Patient guide · Cardiology
PLAC test (Lp-PLA₂), lipoprotein-associated phospholipase A₂ — a novel vascular inflammation marker.
The PLAC test measures lipoprotein-associated phospholipase A₂ (Lp-PLA₂), a vascular-specific inflammation enzyme linked to unstable atherosclerotic plaque. Used as an add-on cardiovascular risk marker in intermediate-risk patients.
Why patients choose us
- 01
The right hands
A consultant cardiologist who requests the test and interprets it — one clinician, one plan.
- 02
Fast turnaround
Fasting draw, lab result in 5–7 days, and a structured cardiology review to follow.
- 03
Independent, and free
We are paid by no clinic, so the recommendation is impartial and costs you nothing.
Key facts
The PLAC test at a glance.
The six things worth knowing — what Lp-PLA₂ is, why it’s vascular-specific, and where it fits alongside your other cardiovascular tests.
- 01
Definition
A blood test measuring lipoprotein-associated phospholipase A₂ (Lp-PLA₂) enzyme activity or mass.
- 02
Vascular-specific inflammation
Unlike hs-CRP, Lp-PLA₂ is a vascular-specific marker of arterial-wall inflammation.
- 03
Unstable plaque signal
Elevated Lp-PLA₂ is associated with unstable, rupture-prone atherosclerotic plaque.
- 04
Complementary marker
Complements QRISK3, coronary calcium score and CaRi-Heart perivascular analysis.
- 05
Intermediate-risk stratification
Most useful in reclassifying patients whose baseline QRISK sits in the intermediate range.
- 06
Consultant interpretation
A consultant cardiologist interprets the result alongside lipids, imaging and risk factors.
The pathway
From consultation to plan — what happens, in order.
One consultant cardiologist from first appointment to structured risk-reduction plan — with the assay reporting in 5–7 days.
Phase 1 · Before the draw
Consultation and fasting
Phase 2 · Sample and lab
5–7 days turnaround
Phase 3 · Interpretation
Plan, act, monitor
- 01
Before
Cardiology or preventive-medicine consultation
A consultant reviews your risk profile, lipids, family history and prior imaging to decide whether Lp-PLA₂ will change the plan.
- 02
Before
Fasting blood draw
A morning fasting venous sample — no food for 8–12 hours, water and essential medications only.
- 03
Sample and lab
Serum sample sent to lab
Serum is separated and shipped to an accredited reference laboratory running the validated PLAC assay.
- 04
Sample and lab
Lp-PLA₂ result in 5–7 days
Activity (nmol/min/mL) or mass (ng/mL) result returned to the referring consultant with reference ranges.
- 05
After
Cardiology interpretation
Interpreted alongside advanced lipids, QRISK3, calcium score and imaging — never in isolation.
- 06
After
Structured risk-reduction plan
A written plan: lipid targets, blood pressure, lifestyle, and — if indicated — intensified pharmacotherapy.
- 07
After
Repeat testing to monitor therapy
Repeat Lp-PLA₂ at 3–6 months to gauge response to statin, ezetimibe or PCSK9 therapy.
Typical end-to-end: 10–14 days. Fast-track: 1 week.
What it shows
What Lp-PLA₂ tells you, and where the red flag is.
The eight ways a PLAC result is used in practice — from reassurance to reclassification, monitoring and post-ACS escalation.
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Normal Lp-PLA₂ (< 200 ng/mL activity)
A reassuring vascular-inflammation signal that lowers the probability of unstable plaque.
-
Elevated Lp-PLA₂ (increased CV risk)
Raised activity or mass associates with higher risk of coronary and cerebrovascular events.
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Reclassification of intermediate risk
Moves a QRISK3 intermediate-risk patient up or down the risk ladder, changing the plan.
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Response to statin or niacin therapy
Falling Lp-PLA₂ on repeat testing supports that lipid-lowering therapy is working biologically.
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Complement to an advanced lipid panel
Adds a vascular-inflammation dimension to ApoB, Lp(a) and particle-count testing.
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Post-ACS monitoring
Trends Lp-PLA₂ after an acute coronary syndrome to gauge residual inflammatory risk.
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Baseline before intensification
Captures a pre-treatment number before adding ezetimibe, PCSK9 inhibitor or bempedoic acid.
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Red flag: very high Lp-PLA₂ + prior ACS — aggressive risk reduction
Very high Lp-PLA₂ after a prior event triggers intensified secondary prevention.
Next steps
What happens after an elevated PLAC result.
The eight most common actions — from intensified statin and PCSK9 add-on to rehabilitation, aspirin, monitoring and cardiology follow-up.
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Intensified statin therapy
Escalation to a high-intensity statin, targeting LDL-C < 1.4 mmol/L in high-risk patients.
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Ezetimibe or PCSK9 inhibitor
Add-on lipid-lowering when statin alone doesn’t reach target, or when statin-intolerant.
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Niacin (specialist selective)
Occasionally used in specialist practice where lipid targets remain unmet on standard therapy.
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Aspirin for secondary prevention
Low-dose aspirin after a prior cardiovascular event, in line with current guidance.
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Cardiovascular risk optimisation
Blood pressure, glycaemic, weight and smoking-cessation targets addressed in parallel.
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Structured cardiac rehabilitation
Supervised exercise, education and psychological support after a coronary event.
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Repeat PLAC to monitor response
Repeat Lp-PLA₂ at 3–6 months to demonstrate that treatment is lowering vascular inflammation.
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Cardiology follow-up
Structured cardiology review every 6–12 months to reassess targets and imaging.
Red flags
When Lp-PLA₂ demands escalation.
The nine clinical contexts where a raised Lp-PLA₂ pushes the plan up a gear — from FH and post-ACS to CKD, PAD and post-CABG failure.
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Very high Lp-PLA₂ + prior CV event
The strongest signal for aggressive secondary prevention — intensified statin and add-on therapy.
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Familial hypercholesterolaemia
Genetic dyslipidaemia carries very high lifetime risk — PLAC contextualises inflammation on top.
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Post-ACS with high residual risk
Persistently raised Lp-PLA₂ after an acute coronary syndrome warrants escalation.
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Family history of premature CAD
First-degree relatives with CAD before 55 (men) or 65 (women) — PLAC adds a functional layer.
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Chronic inflammatory disease
Rheumatoid arthritis, SLE and IBD carry excess CV risk — PLAC helps quantify vascular impact.
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CKD stage 3 or worse
Reduced eGFR amplifies cardiovascular risk; PLAC supports risk stratification.
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Diabetic vasculopathy
Diabetes with microvascular or macrovascular complications — PLAC informs escalation.
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Peripheral arterial disease
Established PAD is a CAD risk-equivalent — PLAC monitors residual inflammatory burden.
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Post-CABG graft failure
Early graft failure or symptomatic ischaemia post-CABG merits vascular-inflammation reassessment.
Reading your report
A PLAC report is a single number in context. Here’s the context.
Whatever the value, the report keeps to the same four parts.
A quiet reminder
Lp-PLA₂ is never read alone — it lands alongside lipids, imaging and your risk score.
If you would like us to walk you through the number before your follow-up, just ask.
- 01 Header
Indication and clinical context
Your details, the reason for testing, baseline risk score and prior CV history.
- 02 Assay
Method: activity or mass
Whether Lp-PLA₂ activity (nmol/min/mL) or mass (ng/mL) was measured, with the assay manufacturer.
- 03 Result
Numeric value and reference range
The measured value against the lab’s reference range, with normal, borderline and elevated cut-offs.
- 04 Impression
The conclusion — read this first
Interpretation alongside lipids, imaging and QRISK3, with the concrete next step.
Recognised by major UK insurers
Cover depends on your policy and clinic; we confirm with your insurer before booking.
Frequently asked
Everything we get asked about the PLAC test.
Quick answers on what it measures, who it’s for, fasting, comparison to hs-CRP and how quickly results come back.
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What does the PLAC test measure?
The PLAC test measures lipoprotein-associated phospholipase A₂ (Lp-PLA₂), an enzyme produced by inflammatory cells inside atherosclerotic plaque. It is a vascular-specific marker — unlike hs-CRP, which reflects systemic inflammation of any cause.
-
Who should consider a PLAC test?
It is most useful in patients whose baseline QRISK3 sits in the intermediate range, where reclassification would change the treatment plan. It also has a role after an acute coronary syndrome, in familial hypercholesterolaemia and in chronic inflammatory disease.
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Do I need to fast?
Yes. A morning fasting sample after 8–12 hours without food is standard, with water and essential medications allowed. Fasting improves the reliability of the accompanying lipid panel.
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How does PLAC compare to hs-CRP?
hs-CRP is a systemic inflammation marker — it rises with any inflammation, from a chest infection to arthritis. Lp-PLA₂ is vascular-specific: it reflects inflammation inside the arterial wall, so it is a cleaner signal for cardiovascular risk.
-
What does an elevated result mean?
An elevated Lp-PLA₂ is associated with unstable plaque and a higher risk of coronary and cerebrovascular events. It doesn’t diagnose disease on its own — it changes the pre-test probability, and the plan is set alongside lipids, imaging and QRISK3.
-
How quickly do I get results?
Lab turnaround is typically 5–7 days. A structured cardiology interpretation follows, usually within a further working week, with a written plan.
Sources
The guidance behind this guide.
- NICE. Cardiovascular disease: risk assessment and reduction (NG238).
- European Society of Cardiology. Guidelines on cardiovascular disease prevention.
- American Heart Association. Scientific statements on Lp-PLA₂ and CV risk.
- PLAC test manufacturer clinical evidence — diaDexus / Diazyme.
Reviewed 2026-07-30 by Pulse Atlas Editorial Board, . Next review 2027-07-30. Estimated reading time 5 minutes.
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In practice, in London
Where plac sits in a private London pathway
With plac, the London question is usually about report turnaround and the radiologist reading it — not whether the scan is available. The NHS route for plac is thorough, but the queue is real. Most patients we speak with have been told to expect anywhere from a handful of weeks to several months, depending on their local trust and how the referral is graded. Going private in London usually collapses that window to a matter of days — often the same week if the diary allows. It isn’t about jumping a queue so much as buying time back while you still have the flexibility to plan around it.
Once you’re in the private system for plac, the pace picks up noticeably. Consultant slots run to time, imaging is usually available in the same building or a short walk away, and the report comes back typed and detailed. It’s the coordination that tends to feel different — one person on the other end of the phone, not a switchboard. For plac specifically, the difference between a routine report and a sub-speciality read is where private care earns its keep.
Honesty about expectations is part of the job. A private plac appointment in London won’t change the underlying medicine — the guidelines, the consultants, and the equipment are largely the same as on the NHS. What it changes is speed, continuity, and the amount of time you get to actually talk through the findings. Everyone we route to is GMC-registered and works within CQC-regulated facilities.