

  • Acute coronary syndrome

    Prolonged central chest pain, sweating, nausea and breathlessness. Call 999. Time-critical assessment for STEMI or NSTEMI.

  • Stroke or TIA

    Sudden face, arm or speech weakness (FAST). Carotid atherosclerosis and cardioembolism are common mechanisms.

  • Intermittent claudication

    Calf, thigh or buttock cramp on walking, relieved by rest, points to peripheral arterial disease.

  • Critical limb ischaemia

    Rest pain, non-healing ulcers, cold or dusky foot. A vascular emergency requiring urgent revascularisation.

  • Renovascular and mesenteric disease

    Uncontrolled hypertension, unexplained kidney decline or post-meal abdominal pain can reflect atherosclerosis elsewhere.

  • Red flag - crushing chest pain

    New central chest pain lasting more than 15 minutes, or any suspicion of stroke, needs 999 not a GP appointment.

Treatment

How atherosclerosis is treated in the UK.

Lifestyle first, then high-intensity statins, add-on lipid therapy, BP control and revascularisation when narrowing is critical and symptomatic.

  • Mediterranean or DASH diet

    The best-evidenced dietary patterns for cardiovascular risk reduction. Emphasise vegetables, legumes, whole grains, nuts, olive oil and oily fish.

  • Exercise and weight

    At least 150 minutes of moderate activity a week, plus resistance work. Weight loss of 5 to 10 per cent meaningfully shifts BP, lipids and glucose.

  • Smoking cessation

    The single highest-impact modifiable factor. Combined behavioural support plus varenicline, NRT or bupropion roughly triples quit rates.

  • High-intensity statin

    Atorvastatin 20 to 80 mg or rosuvastatin 5 to 40 mg. NICE NG238 targets LDL under 1.4 mmol/L in very high risk, under 1.8 for secondary prevention.

  • Ezetimibe and bempedoic acid

    Add-on oral options when statins alone do not reach target or when statins are not tolerated.

  • PCSK9 inhibitors and inclisiran

    Alirocumab and evolocumab (fortnightly) or inclisiran (six-monthly siRNA) for familial hypercholesterolaemia and high-risk residual LDL.

  • Blood pressure control

    Stepped therapy with ACE inhibitor or ARB, amlodipine, indapamide-style thiazide and spironolactone at step 4. Usual target under 130/80.

  • Diabetes and antiplatelets

    SGLT2 inhibitors and GLP-1 agonists cut CV events. Aspirin 75 mg is for secondary prevention only. DAPT with clopidogrel or ticagrelor post-ACS or PCI.

On the horizon

Lipoprotein(a) targeted therapies.

Around one in five people have raised Lp(a), a genetically determined driver of atherosclerosis that statins do not meaningfully lower. Olpasiran (siRNA), pelacarsen (antisense) and other Lp(a)-targeted therapies are in phase 3 trials and may soon add a new lever for high-risk patients. Icosapent ethyl (Vazkepa) is already NICE-recommended for selected patients with high triglycerides and established cardiovascular disease.

What this guide is based on

The sources behind every claim on this page.

UK national guidance and specialist society 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 risk profile, history and medicines and can tell you which parts apply to you. If in doubt, get seen.

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

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

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

  • European Society of Cardiology (ESC). Guidelines on cardiovascular disease prevention and dyslipidaemia.

  • MHRA. Safety updates on statins, PCSK9 inhibitors and inclisiran.

Red flags

When cardiovascular disease needs urgent attention.

Most atherosclerosis is managed in primary care and specialist clinics. These are the situations that need same-day or emergency care.

  • Chest pain suggestive of ACS

    New central chest pain lasting more than 15 minutes, at rest, with sweating, nausea or breathlessness. Call 999 and chew 300 mg aspirin unless contraindicated.

  • Stroke or TIA symptoms

    Sudden face droop, arm weakness or speech disturbance (FAST). Call 999. Time-critical thrombolysis or thrombectomy window.

  • Critical limb ischaemia

    Rest pain in the foot, non-healing ulcer, cold or dusky limb. A vascular emergency needing same-day assessment.

  • Suspected aortic dissection

    Sudden tearing chest or back pain, sometimes with unequal pulses or neurology. Call 999 immediately.

  • Ruptured or symptomatic AAA

    Sudden severe abdominal or back pain with collapse in a man over 65. Emergency vascular referral.

  • Very high LDL or premature CV death

    Untreated LDL over 5 mmol/L or a first-degree relative with heart attack under 55 (men) or 65 (women) warrants familial hypercholesterolaemia screening.

  • Uncontrolled hypertension

    Home BP consistently above 180/120 or symptomatic hypertension needs same-day review.

  • Statin intolerance concerns

    Persistent muscle pain, dark urine or a marked CK rise deserves a proper assessment rather than silent discontinuation.

  • New atrial fibrillation with vascular risk

    AF adds a large stroke risk on top of atherosclerosis. Needs prompt CHA2DS2-VASc assessment and anticoagulation review.

Living with it

A treatable condition, with a clear plan.

Four things that make the biggest daily difference. Diet, movement, quitting smoking and taking prescribed medicines reliably.

A quiet reminder

Consistency beats intensity, every time.

Steady, boring habits kept up for years do more for your arteries than any short burst of heroic effort.

  1. 01 Diet

    Eat like the Mediterranean

    Vegetables, legumes, whole grains, nuts, olive oil and oily fish. Less ultra-processed food, less added sugar, moderate red meat.

  2. 02 Move

    150 minutes a week, most weeks

    Brisk walking, cycling, swimming or dancing plus two sessions of resistance work. Consistency beats occasional heroics.

  3. 03 Quit

    Stop smoking - fully

    The biggest single win. Combined behavioural support with varenicline or NRT roughly triples your chance of quitting for good.

  4. 04 Adhere

    Take the tablets, every day

    Statins, BP medicines and antiplatelets only work when taken. If side effects appear, ask about alternatives rather than stopping silently.

Frequently asked

Everything we get asked about arteriosclerosis and atherosclerosis.

Quick answers on statins, LDL targets, Lp(a), aspirin and revascularisation.

  • What is the difference between arteriosclerosis and atherosclerosis?

    Arteriosclerosis is the general term for arterial wall thickening and stiffness. Atherosclerosis is the specific, lipid-driven form with intimal plaques of cholesterol, inflammatory cells and a fibrous cap. Monckeberg medial calcification and arteriolosclerosis are two other subtypes that sit under the arteriosclerosis umbrella.

  • What actually causes atherosclerotic plaque?

    It begins with endothelial dysfunction driven by LDL cholesterol, hypertension, smoking, hyperglycaemia and oxidative stress. Monocytes are recruited into the intima and become foam cells, smooth muscle cells migrate in and a fibrous cap forms over a lipid core. Plaques progress and calcify over decades. Rupture of an unstable cap triggers thrombosis and the acute event, whether that is a heart attack, ischaemic stroke or acute limb ischaemia.

  • What is my target LDL cholesterol?

    NICE NG238 recommends an LDL under 1.4 mmol/L in patients at very high cardiovascular risk, and under 1.8 mmol/L for most people with established cardiovascular disease. Your absolute risk, whether you have already had an event and any inherited component all shape the target with your clinician.

  • What is Lp(a) and should I have it checked?

    Lipoprotein(a) is a genetically determined, atherogenic lipid particle. Around one in five people have a raised level. Most UK guidelines now support a one-off measurement, particularly with premature CV disease or a strong family history. Statins do not lower it meaningfully, but new siRNA and antisense therapies such as olpasiran and pelacarsen are in phase 3 trials.

  • Should I take aspirin to prevent a heart attack?

    For most people without established cardiovascular disease, no. Aspirin 75 mg is recommended for secondary prevention after a heart attack, stroke or coronary intervention, and for a short period of dual antiplatelet therapy after ACS or PCI. In primary prevention, the bleeding risk generally outweighs any modest reduction in events.

  • How is atherosclerosis actually treated when a vessel is critically narrowed?

    Symptomatic critical narrowing is managed with a combination of optimised medical therapy and interventional procedures. Options include percutaneous coronary intervention with stenting, coronary artery bypass grafting, carotid endarterectomy or stenting, and peripheral bypass or endovascular procedures for PAD. The choice depends on the vessel, the anatomy, symptoms and surgical risk.

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