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Study with 20,070 patients shows that Lp(a), a little-measured cholesterol particle, increases the risk of stroke and cardiovascular death even with standard treatment.
According to ScienceDaily, researchers analyzed stored plasma samples from 20,070 participants aged 40 and over, enrolled in three major randomized studies by the National Institutes of Health in the United States: ACCORD, PEACE, and SPRINT. The results were presented as late-breaking research at the scientific conference of the Society for Cardiovascular Angiography & Interventions, SCAI 2026, in Montreal, on April 24.
The study identified that very high levels of Lp(a), lipoprotein(a), significantly increase the risk of stroke, cardiovascular death, and severe cardiac complications, even in people already receiving standard treatment with medications such as statins and antihypertensives.
Lp(a) is a cholesterol-carrying particle similar to LDL, known as “bad” cholesterol, but it does not appear in routine lipid profile tests. Approximately one in five adults has elevated Lp(a), and most are unaware because the specific test is still rarely requested.
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Lp(a) is a type of dangerous cholesterol that escapes conventional testing
The routine cholesterol test measures total cholesterol, LDL, HDL, and triglycerides. This panel was developed based on cardiovascular knowledge consolidated in the 1960s and 1970s.
Lp(a) is different from regular LDL because it carries an additional protein called apolipoprotein(a). This structure makes the particle more dangerous, as it interferes with clot dissolution and can increase the risk of blockages in vessels already affected by atherosclerosis.
This means that a person can have normal LDL levels and still have an elevated cardiovascular risk due to Lp(a). The traditional lipid profile does not show this hidden risk.
Lp(a) cholesterol increases the risk of stroke and cardiovascular death even with controlled LDL
The most concerning data from the study is not just the association between Lp(a) and cardiac risk, but the fact that this risk persists even with standard medical treatment. The participants analyzed were already part of clinical studies and received conventional care.
Statins reduce LDL, but do not significantly reduce Lp(a). This creates a dangerous situation: the patient takes medication, improves common cholesterol numbers, and believes they are protected, but may still carry a high genetic risk factor.
This is called residual cardiovascular risk. Even with controlled LDL, treated blood pressure, and medical follow-up, high Lp(a) can keep the risk of stroke, heart attack, and cardiovascular death above expected levels.
Study with 20,070 patients showed persistent risk in already treated individuals
The research used samples from three large NIH clinical trials. The ACCORD included patients with type 2 diabetes and high cardiovascular risk; the PEACE evaluated people with stable coronary disease; and the SPRINT analyzed patients with hypertension.
Researchers measured Lp(a) in the samples using a standardized test and reported the results in nmol/L, a unit considered more accurate for this particle than mg/dL. The analysis showed that very high levels were linked to severe cardiovascular events.
The finding reinforces an important shift in preventive medicine. It is not enough to look only at LDL, HDL, and triglycerides when there is a family history, early events, or unexplained cardiac risk.
High Lp(a) is primarily genetic and does not depend solely on diet or weight
The most important characteristic of Lp(a) is that its levels are primarily determined by genetics. Unlike LDL, which can vary significantly with diet, weight, physical activity, and medications, Lp(a) tends to remain relatively stable throughout life.
It is estimated that about 90% of the Lp(a) level is defined by genes inherited from parents. Therefore, people with a family history of early heart attack, stroke, or heart disease without an apparent cause should consider investigation.
If a father or mother has elevated Lp(a), the children may also have an increased risk. This is a marker that can be present even in slim, active people with a balanced diet and apparently normal common cholesterol.
New 2026 guidelines recommend measuring Lp(a) at least once in a lifetime
In March 2026, the American College of Cardiology and the American Heart Association published new guidelines for dyslipidemia management. For the first time, they recommended measuring Lp(a) at least once in every adult’s lifetime.
The guidelines recognize elevated Lp(a) as an independent cardiovascular risk factor. In general, levels above 50 mg/dL or 125 nmol/L are considered elevated and may influence treatment decisions.
The recommendation also includes earlier screening in people with a strong family history. In some cases, children between 9 and 11 years old may be evaluated when there is early heart attack, stroke, or hereditary heart disease in the family.
Lp(a) test is still rarely requested in Brazil, despite cardiovascular risk
In Brazil, the specific Lp(a) test is available in many laboratories, but it is still not part of the routine panel requested by most doctors. In many cases, it needs to be requested separately.
This low request rate occurs because much of the clinical training was done at a time when Lp(a) was not yet strongly featured in the guidelines. With the new recommendations, the trend is for the test to gain more space in preventive cardiology.
The practical guidance is clear: adults with a family history of early heart attack, stroke, sudden death, or apparently normal cholesterol with cardiac events should talk to their doctor about measuring Lp(a).
What to do when Lp(a) is high and there is still no approved specific medication
Today, there is still no widely approved direct treatment to specifically reduce Lp(a). Even so, knowing that it is elevated has real clinical value because it changes the way cardiovascular risk is interpreted.
When Lp(a) is high, doctors may choose to reduce LDL more aggressively, control blood pressure more strictly, treat diabetes, combat smoking, and reinforce physical activity, appropriate weight, and heart-protective diet.
The logic is simple: when it is not possible to directly reduce Lp(a), it is necessary to control all other modifiable factors to the maximum. Genetic risk cannot be ignored, but it can guide more intense prevention.
New medications against Lp(a) are in advanced stages of clinical studies
Research is also gaining importance because specific medications against Lp(a) are in development. Among them are RNA silencing-based therapies, such as pelacarsen and olpasiran.
Pelacarsen is an antisense oligonucleotide that can reduce Lp(a) by up to 80% in clinical studies. Olpasiran, based on siRNA, showed reductions of over 90% in phase II studies.
These medications still depend on further validation and approval stages. But identifying patients with elevated Lp(a) now can put them in a better position when these therapies reach the market.
Lp(a) may explain hidden cardiac risk in seemingly controlled people
The discovery reinforces an important shift in cardiovascular prevention. For decades, the main focus was on LDL, HDL, and triglycerides, but Lp(a) shows that part of the risk may remain invisible in conventional testing.
A person with controlled LDL, proper diet, and correct use of statins may still have an elevated risk if they carry high levels of Lp(a). This risk is especially relevant when there is a family history of early cardiovascular disease.
The study presented at SCAI 2026 reinforces that measuring Lp(a) at least once in a lifetime can reveal a silent, genetic, and clinically important factor. For many patients, this test can be the difference between believing the heart is protected and discovering a risk that never appeared in common cholesterol tests.
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