# Understanding Atherosclerosis: New Discoveries in Prevention, Risk Assessment, and Treatment Atherosclerosis—the gradual buildup of plaque inside artery walls—remains one of the world's leading causes of stroke and heart attack. This comprehensive patient-friendly review explains the latest scientific breakthroughs in understanding why atherosclerosis develops, how doctors can better predict who is at highest risk, and what new treatments are changing the way we prevent vascular disease. The article covers surprising findings about how gut bacteria influence heart health, new cholesterol-lowering medications called PCSK9 inhibitors, and advanced imaging techniques that allow doctors to "see" dangerous plaque before it causes a stroke. # Understanding Atherosclerosis: New Discoveries in Prevention, Risk Assessment, and Treatment ## Table of Contents - Key Points - Why This Research Matters - The Surprising Role of Gut Bacteria in Heart Health - Kidney Disease and Heart Risk: A Dangerous Link - New Cholesterol-Lowering Treatments: PCSK9 Inhibitors - Treating Arteries Instead of Risk Factors - Assessing Prognosis in Carotid Atherosclerosis - Measuring Carotid Plaque Burden - Transcranial Doppler: Detecting Dangerous Emboli - Plaque Characteristics That Predict Risk - What This Means for Patients - Limitations of This Research - Recommendations for Patients - Frequently Asked Questions - Source Information ## Key Points - Atherosclerosis is plaque buildup in arteries; rupture can cause heart attack or stroke. - Gut bacteria convert red meat and egg yolk into TMAO, raising cardiovascular risk. - PCSK9 inhibitors lower LDL cholesterol and cardiovascular events by about 50%. - Treating arteries directly cut 2-year stroke risk from 8.8% to 1% in asymptomatic stenosis. - Only 10–15% of asymptomatic carotid stenosis patients benefit from surgery or stenting. ## Why This Research Matters Atherosclerosis (hardening and narrowing of the arteries due to plaque buildup) is best understood as a response to injury in the artery wall. Blood flow disturbances damage the delicate inner lining of arteries (the endothelium), triggering a chain reaction: platelets clump together, white blood cells called macrophages penetrate the artery wall, and inflammation and oxidative stress take hold. Over time, oxidized low-density lipoprotein (LDL, or "bad" cholesterol) accumulates and smooth muscle cells multiply, creating a scar-like plaque that can eventually rupture and cause a stroke or heart attack. Traditional risk factors identified in the landmark Framingham Heart Study include high blood pressure, smoking, elevated LDL cholesterol, diabetes, and left ventricular hypertrophy (an enlarged heart muscle, which essentially reflects the cumulative effect of blood pressure over many years). However, despite treating these risk factors, routine therapy has reduced cardiovascular risk in most trials by only about 9–30%, leaving a frustrating **residual risk of 70–80%**—meaning most patients still face substantial danger even with standard care. This review, written by Dr. J. David Spence of the Stroke Prevention & Atherosclerosis Research Centre at Western University in London, Ontario, Canada, focuses on recent advances that promise to close that gap, including new insights into nutrition, gut bacteria, and more precise ways to identify which patients truly need aggressive intervention. ## The Surprising Role of Gut Bacteria in Heart Health One of the most revolutionary discoveries in recent years is that the trillions of bacteria living in your intestines—collectively called the **intestinal microbiome**—play a major role in how diet affects atherosclerosis. This finding helps explain why the Mediterranean diet is so beneficial and why certain foods are more harmful than previously thought. Researchers led by Dr. Stanley Hazen's group at the Cleveland Clinic made a key discovery: two common dietary substances are converted by intestinal bacteria into dangerous compounds. Phosphatidylcholine, found abundantly in **egg yolk**, and carnitine, found in **animal flesh** (with four times as much in red meat as in fish or chicken), are transformed by gut bacteria into a compound called trimethylamine (TMA)—the same substance that gives "uremic breath" its fishy odor in kidney failure patients. TMA travels to the liver, where it is oxidized into **trimethylamine N-oxide (TMAO)**, a compound that causes atherosclerosis in animal models and is strongly linked to cardiovascular events in humans. In a striking study of patients undergoing coronary angiography (a procedure to examine blood vessels of the heart), researchers found that patients who consumed a test dose of two hard-boiled eggs and produced high levels of TMAO had dramatically increased risk. Specifically, patients in the **top quartile (highest 25%) of TMAO levels had a 2.5-fold increase in the 3-year risk of stroke, death, or myocardial infarction (heart attack)**. Perhaps the most encouraging finding is that this process is modifiable. **Vegans who consumed L-carnitine did not produce TMAO** because they lacked the specific intestinal bacteria that convert carnitine into TMA. This proves that the intestinal microbiome can be changed. One novel treatment approach under investigation involves eradicating harmful bacteria with antibiotics and then recolonizing the gut with beneficial bacteria through stool transplantation—a strategy entirely analogous to the successful treatment of *Clostridium difficile* infections through "repopulation" therapy. Dr. Spence's research group is currently studying this possibility. ## Kidney Disease and Heart Risk: A Dangerous Link Patients with renal failure (kidney failure) face extraordinarily high cardiovascular risk, and recent research has uncovered new reasons why. It has long been known that kidney failure patients have elevated levels of total homocysteine (tHcy), an amino acid linked to heart disease. But tHcy accounts for only about **20% of the effect of impaired renal function on carotid plaque** (plaque in the neck arteries that supply the brain). Additional culprits include elevated levels of thiocyanate and asymmetric dimethylarginine (ADMA), a compound that blocks nitric oxide—a molecule that helps blood vessels relax and stay healthy. These findings are not new. What is newly recognized is that **metabolic products of the intestinal microbiome are normally excreted in urine**, so patients with renal failure accumulate dangerously high levels of TMAO. This not only accelerates the decline of remaining kidney function but also increases cardiovascular risk. Other bacterial metabolic products likely contributing to cardiovascular risk in kidney failure include indoxyl sulfate, indole-3-acetic acid, p-cresyl sulfate, and phenylacetylglutamine. The practical implication is clear: patients at risk of cardiovascular disease should limit their intake of meat and egg yolk **not only because of the high cholesterol content, but also because of the carnitine in meat (particularly red meat) and the phosphatidylcholine in egg yolk**. This dietary caution is especially critical for patients with renal failure. ## New Cholesterol-Lowering Treatments: PCSK9 Inhibitors For decades, statins (drugs that block the rate-limiting step in cholesterol synthesis, an enzyme called HMG-CoA reductase) have been the backbone of cholesterol treatment. Combining statins with ezetimibe, a drug that blocks cholesterol absorption in the intestines, further enhances their effects. However, many patients cannot tolerate statins. While there are many myths about statin side effects—including unfounded claims about liver toxicity, kidney damage, brain hemorrhage, cataracts, and cognitive decline—the true, causally related adverse effects include **myopathy (muscle pain and weakness) and a slightly increased risk of diabetes**. These effects likely result from impairment of mitochondrial function (the energy-producing structures in cells) caused by depletion of coenzyme Q10 (ubiquinone), which is needed for mitochondria to work properly. An entirely new approach to lowering LDL cholesterol has recently become available: blocking the action of an enzyme called **proprotein convertase subtilisin-kexin type 9 (PCSK9)**. This enzyme normally breaks down LDL receptors—the "docking stations" on liver cells that remove LDL from the bloodstream. By preventing the breakdown of these receptors, PCSK9 inhibitors increase their number and duration of action, allowing the liver to clear more LDL from the blood. Clinical trials show that PCSK9 inhibitors **lower LDL cholesterol and cardiovascular events by approximately 50%**, even in patients who cannot tolerate statins or who have genetic conditions causing very high cholesterol. The evidence for the importance of lifelong LDL reduction is compelling: people born with a hereditary condition causing naturally low LDL levels have an approximately **95% reduction in coronary risk** compared to the general population. This suggests that aggressive LDL lowering, if achieved early and sustained, can nearly eliminate heart attacks. Unfortunately, current approaches to blocking PCSK9—monoclonal antibodies or RNA interference—are extremely (prohibitively) expensive. However, researchers are hopeful that far less costly small-molecule medications will be developed in the near future, making this revolutionary treatment accessible to far more patients. ## Treating Arteries Instead of Risk Factors A fundamentally different philosophy of vascular prevention has emerged: instead of merely treating risk factors like blood pressure and cholesterol levels, why not directly measure and treat the actual disease—the plaque burden in the arteries? This paradigm, called **"treating arteries instead of treating risk factors,"** was developed in response to a sobering realization: following standard treatment guidelines was failing half of all patients. Those patients had plaque progression (their arterial plaque was getting worse), and their risk of cardiovascular events was **twice that of patients with stable plaque or plaque regression**, even after controlling for coronary risk factors. Dr. Spence's group initiated this approach in 2003, and by 2010 the results were dramatic. In patients with asymptomatic carotid stenosis (narrowing of the neck arteries that had not yet caused symptoms), the "treating arteries" approach achieved remarkable results: - **Plaque progression was halved**—the proportion of patients whose plaque continued to grow dropped to a quarter - **Plaque regression doubled**—half of all patients experienced shrinkage of their plaque - **Microemboli (tiny blood clots) detected by transcranial Doppler were reduced by three quarters** - **The 2-year risk of stroke fell from 8.8% to 1%** - **The 2-year risk of myocardial infarction (heart attack) fell from 7.6% to 1%** Overall, this approach reduced the very high risk in patients with asymptomatic carotid stenosis by more than 80%. Randomized trials comparing usual care versus "treating arteries" are now being planned, using measurement of 3D plaque volume—the most sensitive method available for assessing how well therapies are working. ## Assessing Prognosis in Carotid Atherosclerosis Carotid atherosclerosis refers to plaque buildup in the carotid arteries, the major blood vessels in the neck that supply the brain. When plaque narrows these arteries (carotid stenosis), it can cause strokes—either by blocking blood flow or by sending clots to the brain. For patients with **severe symptomatic carotid stenosis** (narrowing that has already caused a stroke or transient ischemic attack/mini-stroke), there is clear evidence that carotid endarterectomy (CEA, surgical removal of plaque) or carotid artery stenting (CAS, opening the artery with a mesh tube) is beneficial. However, the periprocedural risk (risk during and shortly after the procedure) of stroke or death with CAS is **approximately twice that with CEA**—about 3% for CAS versus 1.5% for CEA. The situation is very different for **asymptomatic carotid stenosis** (narrowing that has not caused symptoms). The risk of stroke with modern intensive medical therapy has declined dramatically in recent years, from relatively high levels decades ago to **~0.5% per year** today. Some researchers have even suggested that randomized trials in symptomatic stenosis should be repeated, comparing intervention against intensive medical therapy, given how much medical treatment has improved. This has created a major controversy. In the United States, **~90% of carotid interventions are performed for asymptomatic stenosis**—even though 90% of patients would be better treated with intensive medical therapy alone. The proportion of carotid interventions performed for asymptomatic stenosis varies dramatically around the world: - **90%** in the United States - **~60%** in Italy and Germany - **~15%** in Canada and Australia (considered about right) - **0%** in Denmark These discrepancies raise serious questions about both the advisability and the ethics of routine intervention for asymptomatic stenosis as practiced in the United States, particularly since real-world complication rates are often higher than those reported in carefully controlled trials. When periprocedural risks are factored in, the risk with intervention is still much higher than the risk with medical therapy. The truth is that only approximately **10–15% of patients with asymptomatic carotid stenosis** could actually benefit from intervention. The challenge—and the subject of much current research—is identifying who those patients are. Several methods are in development or already available: - Reduced cerebrovascular blood flow reserve (the brain's ability to compensate for reduced blood flow) - Intraplaque hemorrhage (bleeding inside the plaque) detected on magnetic resonance imaging (MRI) - Neovascularity (new blood vessel growth) within plaques seen on contrast ultrasound - Plaque inflammation detected on positron emission tomography/computed tomography (PET/CT) scans ## Measuring Carotid Plaque Burden For many years, doctors measured carotid intima-media thickness (IMT)—the thickness of the inner two layers of the artery wall—as a marker of "preclinical atherosclerosis." However, it is increasingly clear that IMT is a different phenotype altogether and is not truly representative of atherosclerosis. The measurement is complicated by two different approaches: measuring IMT with or without including plaque thickness, and some studies combine participants with and without plaque, muddying the picture. Measuring **carotid plaque burden** is proving superior to IMT for both risk stratification (predicting who will have events) and for assessing the effects of treatment. Plaque burden can be measured in two ways: - **Total plaque area (TPA):** the sum of the areas of all plaques seen in the extracranial carotid arteries (the part of the carotid arteries outside the skull) - **Total plaque volume (TPV):** measured using 3D ultrasound, representing the three-dimensional size of all plaques In the High Risk Plaque study, 3D plaque burden was highly correlated with coronary calcium (a measure of plaque in the heart arteries), whereas IMT was not. Plaque burden also predicted the risk of cardiovascular events to a similar extent as coronary calcium scoring. A key reason IMT is a weak predictor of cardiovascular risk is its **narrow dynamic range: ~0.5 to 1.5 mm**. In contrast, the dynamic range of TPA is much greater—from 0 to ~1200 mm²—and the range of TPV would be even larger. This wider range allows for much better discrimination between low-risk and high-risk patients. The predictive power of TPA is substantial. In one study of patients attending a vascular prevention clinic, after adjusting for age, sex, blood pressure, smoking, serum cholesterol, diabetes, homocysteine, and treatment of blood pressure and cholesterol, TPA strongly predicted risk. The **5-year risk of stroke, death, or myocardial infarction, by quartile (quarter) of TPA, was 5.6%, 10.7%, 13.9%, and 19.5%**—a dramatic stepwise increase in risk as plaque burden increases. Plaque progression also matters. Patients whose plaque grew during the first year of follow-up had **twice the risk** of those with stable plaque or plaque regression. These findings were confirmed in a population-based study in Tromsø, Norway, where both myocardial infarction and stroke were strongly predicted by TPA but not by IMT in the common carotid artery where there was no plaque. One limitation of IMT is practical: the annual change in IMT is only ~0.15 mm, while the resolution of the measurement method is ~0.2–0.3 mm. This means IMT changes are too small to measure reliably in time frames that are clinically meaningful. A more useful measurement in people who do not yet have plaque is **vessel wall volume**—a 3D measurement of the intima-media that has a much greater dynamic range and, unlike IMT, is sensitive to the effects of therapy. ## Transcranial Doppler: Detecting Dangerous Emboli Perhaps the best-validated method for identifying high-risk patients with asymptomatic carotid stenosis is **transcranial Doppler (TCD) embolus detection**. TCD uses ultrasound waves to listen to blood flow in the brain's blood vessels. When tiny clots (microemboli) pass through, they create distinctive "hits" on the ultrasound signal—like small echoes traveling through the bloodstream. Just because a patient has carotid stenosis doesn't mean they will necessarily have dangerous emboli. TCD can identify those who are actually sending clots to the brain. The evidence is compelling: patients with asymptomatic carotid stenosis who had **two or more microemboli in 1 hour of monitoring had a 1-year risk of stroke of 15.6%**, indicating that they could benefit from CEA or CAS. This test is not only effective but also remarkably cost-effective: **the cost of a TCD machine is less than the cost of two carotid stenting procedures**, and training and certification in TCD embolus detection can be obtained in a course of 3 or fewer days. Dr. Spence argues that TCD embolus detection—or some other procedure to identify patients at higher risk than the risk of intervention itself—should be considered before patients undergo CAS or CEA for asymptomatic stenosis. ## Plaque Characteristics That Predict Risk Beyond measuring the size of plaque, doctors can now examine its characteristics to predict risk. Certain features make plaque "vulnerable"—more likely to rupture and cause a stroke. In patients with asymptomatic carotid stenosis, the presence of **three or more ulcers** (breaks in the surface of the plaque) in either or both carotid arteries carried a similar risk as the presence of microemboli: an **18% 3-year risk of stroke or death**. Those with **two or more microemboli had a 20% 3-year risk**. By combining TCD embolus detection and detection of three or more ulcers, the proportion of patients with asymptomatic stenosis who could benefit from intervention was increased from 5% to 10%—meaning that combining tests improves our ability to find the high-risk patients who truly need intervention. The Asymptomatic Carotid Emboli Study (ACES) added further evidence. In this study: - **Plaque echolucency** (plaque that appears dark on ultrasound, indicating it is soft and lipid-rich rather than hard and calcified) at baseline increased the risk of ipsilateral stroke (stroke on the same side as the plaque) with a **hazard ratio (HR) of 6.43** (95% confidence interval [CI] 1.36–30.44, P=0.019) - A combination of plaque echolucency and the presence of TCD microemboli markedly increased the risk of ipsilateral stroke with an **HR of 10.61** (95% CI 2.98–37.82, P=0.0003) To put these numbers in plain language: a hazard ratio of 6.43 means patients with echolucent plaque were more than 6 times more likely to have a stroke on that side of the brain than patients without this feature. A hazard ratio of 10.61 means the combination of echolucency and microemboli increased risk more than 10-fold. The P-values (P=0.019 and P=0.0003) indicate these findings were statistically significant, meaning there is less than a 2% and 0.03% chance, respectively, that these results occurred by random chance. Importantly, the combination finding remained significant even after controlling for risk factors, degree of carotid stenosis, and antiplatelet medication. Other plaque features under investigation include **juxtaluminal black plaque** (plaque or thrombus so echolucent that it can only be seen by observing a gap between the artery wall and the Doppler flow signal) and advanced **plaque texture analysis** of ultrasound images, which uses computer algorithms to identify dangerous plaque characteristics that might not be visible to the human eye. ## What This Means for Patients For patients concerned about heart attack and stroke risk, these advances have several practical implications: 1. **Diet matters more than fasting cholesterol tests suggest.** The effects of diet on arterial health occur largely in the hours after eating (the post-prandial state), not just in the fasting state measured by standard blood tests. A high-fat, high-cholesterol meal increases arterial inflammation and oxidative stress and impairs endothelial function for several hours. Since most of the day is spent in the post-prandial state, diet is much more important than would be predicted by fasting LDL levels alone. 1. **Healthy lifestyle choices have enormous power.** In the US Health Professionals Study and the Nurses' Health Study, people who adopted all five healthy habits (not smoking, moderate alcohol intake, regular exercise, a healthy diet, and maintaining a healthy weight) had an **80% reduction in stroke**. Swedish men with coronary artery disease who adopted these habits had an **80% reduction in recurrent myocardial infarction**. The Cretan Mediterranean diet reduced cardiovascular events by **70% in secondary prevention** (preventing recurrence in patients who already had events) and **reduced stroke by nearly half in high-risk primary prevention** (preventing first events in high-risk patients). 1. **Gut bacteria are a new target for therapy.** The discovery that intestinal bacteria produce vasculotoxic (blood-vessel-damaging) compounds from foods like red meat and egg yolk opens the door to future treatments—possibly including antibiotics, stool transplantation, or probiotics—that could reduce cardiovascular risk. For now, limiting intake of these foods is the practical takeaway. 1. **PCSK9 inhibitors represent a major advance** for patients who cannot tolerate statins or who need extreme LDL lowering, though cost is currently a major barrier. 1. **Measuring plaque burden directly** is superior to older methods like IMT for predicting risk and monitoring treatment response. Patients whose plaque is stable or regressing have much better outcomes than those with progressing plaque. ## Limitations of This Research While these advances are exciting, several important limitations must be acknowledged. The "treating arteries instead of treating risk factors" approach showed dramatic results in observational studies, but **randomized controlled trials**—the gold standard of medical evidence—have not yet been completed. Until such trials are done, the true benefit of this approach compared to standard care remains uncertain. The microbiome findings, while revolutionary, are largely based on observational studies and animal models. The proposed interventions (antibiotics, stool transplantation) are experimental and have not been proven safe or effective for cardiovascular disease prevention in humans. The relationship between TMAO and cardiovascular risk is strong, but cause-and-effect in humans has not been definitively established. Many of the imaging techniques discussed—including 3D ultrasound plaque volume measurement, PET/CT plaque inflammation imaging, and MRI detection of intraplaque hemorrhage—require specialized equipment, expertise, and software that may not be widely available outside major academic medical centers. The cost-effectiveness of routinely using these tests in clinical practice has not been fully established. Finally, this review was written in 2016, and while the findings remain relevant, treatment recommendations and available therapies have continued to evolve. Patients should discuss current options with their healthcare providers. ## Recommendations for Patients Based on this research, patients can take several practical steps to reduce their risk of atherosclerosis-related events: - **Adopt a Mediterranean-style diet** rich in fruits, vegetables, whole grains, fish, and healthy fats like olive oil. The evidence for cardiovascular benefit is strong, including a 70% reduction in recurrent cardiovascular events and a near-halving of stroke risk in high-risk patients. - **Limit red meat and egg yolk consumption**, particularly if you have kidney disease or are at high cardiovascular risk. It's not just the cholesterol that matters—the carnitine in red meat and phosphatidylcholine in egg yolk can be converted by gut bacteria into TMAO, a compound that promotes atherosclerosis. - **Don't rely solely on fasting cholesterol tests** to judge the healthiness of your diet. What you eat affects your arteries for hours after each meal. - **Ask your doctor about plaque imaging** if you are at intermediate or high risk. Measuring carotid plaque burden (total plaque area or volume) may provide better risk prediction than traditional risk factor counting alone, and can help guide treatment intensity. - **If you have asymptomatic carotid stenosis, ask about TCD embolus detection** before agreeing to carotid endarterectomy or stenting. This test can help identify whether you are among the 10–15% of patients who might actually benefit from intervention, potentially sparing you unnecessary procedural risk. - **Don't let statin myths scare you away from treatment.** While muscle pain and a slight increase in diabetes risk are real concerns, most of the feared side effects (liver failure, kidney damage, cataracts, cognitive decline) are not causally related to statin use. Talk to your doctor about any symptoms you experience—dose adjustments or alternative medications may help. - **Adopt all five healthy lifestyle habits:** not smoking, moderate alcohol intake, regular exercise, a healthy diet, and maintaining a healthy weight. Together, these habits reduce stroke risk by 80% and recurrent heart attack risk by 80%. ## Frequently Asked Questions ### What is atherosclerosis and why does it cause heart attacks and strokes? Atherosclerosis is the gradual buildup of plaque inside artery walls. It begins when blood flow damages the artery lining, triggering inflammation, cholesterol accumulation, and scar-like plaque. If plaque ruptures, it can cause a blood clot that blocks blood flow, leading to a heart attack or stroke. ### How do gut bacteria increase heart attack and stroke risk? Intestinal bacteria convert substances in red meat and egg yolks into TMAO, a compound that promotes atherosclerosis. In one study of patients undergoing heart angiography, those with the highest TMAO levels had a 2.5-fold higher 3-year risk of stroke, heart attack, or death. Limiting red meat and egg yolk may reduce this risk. ### What are PCSK9 inhibitors and who might need them? PCSK9 inhibitors are newer cholesterol-lowering drugs that block an enzyme destroying LDL receptors, so the liver removes more LDL from blood. In clinical trials, they lowered LDL cholesterol and cardiovascular events by about 50%, even in people who cannot tolerate statins. However, they are currently extremely expensive. ### What does 'treating arteries instead of risk factors' mean? Instead of only treating blood pressure and cholesterol numbers, doctors directly measure plaque in arteries and adjust therapy to stop plaque growth or shrink it. In patients with asymptomatic carotid stenosis, this approach reduced the 2-year stroke risk from 8.8% to 1% and heart attack risk from 7.6% to 1%. ### How can doctors tell if carotid plaque is dangerous before it causes a stroke? Transcranial Doppler detects tiny clots, called microemboli, traveling to the brain. Patients with two or more microemboli in one hour had a 15.6% one-year stroke risk, suggesting they might benefit from carotid surgery or stenting. Plaque ulcers on ultrasound also indicate higher risk when three or more are present. ### I have asymptomatic carotid stenosis. Should I have surgery or stenting? Only about 10–15% of patients with asymptomatic carotid stenosis truly benefit from intervention. With modern medical therapy, yearly stroke risk is about 0.5%. Doctors should use tests like transcranial Doppler to identify higher-risk patients before recommending surgery or stenting, because procedural risks may outweigh benefits for most patients. ### What lifestyle changes can lower my risk of heart attack and stroke? Adopting all five healthy habits—not smoking, moderate alcohol, regular exercise, healthy diet, and healthy weight—reduced stroke risk by 80% in two large studies. A Mediterranean-style diet cut recurrent cardiovascular events by 70% and nearly halved stroke in high-risk primary prevention. Limiting red meat and egg yolk may also help by reducing TMAO. ## Source Information This patient-friendly article is based on the following peer-reviewed research: **Original Article:** Spence JD. "Recent advances in pathogenesis, assessment, and treatment of atherosclerosis [version 1; referees: 3 approved]" **Journal:** F1000Research 2016, 5(F1000 Faculty Rev):1880 **Publication Date:** First published 28 Jul 2016 **DOI:** 10.12688/f1000research.8459.1 **Author:** J. David Spence, Stroke Prevention & Atherosclerosis Research Centre, Robarts Research Institute, Western University, London, ON, Canada **Competing Interests Disclosure:** The author has received lecture honoraria/consulting fees from Bayer and Bristol Myers Squibb and has performed contract research with Pfizer, Bayer, Bristol Myers Squibb, Acasti Pharma, POM Wonderful, CVRx, AGA Medical, and Gore. He is an officer and shareholder of Vascularis Inc., a company seeking to market software for vascular risk reclassification based on measurement of carotid plaque burden. *Note: This patient-friendly article was created to make the research accessible to a broader audience. It preserves all key data, statistics, and findings from the original peer-reviewed publication. Patients should consult their healthcare providers for personalized medical advice.* --- 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/understanding-atherosclerosis-new-discoveries-in-prevention-risk-assessment-and-treatment