IPM Take
A patient can spend years being treated for psoriasis, lupus or rheumatoid arthritis without ever entering a cardiovascular clinic, even though the inflammatory disease itself may already be changing cardiovascular risk.
That separation is becoming increasingly difficult to justify.
At the Cardiometabolic Health Congress in Boston, Brittany Weber, director of the Cardio-Rheumatology/Cardio-Dermatology Program at UT Southwestern, argued that cardiovascular disease in autoimmune populations requires closer collaboration between cardiologists, rheumatologists and dermatologists. The argument is not simply that these patients have more heart disease. It is that their risk can begin earlier, follow pathways that are not captured completely by traditional atherosclerosis models and remain underestimated by conventional risk calculators.
The 2026 US dyslipidaemia guideline now explicitly lists chronic inflammatory diseases, including systemic lupus, rheumatoid arthritis, advanced psoriasis and inflammatory arthritis, as cardiovascular risk enhancers. It also acknowledges that standard risk calculators tend to underestimate risk in people with chronic inflammatory disease.
That creates a policy mismatch.
Medicine increasingly recognises inflammation as part of cardiovascular risk, while care remains organised as though dermatological, rheumatological and cardiovascular disease belong to separate systems.
Dedicated cardio-rheumatology and cardio-dermatology programmes are one attempt to close that gap, but the more important question is whether the underlying principles can move beyond specialist academic centres.
The goal should not be to send every patient with psoriasis to a cardiologist.
It should be to make cardiovascular prevention part of the disease pathway before a cardiovascular event forces the specialties to meet.
Executive Summary
Inflammatory and autoimmune diseases are increasingly recognised as conditions that modify cardiovascular risk through mechanisms extending beyond conventional factors such as cholesterol, blood pressure, smoking and diabetes.
At the 2026 Cardiometabolic Health Congress Women’s Cardiometabolic Health and Wellness Masterclass, cardiologist Brittany Weber argued that closer collaboration between cardiology, rheumatology and dermatology is needed because cardiovascular risk frequently accompanies systemic inflammatory disease and can emerge at younger ages than conventional prevention pathways anticipate.
This concern is now reflected in major cardiovascular guidance.
The 2026 ACC/AHA multisociety dyslipidaemia guideline lists chronic inflammatory diseases, including systemic lupus erythematosus, rheumatoid arthritis, advanced psoriasis and inflammatory arthritis, among factors that can enhance atherosclerotic cardiovascular risk.
The same guideline states that conventional cardiovascular risk calculators tend to underestimate risk in people with chronic inflammatory diseases and recommends incorporating cardiovascular risk assessment into their clinical care.
Inflammation may also affect the cardiovascular system beyond large-vessel atherosclerosis.
Studies using positron emission tomography have reported impaired coronary microvascular function in patients with psoriasis and systemic lupus, including patients without overt obstructive coronary artery disease. These studies are relatively small and do not justify routine advanced imaging of asymptomatic patients, but they suggest that the cardiovascular phenotype of autoimmune disease cannot always be reduced to conventional coronary plaque.
The emerging policy challenge is therefore one of integration. Cardiovascular risk may need to be identified and managed inside rheumatology and dermatology pathways rather than relying primarily on referral after conventional risk thresholds or cardiovascular symptoms emerge.
Why it matters
- HTA bodies: Multidisciplinary cardio-rheumatology and cardio-dermatology models may improve identification and management of cardiovascular risk, but evidence on their incremental clinical value, resource requirements and outcomes remains limited. The key question is whether integrated pathways improve risk-factor control and cardiovascular outcomes compared with strengthening prevention inside existing specialty services.
- Payers: Creating a new specialist clinic for every inflammatory condition is unlikely to be scalable. Payers may instead need to consider which patients warrant specialist cardiovascular referral and which elements of prevention can be embedded into routine dermatology, rheumatology and primary-care pathways. Risk-based referral could be more sustainable than universal cardiology assessment.
- Industry / innovation partners: The convergence of immunology and cardiovascular medicine creates opportunities around risk stratification, imaging, biomarkers and therapeutics, but it also raises a higher evidence threshold. Demonstrating that an inflammatory pathway affects cardiovascular biology is not the same as proving that targeting it prevents cardiovascular events.
The traditional map of medicine makes intuitive sense on paper.
A patient with psoriasis sees a dermatologist. A patient with rheumatoid arthritis sees a rheumatologist. Someone with high cholesterol, chest pain or coronary disease eventually sees a cardiologist.
The biology has never respected those boundaries quite so neatly.
Systemic inflammation can begin affecting the cardiovascular system while the most visible manifestations of disease remain in the skin, joints or other organs. By the time a cardiovascular problem becomes obvious enough to create a cardiology referral, years of risk may already have accumulated.
That is the clinical gap behind the emerging fields of cardio-rheumatology and cardio-dermatology.
During a presentation at the Cardiometabolic Health Congress in Boston, Brittany Weber described these disciplines as an attempt to recognise cardiovascular disease more systematically in patients who are already known to have an inflammatory or autoimmune condition.
The idea is becoming more relevant because cardiovascular guidance itself is moving in that direction.
The 2026 ACC/AHA dyslipidaemia guideline does not treat systemic lupus, rheumatoid arthritis, advanced psoriasis and inflammatory arthritis as incidental diagnoses. It lists chronic inflammatory disease among the factors that can increase cardiovascular risk beyond what a conventional calculator may show.
Perhaps more importantly, the guideline acknowledges that standard cardiovascular risk calculators tend to underestimate risk in these populations.
That creates a problem precisely where cardiovascular prevention has become increasingly dependent on numerical thresholds.
A calculator may estimate that a younger patient has a low probability of experiencing an event within the next decade largely because age is one of the strongest determinants of short-term risk. Yet a 32-year-old woman with systemic lupus or a 38-year-old man with severe psoriasis may already be exposed to years of systemic inflammation, glucocorticoids, metabolic changes or other disease-related factors that are poorly represented by a conventional score.
The calculator is not necessarily wrong about the next ten years.
It may simply be answering a narrower question than the clinician needs.
For autoimmune disease, the issue is particularly important because cardiovascular risk can begin accumulating well before the age at which formal prevention traditionally becomes prominent.
That does not mean every young patient with autoimmune disease is destined to develop cardiovascular disease, nor that inflammation should replace traditional risk factors as the dominant explanation.
Smoking, blood pressure, cholesterol, obesity, diabetes, kidney disease and physical inactivity remain critical. Some may also occur more frequently in inflammatory disease populations or be influenced by treatment.
The more useful concept is additive and interactive risk.
A patient may have conventional cardiovascular risk, disease-specific inflammatory risk and treatment-related risk operating simultaneously.
That makes ownership of prevention less obvious.
A dermatologist may be managing biologic treatment successfully while assuming lipid management sits with primary care. A rheumatologist may focus appropriately on suppressing disease activity while cardiovascular risk assessment occurs only intermittently. A primary-care clinician may see a young patient whose calculated ten-year risk appears reassuring and therefore defer intervention.
Every individual decision can look reasonable.
The system as a whole can still miss the risk.
This is precisely the kind of fragmentation multidisciplinary models are designed to solve.
UT Southwestern now has a Cardio-Rheumatology/Cardio-Dermatology Program directed by Weber, integrating cardiovascular assessment with expertise in systemic inflammatory disorders. Similar approaches have emerged at other academic centres, reflecting growing recognition that inflammation-related cardiovascular disease is difficult to manage from a single specialty.
The obvious policy question is whether every health system needs another subspecialty.
Probably not.
The deeper value of cardio-rheumatology may lie less in creating a new clinic than in forcing existing specialties to decide who is responsible for cardiovascular prevention.
A scalable pathway might begin much earlier and much more simply.
Blood pressure should not disappear from a dermatology visit because the primary diagnosis is psoriasis. Lipids and smoking history should not become somebody else’s problem because a rheumatologist is concentrating on disease control. Cardiovascular risk should be reassessed when inflammatory disease becomes severe, prolonged or treatment changes materially.
Only the more complex cases may require a dedicated cardiovascular specialist.
That approach also avoids another potential problem: converting awareness of elevated risk into indiscriminate testing.
Inflammatory diseases can produce cardiovascular abnormalities that extend beyond conventional obstructive coronary disease, but the evidence does not justify scanning every asymptomatic patient.
Research in psoriasis provides an example.
In one positron emission tomography study, coronary microvascular dysfunction was identified in 61.3% of patients with psoriasis compared with 38.4% of matched controls. Importantly, the difference was not fully explained by conventional cardiovascular risk factors or the amount of coronary calcification.
A larger study of patients with severe psoriasis subsequently reported coronary microvascular dysfunction in almost one third of participants, with worse psoriasis severity and longer disease duration associated with greater dysfunction.
Systemic lupus has shown a similar signal.
PET imaging studies have identified impaired myocardial flow reserve among patients with lupus even when obstructive coronary disease was not present, suggesting that the coronary microcirculation may be one pathway through which systemic inflammatory disease affects the heart.
That could help explain why some patients with autoimmune disease develop chest pain or cardiovascular symptoms without the obstructive coronary lesions traditionally expected to account for them.
But it is important not to move too quickly from mechanistic evidence to screening policy.
The existing microvascular studies are relatively small and often involve patients referred for imaging because they already had symptoms such as chest pain or dyspnoea. They do not establish that routine PET imaging in asymptomatic autoimmune populations improves outcomes.
Detecting an abnormality is only useful if clinicians know what to do with it.
That evidence gap is particularly relevant as advanced cardiovascular imaging becomes increasingly sensitive. If every signal of vascular dysfunction creates another scan, another referral and another diagnostic label without a proven management pathway, better detection could simply create more healthcare activity.
The stronger immediate opportunity lies in cardiovascular prevention that already has an evidence base.
The 2026 dyslipidaemia guideline recommends incorporating atherosclerotic cardiovascular risk assessment into care for people with chronic inflammatory diseases. It specifically recognises these conditions as risk enhancers that can alter treatment discussions when calculated risk sits near decision thresholds.
European rheumatology guidance has moved in the same general direction. EULAR recommends regular screening and management of modifiable cardiovascular risk factors in patients with multiple rheumatic diseases and acknowledges that disease activity and therapies such as glucocorticoids can themselves influence cardiovascular risk.
This matters because inflammation is not the only bridge between specialties.
Treatment can be another.
Some immunomodulatory therapies may indirectly improve cardiovascular biology by controlling systemic inflammation, while other therapies can influence blood pressure, lipids, thrombosis or heart failure risk. Glucocorticoid exposure, for example, creates cardiovascular and metabolic concerns that have to be weighed alongside its benefits in controlling inflammatory disease.
That means the cardiovascular implications of therapy cannot always be separated from treatment selection.
At the same time, enthusiasm around inflammation as a cardiovascular target needs perspective.
Trials such as CANTOS demonstrated that reducing inflammation with canakinumab could reduce recurrent cardiovascular events without lowering LDL cholesterol, helping establish inflammation as a causal therapeutic pathway in atherosclerosis. Colchicine trials subsequently reinforced the idea that inflammatory pathways could be modified in selected cardiovascular populations.
But those results do not mean that every anti-inflammatory drug used in rheumatology or dermatology will prevent cardiovascular disease.
The immune system is not a single therapeutic pathway.
Different inflammatory conditions involve different cytokines, cell populations and treatment mechanisms, while individual drugs have their own cardiovascular effects. Translating evidence from one anti-inflammatory therapy or disease to another without dedicated outcomes data would be scientifically unjustified.
The value of multidisciplinary care is therefore partly that it prevents simplistic thinking in both directions.
Cardiologists have to understand the inflammatory disease and its therapies rather than treating every patient as an ordinary prevention case with an additional diagnosis.
Rheumatologists and dermatologists have to recognise that controlling visible disease does not necessarily erase cardiovascular risk.
And primary care has to remain involved because much of the prevention work still consists of familiar interventions: blood-pressure control, smoking cessation, lipid management, physical activity, weight management and diabetes prevention.
The emerging specialty therefore poses an organisational question more than a technological one.
Who owns cardiovascular prevention when the cardiovascular risk begins in another specialty?
That question is particularly important for women because many autoimmune diseases disproportionately affect women, often beginning years before conventional cardiovascular risk becomes clinically prominent.
If the first serious cardiovascular assessment occurs at 50 while systemic inflammatory disease began at 25, the health system has effectively treated decades of potential risk as someone else’s responsibility.
Cardio-rheumatology and cardio-dermatology are attempts to break that pattern.
Their success should ultimately be measured not by how many new clinics appear, but by whether patients with inflammatory disease receive cardiovascular prevention earlier and more consistently.
That may mean better referral algorithms rather than universal cardiology referral. It may mean embedding blood-pressure and lipid pathways into specialty clinics. It may mean electronic health-record prompts when inflammatory disease acts as a cardiovascular risk enhancer. It may mean shared protocols between specialties and clearer responsibility for follow-up.
Those solutions are less glamorous than advanced imaging or new biomarkers.
They may also be more scalable.
Medicine already has substantial evidence that autoimmune and chronic inflammatory diseases can alter cardiovascular risk. What remains uneven is the translation of that knowledge into routine pathways.
The problem is no longer simply recognising that inflammation connects the skin, joints and heart.
The policy challenge is building a health system that behaves as though those organs were connected all along.
