الوسم: atherosclerosis

  • Silent Artery Disease Could Begin Before Age 30

    Silent Artery Disease Could Begin Before Age 30

    Credit: Unsplash+.

    A large international study has revealed that fatty deposits within arteries are quite common even in adults who seem healthy and have never been diagnosed with heart disease.

    The results imply that the processes leading to heart attacks and strokes can start many years before any symptoms show up.

    This condition, known as atherosclerosis, occurs when cholesterol, fat, calcium, and other substances accumulate in arterial walls, forming plaques.

    As time passes, these plaques can enlarge and block arteries, restricting blood flow. They can also rupture, causing blood clots that may suddenly obstruct blood flow to the heart or brain, triggering a heart attack or stroke.

    Cardiovascular disease remains one of the top causes of death worldwide. A challenge in preventing it is that atherosclerosis often develops silently for decades before symptoms like chest pain, fatigue, or breathing issues appear.

    These findings come from the REACT project, a comprehensive international study aimed at mapping hidden artery build-up throughout adult life. Led by Professor Henning Bundgaard at Copenhagen’s Rigshospitalet and Dr. Borja Ibáñez from Spain’s CNIC, the research recruited 16,808 adults aged 18 to 70 in Denmark and Spain. None had prior diagnosed cardiovascular issues linked to atherosclerosis at the time of enrollment.

    Participants underwent scans of crucial arteries: the carotid arteries in the neck, femoral arteries in the legs, and coronary arteries supplying the heart.

    The findings were striking. Over half (57.1%) of participants had detectable plaque in at least one examined artery, despite having no previous diagnosis or symptoms.

    Notably, signs of atherosclerosis appeared surprisingly early. About 1 in 13 individuals aged 18 to 29 already showed plaque presence in at least one artery.

    The prevalence increased with age. Among those aged 60 to 70, roughly 90% had detectable plaque, highlighting how artery disease becomes more common as people grow older.

    Patterns also emerged regarding where plaque tends to form. Most people with plaque in the coronary arteries also had signs in either the carotid or femoral arteries.

    This is significant because examining neck and leg arteries with ultrasound is much easier than performing coronary artery scans. Ultrasounds are radiation-free, quick, portable, and increasingly accessible, making them a practical screening tool.

    Typically, doctors estimate future cardiovascular risk through factors such as age, blood pressure, cholesterol levels, diabetes, and smoking habits. While risk calculators are helpful, they don’t directly reveal whether artery plaque has already developed.

    The REACT team found that traditional risk scoring often misses many individuals who already have silent artery disease. This suggests that direct imaging of arteries might complement existing assessments, providing more detailed risk information.

    Significant differences were observed between men and women. Men tended to develop atherosclerosis earlier, with their patterns appearing about 5 to 10 years sooner than women.

    For women, most increases in plaque occurred between roughly ages 40 and 60—coinciding with menopause. Hormonal changes and shifts in cholesterol, blood pressure, and body composition during this period can influence cardiovascular health.

    It’s important to note that finding plaque doesn’t guarantee a heart attack or stroke will happen. Many individuals with atherosclerosis never experience major cardiovascular events. Factors such as the amount, location, type, and progression of plaque all influence risk.

    The first phase of the study, called REACT-DETECT, started in 2024. The project will continue with REACT-PROTECT from 2027 to 2032, aiming to determine whether prevention strategies based on artery imaging produce better health outcomes than current approaches.

    This next step is key. Screening millions of healthy adults would require confirming that detecting silent plaques leads to interventions that genuinely improve health outcomes, justifying the costs, efforts, additional testing, and potential anxiety involved.

    The study’s strength lies in its large sample size, broad age range, and direct assessment of arteries in multiple locations. Nonetheless, since participants were from Denmark and Spain, further research is needed to see how applicable these findings are to diverse populations with different genetics, diets, healthcare systems, and cardiovascular risks.

    Collaborations are underway with researchers in India, Singapore, Tanzania, and Mexico to explore whether the pattern of silent atherosclerosis is consistent across various demographic and geographic backgrounds.

    Results were presented at the ESC Congress 2026 and simultaneously published in the New England Journal of Medicine, offering a thorough insight into how atherosclerosis appears and progresses in adulthood.

    Overall, the study challenges the notion that artery disease mainly affects the elderly. Its primary message is that the biological process underlying heart attacks and strokes can begin quite early in life.

    While this emphasizes the need for improved prevention strategies, it doesn’t mean routine artery scans are recommended for everyone now. More evidence from future research is needed to determine whether screening can truly save lives.

    Until then, managing well-established risk factors—like quitting smoking, controlling blood pressure, lowering LDL cholesterol, managing diabetes, staying active, and eating healthily—remains the cornerstone of cardiovascular prevention.

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  • Scientists Discover Hidden Trigger That Turns Artery Plaques Deadly

    Scientists Discover Hidden Trigger That Turns Artery Plaques Deadly

    Credit: Unsplash+

    Heart attacks and strokes remain leading causes of death globally. These conditions are often associated with atherosclerosis, a process where fatty deposits called plaques accumulate inside arteries.

    As time passes, these plaques can constrict blood vessels, limiting blood flow. It has been understood for some time that not all plaques pose the same threat. Some stay stable for years, while others suddenly become unstable, rupture, and trigger blood clots that can block blood flow to the heart or brain.

    A recent study from The University of Texas MD Anderson Cancer Center offers new insights into why some plaques turn more dangerous. Published in Circulation Research, the research identified a molecular pathway that seems to promote inflammation and clot formation within artery plaques.

    The study zeroed in on a specific group of cells called senescent cells—cells that have become stressed or aged. Unlike normal cells, senescent cells stop dividing but do not die off. Instead, they remain in tissues and can influence neighboring cells. Increasing evidence links these aging cells to diseases such as cancer, heart disease, and age-related conditions.

    The research team aimed to determine how senescent cells impact blood vessels and plaque buildup. They focused on endothelial cells, which line the inside of blood vessels, helping regulate blood flow and maintain vessel stability. The scientists found that removing two key proteins, LATS1 and LATS2, caused endothelial cells to change significantly. Instead of staying stable, these cells entered a senescent-like state but became unusually active.

    This cellular shift promoted inflammation, made blood vessels leakier, stimulated abnormal new vessel growth, and created conditions conducive to clot formation. Further investigation revealed these effects were linked to a notable increase in an enzyme called CD38. This enzyme appears to reprogram cellular energy production, leading cells to consume more energy and shift into a pro-inflammatory, destabilized state.

    This environment made plaques more prone to rupture and blood clot development. The study identified CD38 as a central driver behind this harmful process. Importantly, blocking CD38 activity reversed many of these effects. In both lab tests and animal models, inhibiting CD38 reduced inflammation and enhanced plaque stability. These results point to CD38 as a promising target for new treatments.

    One encouraging aspect is that some drugs targeting CD38 are already approved by the FDA for certain types of cancer. This existing approval could accelerate efforts to explore their use for cardiovascular issues without needing to develop new medications from scratch.

    Researchers also examined human plaque samples, observing similar molecular patterns, which suggests these mechanisms are relevant to humans, not just experimental models. The findings may be especially significant for cancer patients, as many cancer therapies accelerate cellular aging and increase senescent cell counts. Some individuals undergoing treatment experience higher rates of heart attacks, strokes, and blood vessel inflammation. The newly identified pathway could help explain these side effects.

    Understanding how senescent cells affect blood vessel health offers potential opportunities to prevent cardiovascular disease. By targeting the molecular processes that weaken plaques, future therapies might lower the risk of dangerous blood clots that can cause life-threatening events.

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    Source: The University of Texas MD Anderson Cancer Center.