Cardiometabolic risk beyond QRISK3
Why QRISK3 is the start and not the end of cardiometabolic risk assessment: one pathophysiology and many organ failures, the cardiovascular-kidney-metabolic stages, ApoB as the atherogenic particle count, with non-HDL cholesterol as NICE's practical surrogate, lipoprotein(a) once in a lifetime, coronary calcium and inflammation as tie-breakers, and the KDIGO heat map as the reclassifier that moves QRISK-low patients into high-risk management. About 60 minutes, for GPs, GP trainees, pharmacists, nurses, advanced clinical practitioners and physician associates. A 10-item knowledge check is marked on our learning platform; pass at 70% and a numbered, verifiable Certificate of CPD (1 hour) from New Vision University (UK) is issued to you.
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Cardiovascular disease prevention
Knowledge Green · Evidence Green · Real-world Red
Not yet at the Equinox · UK (NHS England) · as of 7 October 2026 · How the triangle works
A 52-year-old woman whose QRISK3 says "low"
Mrs K, 52, comes for a blood-pressure check. BMI 31, waist 99 cm, BP 138/86, non-smoker. Her mother had a stroke at 63 and her brother a stent at 54. Bloods: HbA1c 43 mmol/mol, total cholesterol 5.8, HDL-C 1.2, non-HDL 4.6 mmol/L, eGFR 84. QRISK3: 6.8%. The template says no statin, review in five years.
The CVRM-HF clinic looks harder. A urine ACR is 6 mg/mmol, repeated at 7: G2 A2 on the KDIGO heat map, moderately increased risk, and a marker QRISK3 does not see. Lp(a), measured once, is 190 nmol/L, above the ESC/EAS risk-enhancer threshold (105 nmol/L) and "moderate" on the HEART UK bands: inherited, unmodifiable, and the likely thread through the family history. ApoB is 1.2 g/L. She is cardiovascular-kidney-metabolic stage 2: dysfunctional adiposity (prediabetes) with a blood pressure that is hypertensive on the 130/80 definition the CKM staging uses (below the 140/90 NICE NG136 threshold), metabolic syndrome, dyslipidaemia and G2 A2 kidney disease, which is itself a stage 2 criterion, two decades before the event her calculator cannot predict.
The plan changes. Once albuminuria is confirmed NICE NG238 says she should not be scored with QRISK3 at all and offers atorvastatin 20 mg on its CKD recommendation; the clinic then treats her as higher risk than the original score: lifestyle and weight-management referral, blood pressure to target, atorvastatin 20 mg with an ApoB and non-HDL goal, an ACR and HbA1c every year, cascade Lp(a) testing offered to her children, and a PREVENT 30-year estimate used in the conversation about why now matters. That is what "beyond QRISK3" means, and it is this module.
By the end of this module you will be able to…
One pathophysiology, many organ failures
The continuum, the 2024–2026 consensus that dismantled single-organ care, and the CKM staging that tells you where a patient is.
Diabetes, atherosclerotic cardiovascular disease, chronic kidney disease, heart failure, obesity and MASLD are the dominant preventable burden in UK primary care. They cluster in the same person because the same upstream mechanisms — insulin resistance, ectopic adiposity, low-grade inflammation, neurohormonal activation, endothelial dysfunction and lipid retention — produce every downstream organ injury. Treat the upstream biology and the syndromes converge: an SGLT2 inhibitor lowers glucose, weight, blood pressure, albuminuria, eGFR decline, heart-failure admission and progression to dialysis, in people with and without diabetes.
What changed. A run of convergent statements replaced "the diabetologist treats glucose, the cardiologist the arteries, the nephrologist the kidneys": DCRM 2.0 (Handelsman et al., Metabolism 2024, 22 multispecialty recommendations); the first AHA/ACC/ADA/ASN cardiovascular-kidney-metabolic guideline (2026, upgrading the 2023 advisory to graded recommendations with the PREVENT equations); NICE NG28 (February 2026), which now offers an SGLT2 inhibitor with metformin to adults with type 2 diabetes, with or without heart failure, ASCVD or CKD (eGFR 30 or more), for its cardiovascular and renal benefit, and NG106 (September 2025), which makes an SGLT2 inhibitor one of the four core medicines for heart failure with reduced ejection fraction; the ESC/EAS 2025 dyslipidaemia update; and the 2026 Lancet Series on cardiometabolic multiple long-term conditions (Khunti, Lim and Valabhji et al.), whose epidemiology paper cites a UK primary-care study (Head et al., Lancet Healthy Longevity 2021) in which the median age at onset of multiple long-term conditions of any kind fell from 56 to 46 years between 2004 and 2019, seven years earlier still in the most deprived areas. Together they point to one integrated plan per patient across glucose, lipids, blood pressure, kidney, weight and (in DCRM 2.0) inflammation.
The CKM stages
| Stage | Definition | Primary-care action |
|---|---|---|
| 0 | No CKM risk factors | Keep it that way; lifestyle |
| 1 | Excess or dysfunctional adiposity (BMI, waist, prediabetes-range glycaemia from adiposity) | Weight management; screen for stage 2 |
| 2 | Metabolic risk factors — hypertension (130/80 or higher, or treated), hypertriglyceridaemia (1.7 mmol/L or more), metabolic syndrome or type 2 diabetes — and/or moderate-to-high-risk CKD on the KDIGO heat map; prediabetes alone is stage 1 | Treat every driver now; measure ACR and Lp(a); calculate risk with a 30-year horizon |
| 3 | Subclinical cardiovascular disease (coronary calcium, raised natriuretic peptide or troponin, or structural heart disease) or a risk equivalent: very-high-risk CKD, or high predicted risk (10-year PREVENT-CVD 20% or more) | Secondary-prevention intensity; the pre-heart failure pathway (F4) |
| 4 | Clinical cardiovascular disease; 4a without, 4b with kidney failure | Secondary prevention; the full CVRM-HF ladder |
Stage 2 is where the practice population sits and where most preventable events are lost. The rest of this module is about seeing stage 2 and 3 patients whom QRISK3 scores as low.
Checkpoint 1 · BMI 33, HbA1c 44, BP 142/90 untreated, non-HDL 4.6, eGFR 92, ACR 1.5, no cardiovascular disease. Which CKM stage?
Stage 2: untreated hypertension (142/90, above the CKM 130/80 threshold), which is sufficient on its own; prediabetes alone would be stage 1, and the raised non-HDL is a reason to calculate risk, not a staging criterion. Treat each driver now, calculate QRISK3 (and PREVENT for the 30-year view), and measure Lp(a).
QRISK3 done properly, and its blind spots
The NICE NG238 rules, who should never be scored, and what the other calculators add.
NICE NG238 in three lines
Use QRISK3 for first-pass triage in primary prevention. Offer atorvastatin 20 mg at a 10-year risk of 10% or more after shared decision-making and lifestyle advice; consider it below 10% where the person wants it or has risk the tool under-estimates. In primary prevention aim for a non-HDL cholesterol reduction above 40%; escalate with ezetimibe (F2). In secondary prevention aim for LDL-C 2.0 or non-HDL 2.6 mmol/L or less (1.7.1).
Do not score these people
Type 1 diabetes; eGFR below 60 and/or albuminuria; familial hypercholesterolaemia or another inherited lipid disorder. They are already at increased risk: atorvastatin 20 mg in CKD, high-intensity therapy in FH. Aged 85 or older: consider atorvastatin 20 mg without a score (NG238 1.1.11, 1.6.9).
What QRISK3 cannot see
QRISK3 includes CKD stage 3–5, rheumatoid arthritis, severe mental illness, atypical antipsychotics, erectile dysfunction, lupus, migraine and ethnicity. It does not include albuminuria, Lp(a), ApoB, coronary calcium, family history beyond a first-degree relative under 60, or heart failure as an outcome, and QRISK3 itself gives only a 10-year horizon, so a 45-year-old with stage 2 disease and a 5% ten-year risk looks reassuring while a lifetime of exposure accrues. NICE NG238 (1.1.16) already asks you to consider a lifetime tool such as QRISK3-lifetime for people with a 10-year score below 10% and for under-40s with risk factors.
| Calculator | Population and status | Signature features |
|---|---|---|
| QRISK3 | England primary care; NICE NG238 | 10-year fatal and non-fatal CVD; CKD, RA, SMI, ethnicity; the tool for treatment thresholds in England |
| SCORE2 / SCORE2-OP / SCORE2-Diabetes | Europe; ESC 2021 (SCORE2, SCORE2-OP) and 2023 (SCORE2-Diabetes); adopted in ESC/EAS 2025 | Region-stratified fatal and non-fatal CVD; older-person and diabetes variants |
| PREVENT | USA; AHA 2024 | 10- and 30-year total CVD including heart failure; eGFR in the base model, BMI for heart failure, urine ACR, HbA1c and deprivation optional; built on the CKM concept |
| ASSIGN | Scotland; SIGN | Deprivation integrated |
PREVENT's 30-year estimate adds eGFR, BMI and heart failure to that conversation with younger stage 2 patients; use QRISK3 for the NICE threshold. NICE has no scheduled update of NG238 (last reviewed September 2025; it will be reviewed only if new evidence emerges), so until a future review adopts a CKM-aware calculator, the additions in Lessons 3–6 are how you correct the score.
Checkpoint 2 · A 49-year-old with eGFR 52 and ACR 40 mg/mmol has QRISK3 9%. Statin?
Yes, without the score. NICE NG238 says not to use a risk tool in people with eGFR below 60 and/or albuminuria; offer atorvastatin 20 mg (F5 covers the rest of the CKD ladder). G3a A3 is very high risk on the heat map.
ApoB and non-HDL cholesterol: measuring atherogenic particles and the cholesterol they carry
Why LDL-C under-estimates risk in diabetes, MASLD and obesity, and the risk-tiered targets.
LDL-C measures cholesterol mass; ApoB counts atherogenic particles (one ApoB per LDL, VLDL, IDL and Lp(a) particle). When particles are small and dense, as in type 2 diabetes, MASLD, obesity and hypertriglyceridaemia, LDL-C systematically under-estimates the burden and ApoB is the more accurate, more reproducible and more recommended measure. ESC/EAS (ApoB goals from 2019; the 2025 focused update confirms the LDL-C goals are unchanged) use ApoB as the secondary goal once LDL-C is at goal; NICE NG238 uses non-HDL cholesterol (total minus HDL) as the practical surrogate: a reduction above 40% in primary prevention and LDL-C 2.0 or non-HDL 2.6 mmol/L or less in secondary prevention. Neither needs a fasting sample.
| Risk category | Source | LDL-C goal (mmol/L) | ApoB (g/L) · non-HDL (mmol/L) |
|---|---|---|---|
| Low (SCORE2 below 2%) | ESC/EAS 2019; LDL-C goal confirmed unchanged in 2025 | < 3.0 may be considered | No secondary goal |
| Moderate (SCORE2 2% to below 10%; young people with diabetes under 10 years and no other risk factors) | ESC/EAS 2019; LDL-C goal confirmed unchanged in 2025 | < 2.6 | ApoB < 1.0 · non-HDL < 3.4 |
| High (SCORE2 10% to below 20%; LDL-C above 4.9 or BP 180/110 or more; FH without other major risk factors; diabetes without target-organ damage but of 10 years or more or with another risk factor; eGFR 30–59) | ESC/EAS 2019; LDL-C goal confirmed unchanged in 2025 | < 1.8 and ≥ 50% reduction | ApoB < 0.8 · non-HDL < 2.6 |
| Very high (documented ASCVD; diabetes with target-organ damage or three or more major risk factors; eGFR < 30; SCORE2 20% or more; FH with ASCVD or another major risk factor) | ESC/EAS 2019; LDL-C goal confirmed unchanged in 2025 | < 1.4 and ≥ 50% reduction | ApoB < 0.65 · non-HDL < 2.2 |
| Recurrent vascular events on maximally tolerated statin-based therapy, or polyvascular disease | ESC/EAS 2025 Figure 1 (Class IIb, may be considered); goal carried over from 2019, where the trigger was a second vascular event within 2 years | < 1.0 may be considered | ApoB and non-HDL equivalents are shown in the guideline figure; otherwise the very-high-risk goals apply |
| Extreme (the DCRM 2.0 tier between very high and extreme-plus) | DCRM 2.0 expert target (not a graded recommendation) | < 1.4 (DCRM states LDL-C < 1.42 as the level already achieved before extreme-plus applies) | ApoB < 0.7 · non-HDL < 2.1 |
| Extreme-plus (extreme risk with further events despite an achieved LDL-C < 1.4) | DCRM 2.0 expert target (not a graded recommendation) | < 1.04 | ApoB < 0.6 · non-HDL < 1.7 |
ESC/EAS and DCRM 2.0 use different ApoB tiers, so quote the source with the number: DCRM 2.0 also quotes ApoB below 0.9 g/L at high risk and below 0.8 g/L at very high risk. NICE NG238 uses non-HDL (a reduction above 40% in primary prevention; LDL-C 2.0 or non-HDL 2.6 mmol/L or less in secondary prevention).
Discordance is the signal. LDL-C 1.7 with ApoB 1.05 g/L in a man with coronary disease, diabetes and MASLD means residual particle risk: intensify (ezetimibe, which NG238 1.7.10 allows even at target; a PCSK9 inhibitor or inclisiran only if LDL-C met the TA733/TA393/TA394 thresholds, which at 1.7 mmol/L it does not; the ladder is F2). Measure ApoB once lipids are on treatment in anyone with diabetes, MASLD, obesity or triglycerides above 1.7 mmol/L, and let it set the goal.
Checkpoint 3 · Type 2 diabetes with coronary disease on atorvastatin 80 mg: LDL-C 1.7, triglycerides 2.6, ApoB 1.05. At target?
No. ApoB is above the very-high-risk goal (0.65 g/L ESC/EAS; 0.8 g/L DCRM 2.0), so LDL-C is under-estimating his particle burden. Intensify lipid lowering (ezetimibe next). A fibrate does not address the ApoB goal.
Lipoprotein(a): once in a lifetime, then act on it
The most prevalent inherited dyslipidaemia, what it changes today, and what is in trials.
Who, when, how often
ESC/EAS (2019, reaffirmed 2025: should be considered, Class IIa) and DCRM 2.0 (once, at initial screening, in all adults) both ask for Lp(a) at least once in every adult's life; a family history of premature cardiovascular disease, familial hypercholesterolaemia, calcific aortic stenosis, or events despite controlled LDL-C make it urgent. It is more than 90% genetically determined, so one result is recorded permanently and is not repeated routinely; the ESC/EAS 2025 update notes that levels may rise after the menopause and that a second measurement is reasonable then, particularly if a pre-menopausal result was borderline. Report in nmol/L. NICE NG238 makes no recommendation on Lp(a). ESC/EAS 2025 treats Lp(a) above 50 mg/dL (105 nmol/L), present in at least one adult in five, as a risk-enhancing factor in all adults; the EAS 2022 consensus uses a rule-in of 125 nmol/L with a 75–125 nmol/L grey zone, because mass-to-molar conversion varies with the assay. HEART UK (2019 consensus) bands risk at 32–90 minor, 90–200 moderate, 200–400 high and above 400 nmol/L very high, and advises managing Lp(a)-associated risk above 90 nmol/L with a non-HDL cholesterol goal below 2.5 mmol/L.
What it changes today
Lifestyle does not move it and statins do not lower it (they raise it slightly). A raised Lp(a) is a reason to treat the person as higher risk than the calculator shows: offer a statin and aim lower on LDL-C and ApoB; control blood pressure and glycaemia; and offer cascade testing to first-degree relatives. At about 250 nmol/L (100 mg/dL) the risk of atherosclerotic disease is roughly doubled whatever the baseline risk, equivalent in coronary-risk terms to about an extra 1 mmol/L of LDL-C carried for life; above about 430 nmol/L (180 mg/dL) lifetime risk approaches that of untreated heterozygous FH.
What is not available. No UK-licensed Lp(a)-lowering drug exists. PCSK9 inhibitors lower Lp(a) modestly but are prescribed on NICE LDL-C criteria; niacin is not recommended. The first outcome trial, Lp(a)HORIZON with the antisense agent pelacarsen (8,323 patients with established cardiovascular disease), reported in September 2026 and did not meet its primary endpoint although Lp(a) fell; the siRNA agents olpasiran and lepodisiran and oral muvalaplin remain in cardiovascular outcome trials, so whether lowering Lp(a) prevents events is still unproven. Until they report, treat a high Lp(a) as a risk marker, not a drug target: treat the person as higher risk and intensify every other lever. Trial enrolment remains a legitimate offer for very high values.
Checkpoint 4 · Lp(a) 210 nmol/L, LDL-C 3.0, QRISK3 9%, no diabetes. "Is there a tablet for the Lp(a)?"
Not yet. Treat him as higher risk than the score: a statin now with LDL-C and ApoB goals, every other risk factor addressed, and Lp(a) testing offered to his children and siblings. Do not repeat the Lp(a).
Coronary calcium and inflammation
The power of zero, CAC ≥ 100 as a reason to favour a statin, and residual inflammatory risk with the colchicine decision.
Coronary artery calcium (CAC)
For statin-hesitant patients close to the NICE 10% threshold, a CAC score reclassifies a meaningful proportion (the US guidelines use their own intermediate bands for this: PCE 7.5–20% in the 2018 ACC/AHA cholesterol guideline, PREVENT-ASCVD 5–10% in the 2026 ACC/AHA dyslipidaemia guideline; there is no NICE-defined QRISK3 band). CAC 0 in an asymptomatic adult over 50 who is not a smoker and has no diabetes, no familial hypercholesterolaemia and no strong family history of premature disease carries a 10-year ASCVD event rate almost always below 5% (MESA, the "power of zero": 1.3–5.6% across the age, sex and ethnic subgroups of all participants with a score of 0, including smokers and people with diabetes) and supports deferring a statin with a repeat scan in 3–7 years. CAC ≥ 100 puts 10-year risk above 7.5% in every MESA subgroup and favours a statin whatever the score, subject to the shared decision. NICE NG238 does not recommend it for routine risk assessment and NHS access is patchy, so it is a tie-breaker for a shared decision, never a screening test, and never in symptomatic patients (who need the chest-pain pathway).
Residual inflammatory risk
DCRM 2.0 makes inflammation its own recommendation. Once lipids, blood pressure and glycaemia are controlled, a persistent hsCRP of 2 mg/L or more (no acute cause) defines residual inflammatory risk. Colchicine 0.5 mg daily reduced major adverse cardiovascular events in stable coronary disease (LoDoCo2) and after myocardial infarction (COLCOT), although the larger CLEAR SYNERGY trial found no benefit when it was started soon after infarction, so the evidence is strongest in stable coronary disease; the ESC 2024 chronic coronary syndromes guideline says it may be considered. It is unlicensed for this in the UK: a documented shared decision, with attention to eGFR, myopathy with statins, and CYP3A4 and P-glycoprotein interactions.
Checkpoint 5 · Stable coronary disease on high-intensity statin and ezetimibe: LDL-C 1.3, ApoB 0.6, hsCRP 3.1 twice, no infection. What does it add?
Residual inflammatory risk. Low-dose colchicine may be considered (ESC 2024 chronic coronary syndromes guideline) after a discussion of benefit, harm and its off-label status; a PCSK9 inhibitor does not treat the CRP, and steroids are not indicated.
The KDIGO heat map as a risk tool, and the searches that reclassify the practice
Albuminuria is a cardiovascular risk factor. Here is how it moves patients, and how to find them.
The KDIGO 2024 heat map gives albuminuria prognostic weight equal to GFR: a patient with eGFR 80 and ACR 50 mg/mmol is at higher cardiovascular risk than one with eGFR 50 and ACR 1. Read the grid as GFR category × albuminuria category; the band sets monitoring and points to the treatment options where the NICE criteria are met: an SGLT2 inhibitor (TA1075, TA942: on the highest tolerated ACE inhibitor or ARB, with eGFR 20–44, or eGFR 45–90 with ACR 22.6 mg/mmol or more or type 2 diabetes; and, with metformin, for adults with type 2 diabetes and eGFR 30 or more, with or without heart failure, ASCVD or CKD, under NG28, February 2026) and, in type 2 diabetes with CKD, finerenone (TA877). A patient with eGFR above 60, no diabetes and an ACR below 22.6 mg/mmol is reclassified for risk and monitoring, not for an SGLT2 inhibitor. The full table and the ladder are in F5; here the point is reclassification.
| eGFR (mL/min/1.73 m²) | A1 · ACR < 3 mg/mmol | A2 · 3–30 | A3 · > 30 |
|---|---|---|---|
| G1–G2 · ≥ 60 | Low risk (not CKD unless another marker of kidney damage is present) | Moderately increased | High |
| G3a · 45–59 | Moderately increased | High | Very high |
| G3b · 30–44 | High | Very high | Very high |
| G4–G5 · < 30 | Very high | ||
Translational pearl. Most practices hold the ACR as a tick-box inside the diabetes annual review. KDIGO 2024 names diabetes, hypertension and cardiovascular disease as the highest-priority groups for CKD detection and asks for both eGFR and a urine ACR in everyone at risk, annually in diabetes (ADA–KDIGO consensus) and at least annually once CKD is present (KDIGO 2024 Practice Point 2.1.1); DCRM 2.0 asks for an annual ACR in everyone with diabetes, ASCVD, obesity or CKD. The heat map is the single most powerful tool for moving QRISK-low patients into high-risk management. Run the searches; the denominator will surprise you.
Three searches
The found patients enter the CVRM-HF clinic, where F2 (lipids), F3 (diabetes), F4 (heart failure) and F5 (kidney) supply the ladder. One list, one prescriber, one set of safety bloods.
Practice task
Run search 1 on your own system this week and count the patients with diabetes, hypertension or cardiovascular disease who have no ACR in the last year. Record the number and what you will do with it in the reflection box below; it prints on your certificate.
Checkpoint 6 · Which single search reclassifies most patients into high-risk management?
The missing or untreated ACR in diabetes, hypertension and cardiovascular disease: the KDIGO heat map moves a large proportion of QRISK-low patients into high-risk groups with treatment indications.
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New Vision University (UK)
Acumen Focus · CVRM-HF Foundation series · delivered by MD Acumen Ltd
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Acumen Focus F1 · Cardiometabolic risk beyond QRISK3
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Authored by Prof Rajesh Varma · MD Acumen Ltd · mdacumen.com
CPD authorised by Prof Rajesh Varma, Convenor for CPD, New Vision University (UK)
Signed against: NICE NG238 (December 2023) · ESC/EAS 2025 · DCRM 2.0 (2024) · AHA/ACC/ADA/ASN CKM guideline (2026) and AHA CKM advisory (2023) · PREVENT (2024) · KDIGO 2024 · ESC 2024 chronic coronary syndromes · Lancet 2026 cardiometabolic MLTC series
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F1 opens the CVRM-HF Foundation series (F1 cardiometabolic risk · F2 lipids · F3 type 2 diabetes · F4 heart failure · F5 kidney disease · F6 obesity and MASLD). Complete all six for the series certificate (6 CPD); the series counts as recognised prior learning for the Certificate of Advanced Studies in CVRM-HF.
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