Patient Experience of Heart Disease with Elevated Lipoprotein(a): Views from a Patient, His Physician, and a Patient Association

Abstract

This article presents three points of view on lipoprotein(a) [Lp(a)]: that of a patient, his endocrinologist, and a patient association, the Association Nationale des Hypercholestérolémies familiales et Lipoprotéines (a) (ANHET). By sharing his story, the patient reveals the severe impact his high Lp(a) levels had on his health, his daily life, and his family. The endocrinologist explains what Lp(a) is and its role as a risk factor for cardiovascular disease. As an expert in the field, he reviews the recommendations for the screening and management of Lp(a). The vice-president of ANHET describes the association’s fight to increase awareness of this risk factor among patients, the medical profession, and even politicians, and to bring about changes in the healthcare system. Given the large number of people concerned, the perspectives of the patient, the physician, and the patient association converge in raising awareness of the negative impact of high levels of Lp(a) on health and the importance of intensifying Lp(a) screening.

See the Supplementary Material for a French-language version of this abstract.

Supplementary Information

The online version contains supplementary material available at 10.1007/s40119-025-00416-6.

Plain Language Summary

Lipoprotein(a), also known as Lp(a), is a lipoprotein that transports cholesterol in the blood. Levels of Lp(a) are genetically determined and vary considerably between people. High Lp(a) levels are a causative, independent risk factor for premature cardiovascular disease, stroke and calcific aortic stenosis, but are not usually measured by doctors, because there is low awareness of the risk Lp(a) poses. This article presents three points of view on Lp(a): that of a patient, his endocrinologist, and a patient association, the Association Nationale des Hypercholestérolémies familiales et Lipoprotéines (a) (ANHET). Unlike most types of lipoproteins/cholesterol, Lp(a) levels are not influenced by lifestyle. The patient in this article was lean, exercised regularly, and had a healthy diet, yet he had a heart attack before 40 years of age, and has had two more since, because of very high Lp(a) levels. The physician describes what Lp(a) is, how it is treated currently, and what the future holds. The only available treatment now is lipoprotein apheresis, which involves removing Lp(a) by pumping blood through a “purifying” machine, which is expensive, time-consuming, and inconvenient. Promising new treatments for reducing Lp(a) levels are being investigated in clinical trials, and the first of these treatments (pelacarsen) is likely to be available within a few years. The vice-president of ANHET describes the association’s role in supporting patients, educating physicians, and driving awareness at a government and policy level to improve rates of testing and screening, and improve access to effective treatment.

Supplementary Information

The online version contains supplementary material available at 10.1007/s40119-025-00416-6.

Key Summary Points

Lipoprotein(a) [Lp(a)] is the combination of a low-density lipoprotein-like particle and apoprotein(a).

Levels are genetically determined and vary considerably between individuals, but have a linear relationship with atherosclerotic cardiovascular event rates, with a clinically significant risk at levels >125 nmol/L (0.50 g/L).

The experience of a patient with very high Lp(a) levels (>330 nmol/L [1.50 g/L]) is illustrative, with repeated myocardial infarctions starting at a young age (39 years), despite a healthy lifestyle.

Physicians should screen all adults at least once; a finding of elevated Lp(a) should prompt familial cascade screening, as per familial hypercholesterolemia recommendations.

Current treatment is limited to lipoprotein apheresis, but new treatments are in phase 2 and 3 clinical development, and will likely be available within a few years.

Greater awareness of Lp(a) and more proactive screening is required, especially with the imminent availability of effective treatments that will markedly reduce cardiovascular risk for individuals with high Lp(a) levels.

Patient Perspective: Mr. Stéphane Favereaux

Finding out that I had cardiovascular disease (CVD) came as a great shock to me. Thirteen years ago, in 2011, when I was 39 years old, I had a heart attack. I was in excellent shape at the time; I used to go running twice a week and had a very healthy lifestyle. There were no warning signs, and it happened very suddenly. One afternoon, I was washing my car and felt a heaviness in my chest, a pain in my left arm, a strange sensation in my jaw, and a cold sweat. I became very short of breath. My wife phoned the emergency services, but I thought it was just a passing episode, so I refused to let them send a medical team. Later in the afternoon, the same symptoms returned, and we went straight to the emergency room. I was told that I was having a myocardial infarction (MI) and I had an operation to place three stents in my coronary arteries. Afterwards, I underwent cardiac rehabilitation, and I was started on treatment, consisting of a statin, an angiotensin-converting enzyme (ACE) inhibitor (ramipril), a beta-blocker (acebutolol), and two antiplatelet agents. My cardiologist at the time did not ask for a lipoprotein(a) [Lp(a)] test. I was also referred to a dietician, but because I have always been careful to eat a healthy diet and was not overweight, I was told that I did not need to change my diet.

Once my cardiac rehabilitation was complete, I resumed playing sport and quickly regained my pre-infarction level of fitness. My life went on as before. However, about 10 years later in 2021, when I was 49 years old, some of the symptoms returned, and I was sent for a scintigraphy scan. The examination revealed that my coronary arteries had become obstructed again and, as a result, I underwent an emergency procedure to place two additional stents. At this point I met Prof. Vincent Durlach, who was the first doctor to tell me about Lp(a) and the way it raises cardiovascular risk. He suggested that this may be the reason why my coronary arteries had become obstructed again despite treatment. A simple blood test showed that I had a very high Lp(a) level of 330 nmol/L (1.50 g/L). My level of low-density lipoprotein cholesterol (LDL-C)—the “bad” cholesterol—had always been normal, so this was a huge surprise. We had a long discussion with Prof. V. Durlach in which he explained the harmful consequences of the very high levels of Lp(a) in my blood for my heart and my health. The news was so very unexpected—it was like a sledgehammer. He asked about CVD in my family. The only person I could think of was my paternal grandmother, who had a history of CVD and had undergone amputation of both lower limbs due to peripheral arteriopathy.

After that conversation, I went home and searched the internet for information about Lp(a), including patient opinions and experiences, but I did not find much. That is one of the reasons that I was keen to contribute to this article! Because having elevated Lp(a) levels is a genetic condition, Prof. V. Durlach recommended that my family members should be tested. I explained to my three children (aged 27, 25, and 12 years) in my own words what Lp(a) was, and the health risks associated with its elevation. This was another hard blow: the tests revealed that all three of our children had high levels of Lp(a). Later, my sister and her two children also got tested and, unfortunately, all three were positive. For reasons of their own, my parents have refused to take the test, although I feel sure that I inherited this from my grandmother.

After the second cardiac event, I carried on with the same medical treatment, but Prof. V. Durlach proposed two other options. One was to take part in a 5-year clinical trial of a new drug capable of lowering Lp(a) levels. The second was to undergo lipoprotein apheresis sessions to partially purify my blood of Lp(a). I was still considering these options when I had another cardiac event in 2023. I suddenly felt breathless, tired, nauseous, and dizzy, so we went to the emergency department of Reims University Hospital. They did a coronary angiogram to check the state of my coronary arteries, and it revealed that the stents had become occluded again. I had to undergo major cardiac surgery with a quadruple bypass at the Pitié-Salpêtrière Hospital in Paris. In October 2023, I started my third cardiac rehabilitation program. At this point, my cardiologist suggested that I consult a psychologist, but I refused. Following the bypass operation, my decision was clear: I did not want to take part in a long clinical trial without certainty of success; I wanted to maximize my chances. I therefore opted for the lipoprotein apheresis, which is currently the most effective option to reduce Lp(a) levels.

An arteriovenous fistula was implanted in my biceps, and I started my first session of lipoprotein apheresis in the Nephrology Intensive Care Unit at Reims University Hospital in January 2024. Since then, I have been going to the hospital for a session every 2 weeks. It takes about 2 h to purify 8 L of my blood. This brings my Lp(a) level down to around 150 nmol/L (0.70 g/L). A rebound effect causes my level to rise to 350 nmol/L (1.60 g/L) just 2 weeks after apheresis.

The last cardiac event and the subsequent decision to begin lipoprotein apheresis totally changed my life. After the sternotomy during my bypass, I started to experience heart rhythm problems. My beta-blocker treatment (atenolol) was adjusted to try to resolve these arrhythmias. I have not had to make any changes to my diet, as I have always been careful about what I eat. However, due to the implantation of the arteriovenous fistula, I was no longer able to do any sport or carry heavy loads. That has had the biggest impact on my daily life. Before this, I was very sporty and really enjoyed manual work, but suddenly I was not able to do anything like that anymore. To relax and try to improve my arrhythmia problems, I started yoga, but it is not the same. Although I had been well informed by Prof. V. Durlach and the nephrology team about the constraints associated with the implantation of a fistula, living with it on a day-to-day basis is different. For example, now I have to hire someone to trim my hedges, whereas I used to do it myself. Overall, I feel like I have suddenly aged 20 years. I have been on long-term sick leave from my job as a prison guard for a year.

Since my diagnosis of elevated Lp(a), I have been living with the sword of Damocles hanging over my head, with the anxiety that a serious cardiac event could happen again. I am the only one in my family to have had all these heart problems and interventions, despite the fact that I have always been careful about my lifestyle, and my cholesterol levels have always been normal. My wife and I really hope, for our children’s sakes, that their condition will not develop as it has in my case. My second daughter consulted Prof. V. Durlach for herself. He advised her to stop smoking, and gave her a few recommendations about her lifestyle. It reassured her to talk to him. She stopped smoking completely, which was a great achievement. Otherwise, my children continue living a normal life. I do not want my children to have to live with the anxiety of this disease and I have advised them to continue to live healthily, but without thinking about it. In fact, this is the overall message I would like to send to other patients who discover they have high levels of Lp(a): try to live a normal life, without thinking about the disease.

Physician Perspective: Prof. Vincent Durlach

I am an endocrinologist who specializes in lipids at Reims University Hospital, France, where I am the local expert in the field of dyslipidemia. This means that I frequently work with cardiologists who treat patients with MI, and it was in this context that I met Mr. Stéphane Favereaux. I am also a member of the Nouvelle Société Francophone d’Athérosclérose (NSFA), which brings together all the lipid specialists in France.

Dyslipidemias are diseases linked to elevated lipoproteins, some of them being genetically transmitted. Lp(a) has been described in the literature since the 1960s and was initially mentioned by the Norwegian Kare Berg in 1963 [1]. My interest in Lp(a) dates back to the 1990s, when Lp(a) was the subject of numerous studies. For about 10 years, we conducted research into this lipoprotein with Dr Eduardo Anglés-Cano, a thrombosis specialist who was working on Lp(a) in patients with coronary artery disease or diabetes. Because no treatment was able to lower it effectively, the scientific community seemed to lose interest in Lp(a) for around 20 years. Interest has been renewed over the last 5 years, thanks to new research and the prospect of new therapies that could significantly reduce the circulating concentration of Lp(a).

Lp(a) is the combination of an LDL-like particle and apoprotein(a) [apo(a)], which is composed of repeating structures called kringles (pretzel-shaped helical structures), similar to plasminogen. The molecular weight of apo(a) varies from 250 to 800 kDa, depending on the number of kringle domains and the extent of glycosylation [2], explaining 70–90% of the variability in Lp(a) levels between individuals [3, 4]. There is considerable genetic heterozygosity (> 95%), with most people carrying two differently sized apo(a) alleles [2]. The low-molecular-weight isoforms of apo(a) are associated with high Lp(a) levels (median of ~100 nmol/L or 0.40 g/L), whereas the high molecular weight forms are associated with lower levels (median ~25 nmol/L or 0.10 g/L) (Fig. 1) [2]. As apo(a) shares a high degree of structural homology with plasminogen, Lp(a) may interfere with fibrinolysis processes (Fig. 2) [2, 5–7]. Lp(a) has been associated with increased risk for atherosclerosis, thrombosis, and aortic valve calcification. Numerous longitudinal, and prospective clinical studies in primary and secondary prevention have demonstrated a link between elevated Lp(a) levels and the development of atherosclerotic CVD, particularly MI and ischemic stroke, in young patients and, more recently, aortic valve stenosis [8–16]. The relationship between the Lp(a) levels and the risk for major cardiovascular events is linear, meaning that the higher the Lp(a) level, the greater the cardiovascular risk [17, 18]. In clinical practice, the threshold of 125 nmol/L (0.50 g/L) is considered to translate to a clinically significant increase in cardiovascular risk [2, 17, 19].

Fig. 1.

Lipoprotein(a) [Lp(a)]: mechanistic insights. Pathophysiological pathways providing a causal link between high plasma concentrations of Lp(a) and atherosclerotic vascular disease and aortic stenosis. Clinical outcomes are related to atherosclerotic stenosis complicated by thrombosis (myocardial infarction, stroke), peripheral artery disease (PAD), or aortic valve replacement (AVR) caused by valve calcification and aortic stenosis [2]. Apo(a) apolipoprotein(a); LDL low-density lipoprotein; OxPL oxidized phospholipids. Used with permission of Elsevier, from Durlach V, et al. Lipoprotein(a): Pathophysiology, measurement, indication and treatment in cardiovascular disease. A consensus statement from the Nouvelle Société Francophone d’Athérosclérose (NSFA). Arch Cardiovasc Dis. 114, 2021. Permission conveyed through Copyright Clearance Center, Inc.

Fig. 2.

Contribution of apolipoprotein(a) [apo(a)] polymorphism to inhibition of fibrinolysis, a mechanism that may favor thrombus development. Lipoprotein(a) [Lp(a)] competes with plasminogen for binding to fibrin and cell plasminogen receptors. Inhibition of plasminogen binding and activation impairs fibrinolysis/pericellular proteolysis, and is related to high Lp(a) concentrations and small apo(a) isoforms (< 22 kringles [K]; 17 K in the figure), but not to large apo(a) isoforms (30 K in the figure) [2]. t-PA tissue plasminogen activator. Used with permission of Elsevier, from Durlach V, et al. Lipoprotein(a): Pathophysiology, measurement, indication and treatment in cardiovascular disease. A consensus statement from the Nouvelle Société Francophone d’Athérosclérose (NSFA). Arch Cardiovasc Dis. 114, 2021. Permission conveyed through Copyright Clearance Center, Inc.

A significant number of people have high or very high levels of Lp(a). It is estimated that 20% of the European population has Lp(a) levels above 125 nmol/L (0.50 g/L) [20]. In France, this means about 10 million people. Between 13% and 35% of patients with CVD have Lp(a) levels above 125 nmol/L (0.50 g/L) [18, 21–23]. Lp(a) levels are predominantly determined by genetics, which means that the risk associated with this factor is largely unmodifiable. Lifestyle factors, such as diet and physical activity, have minimal or no influence on Lp(a) levels [17]. Mr. S. Favereaux is a perfect example of this: even though he led an exemplary lifestyle, he experienced his first MI before he was 40 years of age. Lp(a) levels vary with ethnicity, with Black individuals and South Asian populations having higher median Lp(a) levels than white or East Asian populations [18, 24].

To determine which patients should be screened for Lp(a), we follow the 2019 European Society of Cardiology (ESC) and European Atherosclerosis Society (EAS) guidelines [25]. Mr. S. Favereaux had almost all of the criteria set out in the recommendations: a family history of CVD (his grandmother had undergone limb amputation due to peripheral arteriopathy); a premature cardiovascular event (he had an MI before the age of 40 years); and recurrent CVD despite optimal treatment (he had three stents placed and received standard post-MI treatment with the combination of a statin, beta-blocker, ACE inhibitor, and aspirin, but subsequently required a further two stents). These were all indications that an additional risk factor was at play. At around 330 nmol/L (1.50 g/L), Mr. S. Favereaux’s Lp(a) levels are considered to be very high [2, 26]. Mr. S. Favereaux’s diagnosis led to a recommendation for familial cascade screening, involving his children, sister, nephew, and niece, as recommended in the ESC/EAS consensus statement for familial hypercholesterolemia (FH) [25].

According to the ESC/EAS guidelines, Lp(a) assessment should be considered at least once in a lifetime to identify very high inherited Lp(a) levels [25]. Currently, French and European populations are insufficiently tested for Lp(a); less than 0.5% of the general population are tested and less than 5% of patients with CVD [23, 26]. Two reasons may explain this low testing rate. The first is simply the cost of testing. Even though it is a simple blood test, Lp(a) testing is not reimbursed in most European countries, including France. Second, there is a clear lack of knowledge about Lp(a) among practitioners, although this seems to be changing with new treatments on the horizon and changes in the recommendations in the last 5 years [2, 17, 25]. I am convinced that detecting an increase in Lp(a) as early as possible is the best thing to do: we have the resources to reassure families, and the screening consists of a simple blood test.

Ongoing debate surrounds the standardization of the Lp(a) assay because of inherent challenges including the lack of a definitive reference method, and the reporting of Lp(a) values as molar (nanomoles per liter [nmol/L]) or mass concentrations (grams per liter [g/L]) by different assays [27].

If Lp(a) testing reveals an elevated level, the first step is to explain the importance of this cardiovascular risk factor to the patient without causing them excessive concern. Of course, the same applies for other risk factors, such as hypertension, type 2 diabetes, or smoking. I give my patients with moderate to very high Lp(a) levels information on Lp(a) from the French patient association, Association Nationale des Hypercholestérolémies familiales et Lipoprotéines (a) (ANHET). Since its creation, I have been one of the scientific advisers of the association and I am very involved in many of their projects. The patient association plays an extremely important role as the interface between patients, doctors, and scientists, allowing us to learn from one another and move forward hand in hand. I also invite my patients to contact ANHET directly and follow the webinars that are regularly held with learned societies or other associations. These are excellent sources of accessible information. I know that Mr. S. Favereaux was able to attend some of them.

Secondly, it is important to explain to patients that risk factors are multiplicative, so other risk factors will have to be strictly managed to prevent the occurrence of an early cardiovascular event. Management of LDL-C, blood pressure, glucose, and lifestyle factors is recommended [17]. As Mr. S. Favereaux had an excellent lifestyle—he was a slim, physically active, non-smoker—I did not give him any specific recommendations on this point. My only advice was yoga to reduce his stress levels, because he has a stressful job as a prison guard.

The third message for patients is that, while there are currently few therapeutic options for reducing Lp(a), we are going to offer them all that can be done based on the current state of knowledge and treatments. Treatments should be optimized, e.g., lipid-lowering treatments should be intensified in patients with Lp(a) > 250 nmol/L (1.10 g/L) [2]. At the time of discovering Mr. S. Favereaux’s elevated Lp(a), he was already taking the maximum tolerated doses of secondary preventive therapies. Despite his pharmacologic treatment and interventional procedures, his coronary artery disease was always one step ahead of us. For this reason, I offered him two choices: enter a 5-year clinical trial of a drug designed to reduce Lp(a) levels, with a 50/50 chance of receiving the drug because the study was placebo-controlled; or undergo lipoprotein apheresis. This was not an easy decision, and while he was considering these options, he suffered a third coronary event, requiring emergency quadruple bypass surgery. It was a clear demonstration of the aggressiveness of his disease.

This did not prevent the start of lipoprotein apheresis, his chosen option, which has now been underway for almost 1 year. Lipoprotein apheresis remains an exceptional solution for purifying the blood of Lp(a) in patients with very high Lp(a) levels that are not sufficiently reduced by conventional treatments. With reductions of 60–75% after a single session, lipoprotein apheresis is an effective method for lowering Lp(a) levels [28]. However, this solution is expensive (€1400 per session, reimbursed by the health insurance system in France) and time-consuming for the patient, with a 2-h session every 2 weeks. In France, fewer than 150 people receive LDL or lipoprotein apheresis.

Novel treatments for elevated Lp(a) levels are based on modern techniques, such as antisense oligonucleotides (ASO) and small interfering RNAs (siRNAs), which target apo(a) production in the liver [29–32]. On the basis of a single injection per month, or even every 3 months, these molecules can reduce Lp(a) levels by 80–90% [29–32]. We are impatiently awaiting the results of the first international phase 3 study with an ASO, the HORIZON study of pelacarsen [33], which will be published in 2026. The HORIZON study (NCT04023552) is being conducted in patients with CVD and Lp(a) levels ≥ 150 nmol/L (0.7 g/L) [33]. If the results show a reduction in cardiovascular events associated with the targeted reduction in Lp(a) levels achieved with pelacarsen, we will have a new treatment option to propose to our patients between 2026 and 2030. For Mr. S. Favereaux, this would mean stopping lipoprotein apheresis, and no longer having to suffer the constraints associated with this procedure. By controlling this risk factor, we might be able to slow the natural history of coronary artery disease and reduce the severity of future cardiovascular events. In the slightly more distant future, we could also imagine these new treatments being offered as primary prevention to Mr. S. Favereaux’s children to prevent them from developing CVD. Other ongoing phase 3 studies of novel Lp(a)-lowering treatments include the OCEAN(a) and ACCLAIM-Lp(a) studies (NCT05581303 and NCT06292013) of the siRNAs olpasiran and lepodisiran, respectively, in patients with atherosclerotic CVD and elevated Lp(a) levels [34, 35]. Additionally, the ongoing BROADWAY and BROOKLYN studies (NCT05142722 and NCT05425745) are evaluating the selective cholesteryl ester transfer protein inhibitor obicetrapib in patients with atherosclerotic CVD and/or heterozygous FH with elevated LDL-C [36]. Recently completed phase 2 studies with the oral inhibitor of Lp(a) formation muvalaplin [37] and the siRNA zerlasiran [29] have demonstrated good tolerability and persistent reductions in Lp(a) levels of over 80% after 12 and 48 weeks of treatment, respectively. All these advances are very promising for our patients.

Beyond the recommendations of learned societies published over the last 5 years, it is also up to us, medical specialists and scientists, to raise awareness of Lp(a) so that all our colleagues—endocrinologists, cardiologists, and general practitioners—become aware of the importance of this risk factor. Physicians need to know that elevated levels of Lp(a) are common and have a real impact on people’s health.

Patient Association Perspective: Mr. Bernard Vercoustre for the ANHET Patient Association

Thirty years ago, at the age of 40 years, I had an MI due to FH and underwent a triple bypass. This explains my interest in the subject of dyslipidemia. I have been involved with the ANHET patient association for 8 years, since my retirement, and I became vice-president of ANHET 3 years ago.

The primary objective of ANHET is to promote knowledge of FH and Lp(a) to the public as widely as possible. In France, FH affects many people, around 300,000, but only 10% of them are treated. This highlights the scale of the work that still needs to be done to raise FH awareness despite improved knowledge over the last 10 years. Lp(a) became a subject of interest for ANHET 3 years ago, thanks to Prof. V. Durlach, who explained the similarities between its characteristics and FH, which convinced us to include it as a new target. The work of raising awareness about Lp(a) is even more important than it is for FH, with implications for an incredible 10 million people potentially impacted in France! In addition to educating the general population, we also aim to inform healthcare professionals and the health authorities about the risks associated with elevated Lp(a) levels, to ensure that they are properly addressed.

Our second objective is to increase the number of children screened for FH, including Lp(a). Because these conditions are hereditary, identification of children who are affected by the disease can help to diagnose adults and other family members and have a bigger impact.

Our third objective is to promote access to adequate treatments for each patient. In the case of FH, patients are lucky to have one drug available for almost the entire course of the disease. For Lp(a), however, this is not yet the case, though we are very optimistic about future therapies that should become available in the next few years.

The ANHET association has around 400 members, which may not sound like many, but ANHET is often noted as being as active as the larger patient associations. ANHET was set up more than 10 years ago as an extension of La Nouvelle Société Francophone d’Athérosclérose (NFSA) by several of its members to work together on specific issues relating to the FH subgroup of patients. ANHET is part of the European FH patient network, which brings together 31 organizations including the 27 European associations. As part of this European network, we track the same scientific research and share the latest advances in the field.

A patient association is needed to raise awareness on Lp(a), both among patients to encourage them to consult a doctor, but also among physicians to help them diagnose the condition. More generally, we also aim to help medical professionals to guide patients through the correct care pathway. We establish contact with patients through the doctors who have introduced them to our website or Facebook account or referred them directly to the association. We try to answer all their questions, when we can, or refer them to our scientific committee when the patient requires medical expertise. For FH, we have a solid network covering almost the whole of France, but because Lp(a) is a more recent topic of interest, we rely mainly on our scientific committee. We have strong links with the members of our scientific committee (Prof. V. Durlach, Prof. S. Béliard, and Prof. N. Peretti), which enables us to provide effective information to patients. ANHET also helps patients with referral to doctors who specialize in this field. A list of all the reference centers in France can be found on our website (https://www.anhet.fr/). We also provide patients with up-to-date information on the current state of knowledge and treatments. This can take the form of brochures or patient meetings. For example, patients with elevated Lp(a) receive information on the latest advances in treatments and new molecules that are currently in clinical trials, which gives them hope and reassurance.

Our actions have evolved over time. In the case of FH, we used to meet specialist doctors and patients affected by the disease, whereas now we are directing our actions towards the political sphere in order to be more effective. For example, on 21 October 2024, Prof. V. Durlach and I participated in a presentation on pediatric screening for FH to the Chairman of the Senate Social Affairs Committee, Mr. Philippe Mouiller; the presentation had been prepared in collaboration with 14 learned scientific societies. Today, we feel that the importance of FH is increasingly recognized, and we hope that our experience with FH will also benefit patients with Lp(a), as we take on that battle.

In France, much more could be done to raise awareness of the importance of early diagnosis and treatment of FH and elevated Lp(a) to limit the risk these conditions pose to affected individuals. It should be remembered that CVD is the leading cause of death worldwide [38], and that FH and elevated Lp(a), which are cardiovascular risk factors, are major contributors. Worldwide, the current trend is more towards treatment than prevention. By making patients aware of these pathologies from a young age, we can help them to make the most of their chances, for example by adopting a healthy diet and lifestyle, and/or by early initiation of appropriate therapies. The case of Mr. S. Favereaux, which illustrates the most serious consequences of an elevated Lp(a) level, reinforces the idea that we need to raise awareness of this condition to intervene as early as possible. Knowing that our children, if diagnosed with an elevated Lp(a) level, will be able to have preventive treatment, is a great source of hope. In France and in other countries around the world, we are fortunate to have support for research in this field. This should lead to a new way of treating patients with elevated Lp(a) level: an injectable drug every month, or perhaps every year, which will make everyday life easier.

Widespread screening for Lp(a) is an essential first step in enabling patients and, by extension, their families to know whether they are affected by this condition. Such a diagnosis impacts more than just the patient’s physical health; it also affects their psychological state and their family. Therefore, it is essential to put in place an effective healthcare system between detection and treatment. This is why ANHET must fight relentlessly, with the help of patients, doctors and scientists, to get health policies moving. Progress is being made, but there is still a long way to go.

Supplementary Information

Below is the link to the electronic supplementary material.

Author Contributions

Stéphane Favereaux, Vincent Durlach, and Bernard Vercoustre contributed to and commented on previous versions of the manuscript. All authors read and approved the final manuscript.

Funding

The journal’s Rapid Service Fee was funded by Novartis. The authors were responsible for all content and editorial decisions. The authors received no payment for the development of this manuscript. Novartis checked the manuscript for scientific accuracy only.

Data Availability

Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.

Declarations

Conflict of Interest

Vincent Durlach has participated in clinical trials for Amgen, Sanofi, and Bioprojet; attended conferences, symposia, or training activities for Amgen, Sanofi, Servier, MSD, and Proofs and Practices; and has received travel support (transport, hotel, meals) to attend conferences from Laboratoires Servier, Amgen, Sanofi, and Novo Nordisk. Stéphane Favereaux and Bernard Vercoutre declare that they have no competing interests. Novartis provided funding for medical writing support in the development of this manuscript; this funding was not paid to the authors.

Ethical Approval

This article is based on previously conducted studies and does not contain any new studies with human participants or animals performed by any of the authors. The patient has consented to publication of this report.