Most people think of autoimmune diseases—conditions like lupus, rheumatoid arthritis, and Sjögren’s syndrome—as disorders that attack joints, skin, or organs. Fewer realize that they also place a person at significantly greater risk for heart disease.
What’s even less understood is the silent role of Lipoprotein(a)—or Lp(a)—in amplifying this risk.
Lp(a) is a cholesterol-like particle that often flies under the radar. It isn’t included in standard lipid panels, isn’t influenced by diet or exercise, and is rarely tested for unless specifically requested. But recent research is changing that: elevated Lp(a) is now considered a major, independent cardiovascular risk factor—especially dangerous in people with autoimmune disease.
A 2025 study, featured by Medical Xpress, has highlighted how Lp(a) behaves more aggressively in patients with autoimmune conditions. This combination of inflammation and abnormal lipids may help explain why cardiovascular events—like heart attacks and strokes—happen earlier and more frequently in autoimmune populations.
This article explores the science behind the Lp(a)-autoimmune link, what it means for prevention, and how early detection can reshape care strategies for millions.
Table of Contents
What Is Lipoprotein(a)?
Lipoprotein(a), abbreviated as Lp(a) and pronounced “L-P-little-a,” is a cholesterol-carrying lipoprotein particle similar in structure to LDL (low-density lipoprotein). But it carries a twist: an additional protein called apolipoprotein(a), which alters its behavior and risk profile.
This structural addition makes Lp(a):
- More adhesive to arterial walls
- More pro-inflammatory
- More likely to contribute to plaque formation
Unlike LDL cholesterol, Lp(a) is highly heritable and not significantly influenced by lifestyle changes. Approximately 20–25% of people have elevated Lp(a), often without knowing it.
Studies over the past two decades have linked high Lp(a) levels to increased risk of:
- Atherosclerosis
- Coronary artery disease
- Calcific aortic valve stenosis
- Ischemic stroke
But these risks multiply in the presence of chronic inflammation—the kind commonly seen in autoimmune diseases.
The Cardiovascular Burden of Autoimmune Disease
Autoimmune diseases occur when the immune system mistakenly attacks the body’s own tissues. This results in persistent, low-grade inflammation that can affect joints, skin, lungs, kidneys—and importantly, blood vessels.
Research shows that chronic systemic inflammation accelerates:
- Endothelial dysfunction (damage to the inner lining of blood vessels)
- Plaque formation in arteries
- Thrombosis risk, due to immune-triggered clotting mechanisms
In fact, autoimmune diseases like lupus and rheumatoid arthritis double or triple the risk of cardiovascular disease—and cardiovascular events are a leading cause of death in these populations.
The traditional assumption has been that inflammation alone drives this risk. But the emerging science around Lp(a) is painting a more complex—and more dangerous—picture.
The New Science: Lp(a) and Autoimmune Inflammation Combine Forces
A study released in 2025 and covered by Medical Xpress provides compelling evidence that Lp(a) particles interact with immune-driven inflammation in ways that amplify vascular damage.
Researchers examined arterial tissue samples from individuals with autoimmune conditions and compared them to samples from individuals with standard atherosclerosis. They found that:
- Blood vessels in autoimmune patients with elevated Lp(a) resembled those of people with advanced heart disease.
- Lp(a) molecules in these patients triggered stronger inflammatory responses at the cellular level.
- Vascular cell behavior shifted toward a more plaque-promoting phenotype when exposed to Lp(a) in the presence of inflammatory cytokines.
The takeaway? Lp(a) is more dangerous in inflamed environments, and autoimmune disease creates precisely that environment.
Why Most People Don’t Know Their Lp(a) Levels
Despite its serious implications, Lipoprotein(a) testing is still not a standard part of routine cardiovascular screening. This is partly due to a lack of awareness among both healthcare providers and patients. Many clinicians remain focused on traditional risk markers like LDL, HDL, triglycerides, and blood pressure—overlooking the critical role of Lp(a), especially in complex cases. As a result, millions of people may be walking around with dangerously elevated Lp(a) levels, completely unaware of the cardiovascular risk they carry.
Testing for Lp(a) requires a separate, specific blood test, which is not automatically included in standard lipid panels. Insurance coverage can also be inconsistent, leading to further underutilization. Without awareness or a clear trigger—like early heart disease in a family member—most patients never get tested. And for those with autoimmune disease, this can mean missing a major opportunity for early risk detection and intervention.
Who Should Be Tested for Lp(a)?
People with premature cardiovascular disease—defined as a heart attack, stroke, or other vascular event occurring before age 55 in men or 65 in women—should be tested for Lp(a). These early events often indicate an underlying genetic or inflammatory driver that routine cholesterol tests may not detect. Lp(a) may be the missing explanation for why heart disease develops in individuals who otherwise appear healthy.
Those with a strong family history of heart disease should also undergo Lp(a) screening. If multiple family members experienced cardiovascular events at a young age or without traditional risk factors, Lp(a) could be playing a silent but lethal role. Identifying this marker early can help guide more personalized prevention strategies for relatives.
Patients with familial hypercholesterolemia (FH), a genetic condition that causes very high LDL levels, are at particularly high risk when Lp(a) is also elevated. In these patients, the combination of two genetic lipid disorders can create an extremely aggressive form of atherosclerosis. Testing Lp(a) provides a clearer picture of total inherited cardiovascular risk.
People with autoimmune conditions, especially those with active inflammation or a history of cardiovascular symptoms, represent a highly vulnerable group. Chronic systemic inflammation makes blood vessels more susceptible to damage, and elevated Lp(a) adds another layer of risk. Even without traditional red flags, Lp(a) testing can reveal a need for more intensive monitoring and preventive care.
Detecting Risk Before Symptoms Appear
Vascular imaging techniques, such as carotid artery ultrasound or coronary calcium scoring, can identify structural changes in blood vessels long before symptoms develop. These non-invasive tests help detect early plaque buildup, arterial stiffness, or narrowing that could eventually lead to a heart attack or stroke. For patients with autoimmune disease and high Lp(a), these tools are invaluable in assessing silent cardiovascular risk.
Inflammatory markers like high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) offer insight into systemic immune activity that may worsen Lp(a)-driven vascular damage. Elevated levels of these markers, especially in the absence of acute infection or trauma, suggest a higher likelihood of endothelial dysfunction. When combined with high Lp(a), these results should prompt urgent follow-up.
Genetic screening for elevated Lp(a) is also gaining traction. Since Lp(a) levels are determined largely by a person’s DNA, a one-time genetic test can identify those at risk—even from a young age. This can help guide lifestyle, medication, and screening decisions throughout life, long before any cardiac event occurs.
Functional testing of endothelial health, such as flow-mediated dilation or reactive hyperemia index testing, allows clinicians to assess how well blood vessels respond to stress. Impaired endothelial function is often the first measurable sign of cardiovascular disease. When coupled with elevated Lp(a) and autoimmune inflammation, poor test results indicate a significantly elevated risk of a cardiovascular event.
Treating Elevated Lp(a): What Are the Options?
There is no widely available FDA-approved drug that specifically targets Lp(a). This leaves patients and clinicians in a difficult position, especially when Lp(a) is the main risk factor identified. However, research is advancing rapidly, with several promising therapies in late-stage clinical trials.
Apheresis, a procedure similar to dialysis, can physically remove Lp(a) from the blood in patients with extremely high levels. Though not practical for most, it’s used in high-risk cases or in individuals with progressive cardiovascular disease despite optimal management of other risk factors. It’s invasive, costly, and typically reserved for specialized centers.
Antisense oligonucleotides, a new class of gene-silencing drugs, show promise in blocking the production of apolipoprotein(a) in the liver. These therapies, currently in clinical trials, have demonstrated up to 90% reductions in Lp(a) levels. If approved, they could revolutionize how elevated Lp(a) is treated, especially in high-risk populations like those with autoimmune disease.
PCSK9 inhibitors, injectable cholesterol-lowering drugs, have been shown to reduce Lp(a) by 20–30% in some patients. While they are not designed to treat Lp(a) specifically, they may offer partial benefit for those with overlapping high LDL and Lp(a) levels. They are already in use for individuals with statin intolerance or familial hypercholesterolemia.
In the meantime, clinicians focus on managing traditional risk factors aggressively: lowering LDL, controlling blood pressure and blood sugar, reducing inflammation, and promoting lifestyle changes. While these measures don’t directly reduce Lp(a), they can lower the overall cardiovascular risk burden and mitigate complications.
Autoimmune Conditions Most Strongly Linked to Cardiovascular Risk
Systemic lupus erythematosus (SLE) is one of the autoimmune conditions most closely linked to early and aggressive heart disease. Women under 45 with lupus are particularly vulnerable, with some studies suggesting a 50-fold increased risk of heart attack compared to age-matched controls. Persistent inflammation, along with medications like corticosteroids, contributes to endothelial dysfunction and lipid abnormalities that drive plaque buildup.
Rheumatoid arthritis (RA) also carries a significantly higher risk of coronary artery disease—estimated to be up to 50% greater than the general population. Chronic joint inflammation mirrors what’s happening inside the arteries, where immune cells contribute to the thickening and stiffening of vessel walls. Even when RA symptoms are controlled, vascular inflammation may continue silently, requiring proactive cardiovascular surveillance.
Psoriasis, commonly thought of as a skin condition, is actually a systemic inflammatory disease. Patients with moderate to severe psoriasis show early signs of vascular aging and subclinical atherosclerosis—even in their 30s and 40s. Studies suggest that the degree of skin involvement often correlates with the level of systemic inflammation and cardiovascular burden.
Sjögren’s syndrome, a condition that primarily affects moisture-producing glands, is increasingly recognized for its cardiovascular impact. Inflammation in Sjögren’s can lead to endothelial damage, increasing the risk of coronary artery disease and arrhythmias. Because symptoms often appear subtle or non-specific, patients may not receive timely cardiovascular evaluation until complications arise.
Implications for Patients, Clinicians, and Public Health
For patients, this research underscores the importance of being proactive—especially if you live with an autoimmune disease. Knowing your Lp(a) level and inflammatory markers can help you understand your true cardiovascular risk, which may not be obvious through routine lab work or checkups. Asking your provider about comprehensive vascular screening could be a life-saving conversation.
Clinicians must move beyond the one-size-fits-all model of cardiovascular prevention. For autoimmune patients, standard risk calculators may significantly underestimate the true danger, especially if Lp(a) is elevated. Expanding screening protocols to include Lp(a) and inflammation testing allows for earlier intervention and more personalized care.
Public health officials and policymakers should consider updating cardiovascular screening guidelines to include Lp(a) testing for at-risk populations—particularly those with autoimmune diseases. Making these tests more accessible and covered by insurance could prevent thousands of premature heart attacks and strokes annually. Public awareness campaigns may also help close the knowledge gap and empower patients to take initiative in managing their cardiovascular health.
Final Thoughts
As science uncovers deeper links between immunity and vascular health, one message rings loud and clear: it’s no longer enough to treat autoimmune disease in isolation.
Elevated Lp(a) is a powerful, genetically driven marker of cardiovascular risk that becomes especially dangerous in inflammatory environments. For people living with autoimmune conditions, the combination can be deadly—but also predictable and preventable with the right tools.
The future of care lies in early detection, personalized risk profiling, and interdisciplinary awareness. And as this research shows, the arteries don’t lie—even when symptoms stay silent.
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