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Latest Research
A new Mount Sinai study of 547 asymptomatic patients shows that Lp(a) is the only biomarker that independently tracks with the most dangerous type of coronary plaque, even when your calcium score, LDL, and CRP look reassuring.
2026-02-06 • 8 min • By Arvind Srivastav
Most people who get a coronary artery calcium (CAC) score and see a low number walk away feeling reassured. But a new study from Mount Sinai shows that CAC, while excellent at quantifying total plaque, is completely blind to the most dangerous kind: soft, low-density non-calcified plaque. The only blood marker that tracked with that plaque independently? Lipoprotein(a), or Lp(a), a genetically inherited risk factor that most people have never been tested for.
Key finding
Lp(a) is the only biomarker that independently predicts low-density non-calcified plaque
In 547 asymptomatic patients, CAC score, LDL particle count, and hsCRP all failed to predict this high-risk plaque type. Only Lp(a) did.
If you are a health-conscious person who gets regular blood work and maybe even a calcium score, you probably feel like you have a solid read on your heart risk. This study suggests you might be missing a critical piece.
Researchers at Mount Sinai's Icahn School of Medicine looked at 547 asymptomatic adults who had no known heart disease. These were primary prevention patients, meaning the goal was to catch risk before anything goes wrong. Each patient received a coronary CT angiography (CCTA) with AI-powered plaque analysis, along with bloodwork for Lp(a), LDL particle concentration (LDL-P), high-sensitivity CRP (hsCRP), and a coronary artery calcium score.
The question was simple: which of these markers actually tells you about the type of plaque that causes heart attacks?
To understand the results, it helps to know that coronary plaque comes in different forms. Calcified plaque is hard and stable. It shows up clearly on a calcium score scan, and while it signals that atherosclerosis is present, it is not typically the type that ruptures and triggers a heart attack.
Low-density non-calcified plaque (LDNCP) is a different story. It is soft, lipid-rich, and more prone to rupture. When a plaque ruptures, a blood clot forms at the site and can block the artery entirely. This is how many heart attacks happen, often in people who had no prior symptoms.
Think of it this way: a calcium score tells you how much hard plaque has accumulated in your arteries over time. It is like an odometer for atherosclerosis. But it cannot see the soft, unstable plaque that is more likely to actually cause a cardiac event. For that, you need a different signal.
The study found that CAC score was the strongest predictor of total plaque burden, including both calcified and non-calcified plaque. No surprise there. But CAC had no association with low-density non-calcified plaque. None.
Lp(a), on the other hand, was the only biomarker independently associated with LDNCP after adjusting for age, sex, and every other risk marker in the model. It was also associated with higher arterial stenosis and a higher remodeling index, another feature of vulnerable plaque.
LDL particle count and hsCRP, two commonly measured risk enhancers, showed no significant association with any plaque subtype in the multivariable model. They were effectively overshadowed when Lp(a) and CAC were in the picture.
Lp(a) is a lipoprotein particle that is largely determined by your genes. Unlike LDL cholesterol, which responds to diet and statins, Lp(a) levels are set at birth and remain fairly constant throughout life. About 20 percent of the global population has elevated Lp(a), generally defined as 125 nmol/L or higher.
Despite being recognized as an independent cardiovascular risk factor for decades, Lp(a) is rarely tested in routine clinical practice. Many people discover they have elevated Lp(a) only after a cardiac event, or not at all.
Current guidelines from the American College of Cardiology and American Heart Association recommend measuring Lp(a) at least once in a lifetime as a risk enhancer for borderline or intermediate-risk patients. But with studies like this one showing that Lp(a) tracks with the most vulnerable plaque features, there is a growing case that everyone should know their number.
The traditional approach to cardiovascular risk assessment relies heavily on LDL cholesterol, blood pressure, diabetes status, and smoking. If your LDL is in range and your calcium score is low, you generally get a clean bill of health. But this study highlights a gap in that framework.
Among the 547 patients in this study, 72 percent were classified as low risk by the standard ASCVD risk calculator. Yet many still had measurable plaque, and those with higher Lp(a) had more of the dangerous, soft plaque variety. In other words, standard risk tools would have told these people they were fine.
The researchers suggest that Lp(a) and CAC serve complementary roles. CAC gives a broad picture of how much plaque has developed. Lp(a) adds a layer of insight about the nature and stability of that plaque. Using both together could provide a much more complete risk profile than either alone.
If you are not measuring Lp(a), you are flying partially blind in primary prevention. A calcium score tells you how much plaque has hardened in your arteries. Lp(a) tells you whether you are building the kind of plaque that is most likely to cause trouble. Both matter, and knowing both puts you in a stronger position to act early.
This is exactly the kind of insight that drives what we are building at Veevo Health: giving you a more complete picture of your cardiovascular risk so you can take action years before symptoms appear.