# The Changing Landscape of Atherosclerosis: What Every Patient Should Know

Atherosclerosis—the silent buildup of fatty plaque inside artery walls—has undergone a dramatic transformation in recent decades. Once considered a disease of middle-aged Western men, it now contributes to the majority of deaths worldwide, striking younger people, more women, and individuals from diverse ethnic backgrounds than ever before. This comprehensive review by Dr. Peter Libby of Brigham and Women's Hospital and Harvard Medical School examines how shifting risk factors, newly recognized inflammatory pathways, and even bone marrow mutations are reshaping our understanding of the disease. The findings point to exciting new treatment opportunities, including therapies that target inflammation directly and offer hope even for patients whose cholesterol is already well controlled.

# The Changing Landscape of Atherosclerosis: What Every Patient Should Know

## Table of Contents

- Key Points
- Background: Understanding Atherosclerosis and Why It Matters
- The Changing Face of Atherosclerosis: Who Gets It Now?
- Reassessing Cholesterol: From LDL to Triglycerides and Lipoprotein(a)
- Inflammation: The Hidden Driver of Atherosclerosis
- Inside the Artery Wall: How Plaques Form and Progress
- The Bone Marrow Connection: Clonal Haematopoiesis
- Clinical Implications: What This Means for Treatment
- Limitations: What We Still Don't Know
- Recommendations for Patients
- Frequently Asked Questions
- Source Information

## Key Points

- Atherosclerosis now causes most deaths worldwide, affecting more younger women, minorities, and developing countries than before.
- LDL, triglyceride-rich lipoproteins, and lipoprotein(a) all cause atherosclerosis; inflammation is a proven driver of heart attacks and strokes.
- Clinical trials CANTOS, COLCOT, and LoDoCo2 showed anti-inflammatory drugs reduce recurrent events even with controlled cholesterol.
- Clonal haematopoiesis, age-related bone marrow mutations, is a common and potent cardiovascular risk factor in people over 70.
- Know LDL, triglycerides, and hsCRP; manage abdominal weight, sleep, and sugary drinks; lifestyle reduces risk at every genetic level.

## Background: Understanding Atherosclerosis and Why It Matters

Atherosclerosis is the disease process in which cholesterol, fat, and inflammatory cells accumulate inside the walls of arteries, forming plaques that can narrow blood vessels or rupture and trigger blood clots. It is the underlying cause of several life-altering conditions: **myocardial infarction** (heart attack), **ischaemic cardiomyopathy** (weakened heart muscle from reduced blood flow, the most common cause of heart failure), **strokes** (which can rob people of independence, mobility, cognition, or the ability to communicate), and **peripheral arterial disease** (which limits activity and can jeopardize limbs).

For decades, atherosclerosis was viewed primarily as a problem of industrialized, wealthy nations. But the world has witnessed an "epidemiological transition": improved sanitation, vaccination, and treatment of acute infections have dramatically reduced deaths from communicable diseases in developing countries. As a result, more people now survive long enough to develop chronic diseases like atherosclerosis.

This transition has created a phenomenon called **"morbidity extension"** in the developing world. Many individuals escape early death from infection, but they must bear the burden of chronic cardiovascular disease alongside arthritis, depression, and other long-term health impediments. **Today, the major pool of risk for developing cardiovascular disease is no longer in Western countries but in the more populous developing world**, and atherosclerotic cardiovascular disease now accounts for the majority of deaths worldwide.

The numbers are stark. According to the Global Burden of Disease study, the worldwide prevalence of ischaemic heart disease has risen from about **100 million cases in 1990 to over 180 million cases in 2019**. Perhaps even more concerning, in some regions of the United States and the United Kingdom, the decline in heart disease prevalence that had been attributed to successful risk-factor control has **slowed or even halted between 2014 and 2019**. We may be losing ground in prevention even in high-income countries.

## The Changing Face of Atherosclerosis: Who Gets It Now?

The classic picture of a heart attack candidate was a middle-aged white man with high blood pressure, high cholesterol, and a cigarette habit. That image has evolved considerably. While individuals in mid-life still face risk, coronary artery disease now affects an increasing number of **younger women**, and—as populations age—the **very old** now account for a growing proportion of cardiac patients.

Several positive trends are worth celebrating: effective treatments for high blood pressure and lipid disorders have improved control of hypertension and hypercholesterolemia, and reductions in smoking (along with decreased second-hand smoke exposure) have gained a foothold in many societies. However, new challenges have emerged to replace the old ones.

### The Obesity Epidemic and Metabolic Syndrome

An epidemic of obesity has swept across the world. Excess body fat, especially fat accumulated in the abdomen, and fatty liver drive **insulin resistance**, which sets the stage for diabetes and links closely with hypertension. This cluster of conditions—collectively known as the **metabolic syndrome**—includes increased waist circumference, low HDL (protective) cholesterol, high blood pressure, and elevated fasting blood glucose.

The prevalence of the metabolic syndrome in the United States **rose by 35% from 1988–1994 to 2007–2012**. Women, members of minoritized groups, and populations in developing countries now bear an increasing burden of atherosclerotic cardiovascular disease.

There are important ethnic differences in how the body handles excess fat. **Asian and South Asian individuals**, as well as people of some ethnicities in Central and South America, can develop metabolic problems—including glucose intolerance—at lower abdominal girths than white individuals. Given the large populations in Asia, Central and South America, increased prosperity with shifts away from traditional diets, continuing tobacco use, and the growing burden of obesity and diabetes present an enormous public health challenge.

### Air Pollution, Diet, and Other Modern Exposures

Beyond obesity and insulin resistance, researchers are investigating additional environmental contributors: **air pollution, environmental noise, transitions from traditional diets to less healthy ones, and impaired sleep** may all be mitigating some of the advances made in prevention. Among the most readily remedied dietary shifts, the consumption of **sugar-sweetened beverages, often high in fructose**, may contribute to obesity and its adverse metabolic consequences. Modifiable risk factors contribute enormously to the global burden of ischaemic heart disease.

## Reassessing Cholesterol: From LDL to Triglycerides and Lipoprotein(a)

### LDL: Still the Prime Suspect

**Low-density lipoprotein (LDL) cholesterol**—the "bad" cholesterol—is encircled by its signature protein component, apolipoprotein B, and it definitively causes atherosclerosis. Scientists note that if the entire population maintained LDL concentrations similar to those of a newborn baby (or of most adult animals), **atherosclerosis might well become an orphan disease**.

The duration and extent of exposure to above-ideal LDL concentrations matters enormously. Lifelong elevated LDL levels have already sown the seeds of atherosclerosis in millions of people, increasing their lifetime risk of cardiovascular disease. Treating children and adolescents with cholesterol-lowering drugs, however, presents many challenges.

Even with effective treatments for LDL, blood pressure, and other traditional risk factors, a **considerable residual risk** for cardiovascular events remains. Recent clinical trials of novel heart medications, conducted in patients already receiving optimal standard therapy, found that **about 1 in 20 patients will have a recurrent ischaemic event in the year after an acute coronary syndrome**. In the United States, **1 in 10 individuals who survive an acute heart attack will require readmission to the hospital within one month**—at considerable personal and societal cost.

### The HDL Story: A Paradigm Shift

For decades, doctors believed that **high-density lipoprotein (HDL)**—the "good" cholesterol—protected against atherosclerosis. That belief has been seriously challenged. Recent human genetic studies, along with the failure of several independent drug trials that raised HDL levels without reducing heart events, have **called into question HDL's protective effect**.

However, the story is not entirely closed. **Mendelian randomization studies** (which use genetic variations to infer cause-and-effect relationships) that corrected for "pleiotropy" (one gene influencing multiple traits) have provided some support for HDL's protective role. Moreover, the *function* of HDL particles—such as their capacity to remove cholesterol from cells (a process called **cholesterol efflux**) or their anti-inflammatory actions—may still protect against atherosclerosis, even if the simple measurement of total HDL cholesterol level does not tell the whole story.

### The Rise of Triglyceride-Rich Lipoproteins (TGRL)

For many years, plasma triglyceride levels were overlooked as a risk factor. The belief in HDL's protective effect led researchers to "adjust" triglycerides for HDL, which attenuated the risk attributed to triglyceride-rich lipoproteins (TGRL). That approach was a mistake.

A recent ranking of lipid risk factors has **demoted HDL as a protective factor and identified TGRL as a potent predictor of cardiovascular risk**. Unlike HDL, contemporary human genetic studies strongly support a causal role for TGRL in atherosclerosis and its complications.

Here is how the biology works: a crucial enzyme called **lipoprotein lipase** normally breaks down triglycerides in TGRL particles. Several proteins regulate this enzyme:

-
**Apolipoprotein CIII**, **ANGPTL3**, and **ANGPTL4** inhibit lipoprotein lipase, causing TGRL particles to accumulate.
-
**Apolipoprotein V** augments lipoprotein lipase activity and enhances TGRL clearance.

People who inherit genetic variants that raise TGRL experience more atherosclerotic events, while those with variants that lower TGRL have better outcomes. Interestingly, the triglyceride component itself does not appear to be what makes TGRL dangerous. Like LDL, TGRL particles carry apolipoprotein B and contain cholesterol, which they can deliver directly to macrophages (scavenger cells) inside artery plaques. TGRL also provoke inflammation, in part because of their apolipoprotein CIII content. In fact, **TGRL concentrations correlate with inflammatory status better than LDL itself does**.

This refocusing on TGRL as a causal risk factor—combined with the disappointing results of HDL-raising therapies—has significant treatment implications that we will explore later.

### Lipoprotein(a): A Genetic Risk Factor You Can't Change with Diet

Another important player is **lipoprotein(a)**, a special form of LDL that has long been associated with atherothrombotic (plaque + clot) risk. Lipoprotein(a) consists of an LDL particle whose apolipoprotein B has bound covalently to a second protein called apolipoprotein(a). This particle carries oxidized lipids and may inhibit the body's ability to break down blood clots, because it structurally resembles plasminogen (a key clot-dissolving protein).

Concordant human genetic studies provide persuasive evidence that elevated lipoprotein(a) is not just associated with, but actually **causes**, both atherosclerosis and **calcific aortic valve disease**. This is a genetic risk factor that patients cannot modify through diet or exercise—though targeted therapies are in development.

## Inflammation: The Hidden Driver of Atherosclerosis

Beyond abnormal cholesterol levels, a convincing body of experimental and clinical evidence now shows that **inflammation participates fundamentally in atherosclerosis and the triggering of heart attacks and strokes**. Importantly, inflammation does not replace or minimize the role of lipids; rather, inflammatory responses are the pathways that *link* lipids and other traditional risk factors to the disease. For example, remnant lipoprotein levels show links with C-reactive protein (CRP), a biomarker of inflammation, and substantial evidence implicates inflammation in high blood pressure.

### The Immune System's Dual Role

The immune system plays a complex and often contradictory role in atherosclerosis. Both branches of immunity are involved:

-
**Innate immunity** (the older, non-specific arm of the immune system) relies largely on cytokines (chemical messengers) and macrophages (scavenger cells). A simple blood test for **high-sensitivity C-reactive protein (hsCRP)** can measure overall innate immune activity and is a validated, clinically useful gauge of atherosclerotic risk—even independently of all traditional risk factors.
-
**Adaptive immunity** (the targeted, memory-based arm) involves T lymphocytes and B lymphocytes. T-helper 1 (Th1) cells generally *aggravate* atherosclerosis, while T-helper 2 (Th2) and regulatory T cells (Tregs) can *mute* the process. B1 cells produce natural IgM antibodies that *mitigate* experimental atherosclerosis, while B2 cells can produce antibodies that drive the disease. One candidate target identified from mouse studies is the mitochondrial enzyme **ALDH4A1**.

### Metabolic Connections

New links between inflammation, immunity, and metabolism have recently emerged. Inflammatory activation of immune cells and endothelial cells shifts their metabolism toward **glycolysis** (sugar-burning). Altered **tryptophan metabolism** has also drawn attention: cytokines induce an enzyme called indolamine dioxygenase, which breaks down tryptophan and increases production of kynurenine and its metabolites. This pathway may actually serve a counter-regulatory function by dampening inflammation and the cellular immune response.

### Proof from Clinical Trials: CANTOS, COLCOT, and LoDoCo2

The most dramatic validation of the inflammation theory came from large clinical trials showing that **targeting inflammation can reduce cardiovascular events**—even in patients already receiving optimal cholesterol-lowering and blood-pressure-lowering therapy.

**The CANTOS trial** (Canakinumab Anti-inflammatory Thrombosis Outcomes Study) tested canakinumab, an antibody that neutralizes the proinflammatory cytokine IL-1β, in patients with stable coronary artery disease who had experienced a heart attack at least one month earlier. Participants had evidence of ongoing inflammation (hsCRP above 2 mg/L) despite standard medical therapy, and their baseline LDL was approximately 2 mM (81 mg/dL)—already quite well controlled.

Results of CANTOS:

-
**15% relative reduction** in the risk of recurrent heart attack, stroke, or cardiac death with anti-inflammatory therapy.
- In an "on-treatment" analysis, patients who responded with a greater-than-median reduction in hsCRP had a **26% reduction** in the primary endpoint and a decrease in all-cause mortality.
- Because IL-1β helps fight infections, there was a small but statistically significant increase in infections (including fatal infections) in patients receiving canakinumab.
- Exploratory analyses found a highly significant reduction in incident and fatal lung cancer, which counterbalanced the infection risk.

**The COLCOT trial** (Colchicine Cardiovascular Outcomes Trial) tested colchicine—a natural plant-derived anti-inflammatory medication long used for gout and pericarditis—in patients treated early (within 4–30 days) after an acute coronary syndrome. The results:

-
**23% reduction** in the composite primary endpoint, driven primarily by fewer revascularization procedures (procedures to restore blood flow).
- The incidence of pneumonia **more than doubled** in the colchicine-treated group.

**The LoDoCo2 study** (Low Dose Colchicine 2) confirmed the efficacy of low-dose colchicine in reducing recurrent cardiovascular events after acute coronary syndromes.

However, not all anti-inflammatory interventions have succeeded. A trial of **low-dose weekly methotrexate**—a common anti-inflammatory drug—did not improve cardiovascular outcomes, nor did it meaningfully reduce inflammation in the population studied.

### Obesity, Environment, and Inflammation

Adipose (fat) tissue is not inert—it abounds with inflammatory cells and produces proinflammatory mediators. Inflammation mechanistically links obesity, insulin resistance, and atherosclerotic risk. Environmental factors including **air pollution, noise, disturbed sleep, and other stressors** also appear to increase cardiovascular risk, at least in part by activating inflammatory pathways.

## Inside the Artery Wall: How Plaques Form and Progress

Understanding the disease at the cellular level helps explain why new treatments work. A normal artery has three layers: the innermost **intima** (in direct contact with blood), the middle **media** (containing smooth muscle cells), and the outer **adventitia**.

Under healthy conditions, the endothelial cells that line the intima do not attract blood leukocytes (white blood cells). But when activated by proinflammatory cytokines or other irritants related to cardiovascular risk factors, endothelial cells express adhesion molecules such as **VCAM-1**, which interact with their partners (VLA4) on blood monocytes and lymphocytes. This causes the white blood cells to roll along the vessel surface, stick, and eventually migrate into the intima.

Within the intima, **foam cells**—lipid-laden scavenger cells—form by taking up cholesterol. Some foam cells arise from blood monocytes that mature into macrophages. Remarkably, recent evidence in mice shows that **smooth muscle cells can undergo metaplasia** (transform into a different cell type) and give rise to foam cells that carry markers identical to macrophages. T lymphocytes, though fewer in number, orchestrate many functions of these immune cells.

As the plaque grows, smooth muscle cells (both resident in the intima and migrated from the media) produce extracellular matrix—the structural "scaffolding" of the plaque. Growth factors like **PDGF** promote smooth muscle migration and replication.

Plaque progression reflects an ongoing struggle between factors that promote and those that mute the disease:

-
**Pro-inflammatory factors (promote disease):** IL-1, TNF, M-CSF, and IFNγ (produced by Th1 cells) stimulate inflammation and plaque growth.
-
**Anti-inflammatory factors (protect):** IL-10 (from Th2 cells), TGFβ (from regulatory T cells), and natural IgM antibodies from B1 cells quell inflammation and promote tissue stability.

A critical process called **efferocytosis**—the engulfment of dying or dead cells by scavenger cells—helps keep plaques stable. When efferocytosis is inefficient, debris from dead cells accumulates, promoting the formation of the plaque's central lipid core. Researchers now view atherosclerosis as a years-long battle between proliferation and death, involving proinflammatory, anti-inflammatory, and pro-resolving mediators.

## The Bone Marrow Connection: Clonal Haematopoiesis

One of the most surprising recent discoveries links atherosclerosis to the bone marrow. As we age, we accumulate **somatic mutations** (acquired, not inherited genetic changes) in the hematopoietic stem cells in our bone marrow—the cells that produce all blood cells. These mutations occur in genes that, when mutated, can also drive acute leukemia. However, researchers seeking the origins of leukemia found something unexpected: **apparently healthy individuals without any blood cancer can generate clones of leukocytes bearing these mutations** in their circulating blood.

This condition is called **clonal haematopoiesis**. It represents a previously unrecognized but common and potent age-related contributor to cardiovascular disease risk. The prevalence in individuals aged 70 **exceeds 10%**, and the burden increases with further ageing. This discovery opens an entirely new window into why heart disease risk rises so dramatically with age—and may eventually lead to personalized screening or treatments targeting these mutated clones.

## Clinical Implications: What This Means for Treatment

This evolving understanding of atherosclerosis has opened multiple new avenues for prevention and treatment:

1.
**Anti-inflammatory therapy is now proven.** The CANTOS, COLCOT, and LoDoCo2 trials demonstrate that modulating inflammation reduces cardiovascular events independent of cholesterol lowering. Colchicine is already becoming part of standard care for selected patients after heart attacks. Because canakinumab increased infections, its use requires careful patient selection, but the lung cancer finding suggests intriguing possibilities.
1.
**Triglyceride-rich lipoproteins are a treatment target.** The strong human genetic evidence that TGRL cause atherosclerosis has renewed interest in therapies that lower TGRL, including drugs targeting apolipoprotein CIII, ANGPTL3, and ANGPTL4—the proteins that inhibit lipoprotein lipase.
1.
**Lipoprotein(a) is on the radar.** With convincing genetic evidence of causality, new drugs targeting lipoprotein(a) are in development. This is particularly important for patients with a family history of early heart disease or aortic valve disease.
1.
**Genetic risk scores may enable earlier prevention.** Because genetic risk can be detected from birth, these scores may inform early, targeted prevention strategies in younger individuals with an inherited predisposition. Importantly, **lifestyle measures appear to mitigate cardiovascular risk across the entire spectrum of genetic risk**—so even those with high genetic risk can benefit from healthy habits.
1.
**Clonal haematopoiesis may become a biomarker.** Testing for these bone marrow mutations could someday identify older adults at especially high cardiovascular risk, potentially guiding more aggressive prevention.

One important caveat: genetic risk scores' ability to improve prediction of events beyond traditional algorithms remains controversial, so they are not yet ready for routine clinical use in all settings.

## Limitations: What We Still Don't Know

This review article synthesizes current knowledge, but important uncertainties remain:

-
**HDL's role is not fully settled.** Although raising HDL cholesterol has failed to reduce events, the functional properties of HDL (cholesterol efflux, anti-inflammatory actions) may still protect. Standard blood tests may not capture these functions.
-
**Animal models don't perfectly mirror human disease.** For example, humans (but not many small laboratory animals) have resident smooth muscle cells in the intima, which affects how plaques develop. Some findings in mice may not translate to humans.
-
**Anti-inflammatory treatments have side effects.** Both canakinumab (increased infections) and colchicine (more than doubled pneumonia incidence) carry risks that must be weighed against benefits.
-
**Genetic risk scores remain controversial** in their ability to improve prediction beyond traditional risk calculators.
-
**Observational associations** (such as those linking air pollution, noise, and disturbed sleep to heart disease) cannot prove causation, although the inflammatory mechanisms provide plausible biological explanations.
- The **trajectory of prevention is uncertain**: the slowing or halting of heart disease decline in some US and UK regions between 2014 and 2019 suggests that current prevention strategies may be losing ground against rising obesity and other modern exposures.

## Recommendations for Patients

Based on this evolving science, here are practical steps patients can discuss with their healthcare team:

1.
**Know your numbers beyond LDL.** Ask about your triglyceride level and, if you have a family history of early heart disease or aortic valve problems, ask whether testing for lipoprotein(a) is appropriate. TGRL (triglyceride-rich lipoproteins) are now recognized as causal risk factors, not just bystanders.
1.
**Don't stop your statin or other LDL-lowering therapy.** LDL remains a definitive cause of atherosclerosis. Reducing lifelong exposure to elevated LDL is fundamental—even in the era of anti-inflammatory drugs.
1.
**Ask about inflammation.** A simple blood test for hsCRP can gauge inflammatory status. If your hsCRP is elevated despite good cholesterol control, talk with your doctor about whether anti-inflammatory strategies—such as low-dose colchicine—might be appropriate, particularly if you've already had a cardiovascular event.
1.
**Protect your sleep.** Disturbed sleep is increasingly recognized as a contributor to cardiovascular risk, in part through inflammatory pathways. Prioritizing good sleep hygiene is a low-cost, evidence-informed strategy.
1.
**Manage abdominal weight.** Excess fat around the abdomen (visceral adiposity) and fatty liver drive insulin resistance and inflammation. Even modest weight loss can meaningfully reduce metabolic risk. Remember that people of Asian, South Asian, and Central/South American descent may develop metabolic problems at lower waist measurements than white individuals—so don't rely on one-size-fits-all thresholds.
1.
**Minimize environmental exposures where possible.** Air pollution, environmental noise, and second-hand smoke all contribute to cardiovascular risk. Reducing exposure—through air purifiers, avoiding high-traffic areas during peak pollution, or noise protection—may help.
1.
**Limit sugar-sweetened beverages.** Drinks high in fructose contribute to obesity and its adverse metabolic consequences. This is one of the most readily remedied dietary shifts.
1.
**Know that lifestyle helps at every genetic risk level.** Even if you carry a high genetic risk score, lifestyle measures mitigate risk across the entire spectrum of genetic predisposition. Genes are not destiny.
1.
**If you've had a heart attack, don't underestimate residual risk.** Even on optimal therapy, about 1 in 20 patients will have another event within a year, and 1 in 10 survivors of acute heart attack in the US are readmitted within a month. Staying on all prescribed medications and attending cardiac rehabilitation are critical.

## Frequently Asked Questions

### What is atherosclerosis and why does it matter?

Atherosclerosis is the buildup of cholesterol, fat, and inflammatory cells inside artery walls. Plaques can narrow blood vessels or rupture, causing blood clots. It is the underlying cause of heart attacks, heart failure, strokes, and peripheral artery disease. Many people do not know they have it until a serious event happens.

### I already had a heart attack. Even with treatment, how likely is another one?

In recent clinical trials, about 1 in 20 patients had a recurrent heart attack, stroke, or cardiac event within a year after an acute coronary syndrome, despite optimal standard therapy. In the United States, 1 in 10 heart attack survivors is readmitted to the hospital within one month. Staying on medications and attending cardiac rehabilitation are critical.

### Is LDL cholesterol the only cholesterol that causes heart disease?

LDL cholesterol definitively causes atherosclerosis. However, triglycerides and triglyceride-rich lipoproteins are now recognized as causal risk factors too. Lipoprotein(a), a genetic form of LDL, also causes atherosclerosis and aortic valve disease. Ask your doctor about your triglyceride level and, if you have a family history of early heart disease, whether testing for lipoprotein(a) is appropriate.

### What is the hsCRP blood test and why does it matter?

hsCRP stands for high-sensitivity C-reactive protein, a blood test that measures overall innate immune activity and inflammation. It is a validated, clinically useful gauge of atherosclerotic risk, even independently of traditional risk factors. If your hsCRP is elevated despite good cholesterol control, discuss anti-inflammatory strategies with your doctor, especially if you have already had a cardiovascular event.

### Can anti-inflammatory drugs reduce heart attack risk?

Yes. In the CANTOS, COLCOT, and LoDoCo2 trials, anti-inflammatory therapies reduced recurrent cardiovascular events in patients already on optimal cholesterol and blood pressure treatment. Colchicine reduced events by 23% in early post-heart-attack patients. However, these drugs have side effects, including increased infections, so they are not for everyone. Ask your doctor if you are a candidate.

### What can I do about belly fat, sleep, and sugary drinks?

Excess abdominal fat and fatty liver drive insulin resistance and inflammation, increasing heart risk. Disturbed sleep is a contributor. Sugar-sweetened beverages high in fructose contribute to obesity. Even modest weight loss helps. People of Asian, South Asian, and Central or South American descent may develop metabolic problems at lower waist measurements, so do not rely on one-size-fits-all thresholds.

### Should I be tested for lipoprotein(a) if heart disease runs in my family?

Elevated lipoprotein(a) is a genetic risk factor that causes both atherosclerosis and calcific aortic valve disease. It is not something you can change through diet or exercise, but targeted therapies are in development. If you have a family history of early heart disease or aortic valve problems, ask your healthcare team whether testing is appropriate.

## Source Information

This patient-friendly article is based on a peer-reviewed scientific review published in the journal *Nature*.

-
**Original article title:** The changing landscape of atherosclerosis


---
Publisher: Diagnostic Detectives Network (https://diagnosticdetectives.com) — independent multi-expert medical second opinions, worldwide, private-pay.
Author byline: Anton Titov, MD, PhD. Contact: https://diagnosticdetectives.com/pages/contact
Canonical page: https://diagnosticdetectives.com/products/the-changing-landscape-of-atherosclerosis-what-every-patient-should-know