Inflammation and Vascular Disease: What It Is, Why It Matters, and How to Lower Risk

By Joe Barnett On 20 Aug, 2025 Comments (11)

TL;DR

Vascular disease isn’t just “plumbing.” It’s an immune-driven process where chronic inflammation makes artery plaques form, grow, and rupture.
hsCRP is the most practical blood marker for vascular inflammation. Under 1 mg/L is low risk; over 3 mg/L is high. Repeat when you’re well, not during a cold.
Lowering inflammatory risk starts with basics: stop smoking, eat Mediterranean-style, move most days, sleep well, treat gum disease, and manage weight and chronic conditions.
Evidence-backed meds that reduce events by targeting inflammation include statins (partly via inflammation), low-dose colchicine (secondary prevention), and IL-1β inhibitors in select high-risk people.
Ask: what’s my LDL, my blood pressure, my hsCRP, and my plan? Small consistent steps matter more than hacks.

Why inflammation drives vascular disease (and how it actually works)

If heart disease were just clogged pipes, we’d only need a plunger. Arteries aren’t pipes though. They’re living tissue that reacts to stress. When LDL cholesterol slips into the artery wall and gets damaged by free radicals, your immune system spots trouble and sends in first responders-monocytes, neutrophils, and a storm of signals like IL‑1β and IL‑6. That’s inflammation. Helpful in short bursts. Harmful when it smolders for years.

Here’s the loop, minus the jargon. Irritated artery lining becomes “sticky.” White blood cells stick and move in. They eat up modified LDL and turn into foam cells. Those foam cells gather into a fatty streak. Over time you get a plaque with a soft, inflamed core and a thin cap. Inflammatory enzymes weaken that cap. One stressful day-or a spike from flu, air pollution, or even a bad night’s sleep-and the cap can crack. Platelets rush in, a clot forms, and blood flow stops. That’s a heart attack or a stroke.

This isn’t hand‑waving. Imaging studies show plaques with lots of inflammatory activity are more likely to rupture. People with higher high-sensitivity C‑reactive protein (hsCRP)-a liver protein dialed up by IL‑6-have higher rates of heart attacks, even when LDL looks “fine.” The JUPITER trial showed people with normal LDL but high hsCRP did far better on rosuvastatin than placebo. That told us reducing inflammation matters, not just cholesterol.

Zoom in on two key ideas you can act on: first, plaque stability matters more than plaque size. Inflamed plaques are fragile. Second, inflammatory “pushes” add up-smoking, poorly controlled diabetes, sleep apnea, gum disease, psoriasis, rheumatoid arthritis, chronic kidney disease, long‑term air pollution, even repeated viral infections. Each can stoke the fire.

I live in Cambridge and bike along the Cam most days. On damp mornings when my cat Marlowe insists on a 5 a.m. breakfast, I feel the tug to skip the ride. But that half hour of easy pedaling? It’s anti‑inflammatory medicine you don’t swallow. Muscles release myokines that calm immune noise. It’s not about hero workouts; it’s about dosing your day with movement.

How to measure inflammatory risk (and avoid common traps)

No single blood test perfectly captures artery inflammation. The best practical option is hsCRP. It’s widely available, inexpensive, and backed by outcomes data. Here’s how to use it without getting misled.

What to order: high-sensitivity C‑reactive protein (hsCRP), not regular CRP. Same molecule; the high-sensitivity assay detects lower levels relevant to vascular risk.
Cut points (from AHA/CDC guidance): low risk < 1 mg/L; average risk 1-3 mg/L; high risk > 3 mg/L. Over 10 mg/L usually means acute infection or flare-don’t use that for heart risk.
When to test: when you feel well, without a cold or flu. Avoid the week after heavy exercise, dental work, or a vaccine. If high, repeat in 2-3 weeks to confirm.
How to place in context: hsCRP adds to, but does not replace, LDL, blood pressure, smoking status, family history, diabetes, and (if you’re 40-75) your 10‑year risk score. A low hsCRP doesn’t cancel out a very high LDL.

Other markers exist but are less useful day to day:

IL‑6 and GlycA show promise, but they’re not standard in clinics yet.
Lp‑PLA2 can track vascular inflammation in some settings; evidence for routine use is mixed.
ESR (sed rate) is non‑specific; it rises with many conditions.

Imaging that reflects inflammation or risk:

Coronary artery calcium (CAC) scoring: not measuring inflammation, but it refines risk. A CAC of 0 suggests very low short‑term risk; higher scores argue for aggressive prevention. Availability varies across the UK, and it isn’t always funded. Worth discussing if you’re on the fence about statins.
Carotid ultrasound: can show plaque and plaque features. In skilled hands, plaques that look “soft” or irregular can hint at higher risk.

Rules of thumb to stay out of trouble:

Never act on a single hsCRP taken during or right after an illness.
If hsCRP stays above 3 mg/L after repeat testing and you don’t have an infection, scan your life for hidden inflammatory drivers: gum disease, untreated sleep apnea, obesity (especially visceral fat), high blood sugar, autoimmune flares, smoking, and high stress.
In the UK, your GP won’t order hsCRP as a routine screening for everyone. It’s most useful when your overall risk is borderline and you’re deciding how hard to push therapy, or if you already have vascular disease and want to track a modifiable signal.

What actually lowers vascular inflammation (habits, meds, and real evidence)

You can’t supplement your way out of inflamed arteries. But you can stack small, proven changes that shift the biology in your favour. Then, if your risk is high, add medications with outcome data-not just nice lab effects.

Lifestyle with the strongest anti‑inflammatory impact:

Stop smoking and vaping: still the biggest lever. Quitting drops hsCRP and halves heart attack risk within a year or two. If you need help, nicotine replacement or prescriptions like varenicline are worth it.
Eat Mediterranean‑style: extra‑virgin olive oil, nuts, fish, beans, a riot of veg, whole grains, and minimal ultra‑processed foods. In PREDIMED, a Mediterranean diet cut major events by ~30% in high‑risk adults. It also nudged inflammatory markers down.
Move daily: aim for 150 minutes a week of moderate activity or 75 of vigorous. Short bouts count. Resistance work twice a week adds extra anti‑inflammatory punch by improving insulin sensitivity.
Sleep 7-8 hours: sleep loss spikes IL‑6 and hsCRP. If you snore loudly or wake unrefreshed, screen for sleep apnea. Treating it eases vascular stress.
Oral health: gum disease and tooth loss track with higher heart risk. Periodontal treatment can lower CRP. Brush, floss, and see your dentist if your gums bleed when you brush.
Weight and waist: visceral fat pumps out inflammatory signals. Even 5-10% weight loss can lower hsCRP and blood pressure.
Vaccines: flu and COVID vaccines reduce infections that can trigger heart events. Trials and registry data show flu shots reduce major cardiac events, especially in those with recent heart attacks.

Medications with outcome data on inflammation and vascular events:

Statins: yes, they drop LDL, but they also reduce hsCRP. In JUPITER, people with hsCRP ≥2 mg/L and normal LDL had a ~44% relative risk reduction on rosuvastatin. If you’re hesitating, measure both LDL and hsCRP and talk with your clinician about absolute risk and expected benefit.
Low‑dose colchicine (0.5 mg daily): in COLCOT (post‑MI) and LoDoCo2 (stable coronary disease), colchicine lowered recurrent events. It’s anti‑inflammatory at that dose. It’s not for primary prevention and it has interactions (notably with certain antibiotics and antifungals). In the UK it’s licensed for gout, so use in heart disease is specialist‑led. Current ESC and AHA guidance suggests it may be reasonable for select patients with established coronary disease.
IL‑1β inhibition (canakinumab): in CANTOS, people with prior MI and high hsCRP had fewer events on canakinumab despite no LDL change. Infections increased. It’s expensive and used in narrow cases, not routine prevention.
Methotrexate: the CIRT trial showed no reduction in events. Not helpful for atherosclerosis prevention on its own.
Omega‑3s: mixed. High‑dose purified EPA (icosapent ethyl) in REDUCE‑IT cut events, but mineral oil placebo complicates interpretation and not all omega‑3 trials were positive. Omega‑3 capsules from the shop aren’t a substitute for prescribed EPA.
GLP‑1 receptor agonists and SGLT2 inhibitors: these diabetes and weight‑loss drugs reduce events and seem to damp inflammation indirectly through weight loss and metabolic effects. They’re used based on diabetes/obesity indication and overall CVD risk, not hsCRP alone.

Medicines to treat with care in this context:

NSAIDs (e.g., diclofenac, high‑dose ibuprofen): can raise blood pressure and increase CV risk. If you need pain control, discuss safer options.
Aspirin for primary prevention: in 2025, not routine. It can help in specific high‑risk people but raises bleeding risk. For secondary prevention after a heart event or stent, it’s standard-follow your cardiologist’s plan.

How to stack your plan, step by step:

Know your numbers: LDL‑C, non‑HDL‑C, blood pressure, HbA1c (if at risk for diabetes), hsCRP (if testing will change decisions).
Pick two lifestyle actions you can keep for 12 weeks. Example: 30‑minute brisk walks after dinner, Mediterranean lunches on weekdays.
If your 10‑year risk is moderate or you already have plaque, talk about statins. If you’ve already had a heart event, ask whether low‑dose colchicine fits you (checking kidney function and interactions).
Treat hidden drivers: gum disease, sleep apnea, psoriasis/RA flares, smoking, and high stress.
Recheck: repeat hsCRP and lipids after 8-12 weeks of steady changes or new meds.

Intervention	Population	Primary result	Key note	Source/Year
Rosuvastatin (JUPITER)	LDL normal, hsCRP ≥ 2 mg/L	~44% lower major events	Showed benefit tied to inflammation marker	NEJM, 2008
Canakinumab (CANTOS)	Prior MI, hsCRP ≥ 2 mg/L	Reduced recurrent events	LDL unchanged; higher infection risk	NEJM, 2017
Colchicine 0.5 mg (COLCOT)	Post‑MI	Reduced composite CV events	Low dose, watch drug interactions	NEJM, 2019
Colchicine 0.5 mg (LoDoCo2)	Stable CAD	Lowered CV events	Secondary prevention signal	NEJM, 2020
Methotrexate (CIRT)	Stable CAD or multiple risk factors	No event reduction	Not useful for atherosclerosis prevention	NEJM, 2019
Mediterranean diet (PREDIMED)	High‑risk adults	~30% fewer major events	Dietary pattern lowered inflammation markers	NEJM, 2013 (updated)

Checklists, decision cues, FAQs, and next steps

Quick checklist to spot and shrink your inflammatory load:

Teeth bleed when brushing or gums feel tender? Book a dental clean and review.
Snoring, daytime sleepiness, or morning headaches? Screen for sleep apnea.
Waist growing even if weight looks stable? Focus on protein, fibre, and strength work.
Work stress locked at 8/10? Try a 10‑minute daily walk without your phone and a consistent wind‑down routine.
Lab plan set? LDL‑C, non‑HDL‑C, HbA1c if needed, and hsCRP when well.
Vaccines up to date? Flu and COVID help prevent inflammation spikes that tip plaques.

Simple decision pathway you can discuss with your clinician:

If you have known vascular disease: prioritise high‑intensity statin, lifestyle stack, blood pressure control. Consider low‑dose colchicine if no interactions and kidney function is okay. Ask about target LDL (often <1.8 mmol/L for secondary prevention).
If you don’t have known disease and your 10‑year risk is borderline: a single hsCRP >3 mg/L (confirmed) nudges toward statins and lifestyle intensity. A CAC score can help if available and you’re undecided.
If hsCRP is >10 mg/L: look for infection or flare, treat that, then retest before making heart decisions.

Mini‑FAQ

Is all inflammation bad? No. Short, targeted inflammation heals injuries and fights bugs. The problem is chronic, low‑grade immune activation inside artery walls.
Should I take turmeric or curcumin? They may lower CRP a little in small trials, but we don’t have outcome data for heart events. Don’t swap proven treatments for supplements.
What about omega‑3 supplements? Eating fish twice a week is a good bet. Over‑the‑counter fish oil hasn’t consistently reduced events. Prescription icosapent ethyl is different and for select people.
Can I just test IL‑6? Not routinely. It’s more of a research marker. hsCRP is the practical tool for now.
Does stress really affect arteries? Yes. Chronic stress shifts hormones and immune signals, raises blood pressure, and worsens sleep. Small daily stress‑management habits add up.
Do statins help if my LDL is “okay”? If your risk is high or hsCRP is elevated, statins can still help. The JUPITER data is the classic example.
Is colchicine safe? At 0.5 mg daily, many tolerate it well, but GI upset is common and drug interactions matter. It’s a specialty decision, mainly for people who already have coronary disease.

Common pitfalls to avoid:

Chasing supplements while skipping the big rocks: smoking, diet, movement, sleep, blood pressure.
Testing hsCRP while ill and making decisions off that number.
Assuming a clean calcium score means “no rules apply.” It lowers short‑term risk, not lifetime risk.
Ignoring gums. Periodontal disease is a quiet, fixable source of inflammatory drive.

Next steps by scenario

I’m 45-60 with a family history, not on meds: get a proper risk check-lipids, blood pressure, glucose, and consider hsCRP. If risk is borderline, talk about a CAC scan. Start the lifestyle stack today; it compounds.
I have coronary disease already: take your prescribed statin, ACE inhibitor/ARB, and antiplatelets as directed. Ask your cardiology team whether low‑dose colchicine suits you. Double down on oral health, sleep, and daily movement.
My hsCRP is 4.5 mg/L, I feel well: repeat in 2-3 weeks when you’re healthy. If still high, scan for triggers (gums, sleep, weight, smoking, autoimmune issues). Talk with your GP about intensifying prevention.
I live with psoriasis or rheumatoid arthritis: push for tight control of your condition and get a cardiovascular risk review. Many rheum drugs lower inflammation and may cut heart risk. Coordinate care.

What I’d do this week if I were starting from scratch:

Book a blood pressure check and labs (lipids, HbA1c if at risk, hsCRP when well).
Switch breakfast to protein + fibre (e.g., Greek yoghurt, berries, oats, nuts). Easy anti‑inflammatory win.
Walk 20-30 minutes after dinner, five nights. Habit first, pace later.
Floss daily and book a hygienist visit if gums bleed.
Set a phone‑free wind‑down 45 minutes before bed. Morning is easier when you sleep, and your arteries notice.

What the evidence and guidelines say, in short: atherosclerosis is an immune disease sitting on a metabolic base. LDL opens the door; inflammation pushes it open. The best results come from hitting both: lower LDL and calm the immune noise. Trials like CANTOS, COLCOT, LoDoCo2, and JUPITER aren’t perfect, but they point in the same direction. Current European (ESC) and US (AHA/ACC) guidance in 2023-2024 reflects this-lifestyle and statins first, consider colchicine in selected secondary‑prevention patients, keep vaccines up to date, and personalise choices using numbers that match your life.

If this feels like a lot, keep it humble: take the next right step, then the next. That’s how arteries heal. I’ll be doing the same after I feed Marlowe and head out into the Cambridge drizzle.