The 2026 Levels Guide to cardiac health tests

Combined, these markers give a fuller picture of your heart disease risk than standard blood work does.

WRITTEN BY

Dan Wagener

Updated: 02/12/2026|10 min read

Heart disease remains the leading cause of death in the United States and globally, affecting millions of people each year. In 2023, one in every three deaths in the United States was due to heart disease—that’s more than 900,000 people.

Most of these deaths stem from atherosclerosis, the buildup of plaque in arterial walls. Over time, this can narrow the arteries and prevent blood from reaching organs and tissues. Plaques can also burst and form blood clots, which can block arteries and cause heart attacks, strokes, or heart failure.

In addition to other tests such as electrocardiograms, chest X-rays, and heart stress tests, several blood tests can help detect atherosclerosis and assess heart disease risk. After diagnosis, individualized treatments from your provider can halt or even reverse the disease.

Read on to learn about the blood tests used to diagnose atherosclerosis, who should get them, and what the results mean.

This information does not constitute medical advice. This is compiled expert opinion for educational purposes. Your doctor knows you best. Talk to them about your personal lab results.

Why do cardiac health tests matter?

In the early stages, heart disease often doesn’t cause symptoms. Testing can catch the condition before you feel anything—and before it begins to cause significant harm.

Cardiac tests look at several different factors involved in atherosclerosis, including:

• Cholesterol
• Inflammation
• Metabolic health (insulin, blood sugar)
• Cardiac damage

Collectively, these markers help tell the story of atherosclerosis’ development and progression: from initial cholesterol abnormalities and increased inflammation to damaged blood vessels and, eventually, heart damage.

When should you consider cardiac health testing?

You might receive cardiac health tests as part of routine blood work. Your provider may also suggest them if you’re at risk for atherosclerosis due to family history, health conditions, or symptoms of heart disease.

Here are some of the common reasons to get your cardiac biomarkers checked:

• Routine preventive screening: The American Heart Association recommends cholesterol testing every four to six years for adults age 20 and older. This blood work includes high-density lipoprotein (HDL), low-density lipoprotein (LDL), and triglycerides. Your provider may also recommend a hemoglobin A1c test (which measures average blood glucose levels and helps assess cardiovascular risk) as part of an annual physical.
• Family history: If you have first-degree relatives with early heart disease, your provider may want to test your lipoprotein(a) or Lp(a), a type of inherited LDL.
• Existing risk factors: Conditions like hypertension (high blood pressure), diabetes, obesity, high cholesterol, and a history of smoking are risk factors for atherosclerosis and warrant cardiac panel testing.
• Symptoms of heart problems: Atherosclerosis usually has no symptoms in the early stages. But advanced atherosclerosis may cause chest pain, shortness of breath, fatigue, palpitations, numbness or tingling sensations, or worsening ability to exercise. If you notice any of these, it’s smart to seek cardiac testing.
• To monitor treatment effectiveness: Your doctor may recommend follow-up testing to determine whether any medications or lifestyle changes are working to lower your atherosclerotic risk.

What are cardiac health tests, and what do they tell you about heart disease?

Below are some of the most common blood tests used to diagnose atherosclerosis. No single biomarker is used to make a diagnosis. Instead, your provider will compare multiple results to get a clear picture of your condition. They may use other diagnostic tools besides blood tests, such as electrocardiograms (EKGs), computed tomography (CT) scans, chest X-rays, and heart stress tests. These tests reveal additional information about heart function and plaque in the arteries.

Lipids: Core drivers of atherosclerosis

Lipids include fats and cholesterol. High cholesterol levels (specifically LDL) are strongly linked to atherosclerosis and are a red flag that the disease may be present or developing.

LDL, non-HDL, and ApoB

LDL, non-HDL, and apolipoprotein B (ApoB) tests reflect the concentration of potentially harmful particles that can lodge in arterial walls and initiate atherosclerosis. Since ApoB is a protein found in lipoproteins such as LDL, all three biomarkers are likely to be elevated simultaneously.

When lipoproteins penetrate arterial walls and become embedded, they can oxidize, or undergo chemical changes. This triggers an inflammatory response: The immune system thinks these damaged lipoproteins are harmful invaders, so white blood cells called macrophages arrive at the site and try to remove them by engulfing them. As the macrophages swell with lipids, they take on a foamy appearance, becoming what are known as “foam cells.”

Over time, foam cells die and accumulate in the arterial walls, forming “fatty streaks,” the earliest visible signs of atherosclerosis. These streaks can thicken and become plaques, which can grow and harden. Plaques can then block the flow of blood through the arteries and cause cardiovascular complications like heart attack or stroke. They can also rupture, leading to blood clots.

Conditions such as hypertension (high blood pressure) and diabetes can weaken blood vessels and make them more vulnerable to infiltration by lipoproteins.

Standard reference ranges:

• LDL: <100 mg/dL (milligrams per deciliter; goals vary based on risk)
• Non-HDL: <130 mg/dL
• ApoB: <90 mg/dL

Even though these lipid tests are among the strongest indicators of atherosclerosis, healthcare providers consider other markers and conditions when making a diagnosis. For example, high blood sugar can increase the risk of atherosclerosis, and inflammation levels (measured by a high-sensitivity C-reactive protein test) can suggest the existence and progression of the disease.

The primary drivers of high LDL levels are genetics and lifestyle habits, such as eating a diet high in saturated fats, getting inadequate exercise, and chronic stress. Medications such as diuretics and other health conditions, such as hypothyroidism, can also raise levels but are less common culprits.

HDL

High-density lipoprotein (HDL) particles remove cholesterol from peripheral tissues—including artery walls—and transport it back to the liver for elimination. This helps prevent plaque buildup. HDL can also help ​​protect against atherosclerosis by limiting inflammation in arteries. In general, high LDL levels combined with low HDL levels increase the risk of atherosclerosis.

But a healthy HDL level can’t eliminate heart disease risk on its own. Medications that only focus on raising HDL (without also lowering LDL) have not been shown to reduce the risk of atherosclerosis. And some studies suggest that high levels of HDL (above 80 mg/dL) can increase the risk of atherosclerosis because HDL may lose its protective effect at a certain level.

Standard optimal ranges:

Female:

• <20 Years: >45 mg/dL
• ≥20 Years: ≥50 mg/dL

Male:

• <20 Years: >45 mg/dL
• ≥20 Years: ≥40 mg/dL

Triglycerides

Triglycerides are the most common type of fat in the body and the primary component of most dietary fats. Our bodies produce them when we consume excess calories from any food source and store them for energy. Studies have found that elevated triglyceride levels increase the risk of heart disease.

Triglycerides contribute to atherosclerosis in several ways, even though they don’t directly cause it. First, their breakdown in the body creates remnant low-density lipoproteins that can inflame blood vessels, attract macrophages, and initiate atherosclerosis in much the same way as LDL particles. Second, as triglyceride levels rise (above 200 mg/dL), HDL particles absorb triglycerides, become smaller, and are more prone to rapid breakdown, while LDL particles also tend to become more triglyceride-rich, leading to denser particles. Both of these effects increase the risk of atherosclerosis.

Triglycerides typically rise with insulin and glucose levels and with elevated high-sensitivity C-reactive protein, creating a cluster of interrelated risk factors that accelerate atherosclerosis. High triglycerides can also be an independent risk factor for atherosclerosis.

Standard range:

• Optimal: <100 mg/dL
• Normal: <150 mg/dL
• Elevated: >150 mg/dL

Genetic risk enhancers

Lipoprotein(a)

Lipoprotein(a), or Lp(a), is an inherited lipoprotein (up to 90 percent of its concentration in the blood is determined by genetics). It’s essentially an LDL particle, but in addition to containing apolipoprotein B, it has another protein attached to it: apolipoprotein A. This means it can both promote plaque formation and cause blood clotting.

Lp(a) can play several roles in the progression of atherosclerosis. It can bind to artery walls and is more prone to oxidation than LDL particles. This makes it likely to attract macrophages, which eventually become foam cells and form plaques. Lp(a) also transports oxidized phospholipids, which can cause inflammation in artery walls, weaken plaques, and make them more vulnerable to rupturing.

Finally, Lp(a) can increase the activity and clumping of platelets (cells that help form blood clots) and impede the body’s ability to break down clots by preventing activation of the enzyme plasminogen. These clots can block blood flow and cause heart attacks or strokes.

Like triglycerides, Lp(a) operates independently of other risk factors—it’s harmful regardless of LDL levels or inflammation status. However, some studies suggest an increased risk for atherosclerosis if LDL is also high. It’s unclear how Lp(a) interacts with triglycerides and HDL.

Lifestyle changes or statins (which are commonly prescribed to lower LDL cholesterol) have minimal to no effects on Lp(a). Treatments to lower Lp(a) include PCSK9 inhibitors, and apheresis, a dialysis-like treatment that directly removes Lp(a) from the blood.

Standard range:

• Optimal: <30 mg/dL (<75 nanomoles per liter or nmol/L)
• High risk: >50 mg/dL (>125 nmol/L)

Inflammatory drivers

High-sensitivity C-reactive protein

C-reactive protein, or CRP, is a protein produced by the liver that rises in response to inflammation. The high-sensitivity C-reactive protein test, or hs-CRP, can uncover smaller changes in CRP than the standard test. It can detect low-grade, chronic inflammation associated with atherosclerosis, even in people without symptoms.

Inflammation is involved in every stage of atherosclerosis. It can damage blood vessels and make them more vulnerable to penetration by lipoproteins, which are then more prone to oxidation. Macrophages arrive at the site and, along with smooth muscle cells in the vessels, release cytokines that promote further inflammation. Triglyceride lipoprotein remnants circulating in the blood may also cause inflammation in blood vessels.

When the macrophages become foam cells and eventually plaques, inflammation can make the plaques more likely to rupture by weakening the fibrous cap on top of them. After the plaque ruptures, another inflammatory response activates platelets, which can form blood clots that can block vessels and cause a heart attack or stroke.

High inflammation may increase the risk of atherosclerosis even in people with normal LDL cholesterol levels. In this scenario, statins may help. In the JUPITER trial, rosuvastatin reduced events in people with elevated hs-CRP and near-normal LDL, while substantially lowering both LDL and hs-CRP.

Additionally, chronic inflammation can lower HDL and increase triglyceride levels by boosting very low-density lipoprotein (VLDL) production in the liver and reducing the clearance of triglyceride lipoproteins. It can also increase Lp (a) production in the liver.

Standard range:

• Low risk: <1 milligrams per liter (mg/L)
• Average risk: 1 to 3 mg/L
• High risk: >3 mg/L

Metabolic dysfunction markers

Fasting insulin and hemoglobin A1c

Fasting insulin measures baseline insulin levels, while hemoglobin A1c (HbA1c) measures your average blood glucose level over three months. A high fasting insulin level combined with a normal or elevated blood glucose level may indicate insulin resistance.

Insulin resistance means your cells have trouble letting in glucose, which is your body’s primary source of energy. When this happens, your pancreas may boost insulin production to help more glucose enter cells, which can worsen insulin resistance.

Insulin resistance promotes atherosclerosis through multiple mechanisms: It creates oxidative stress that increases the production of free radicals. These molecules reduce the availability of nitric oxide, a molecule that helps blood vessels dilate. Without enough nitric oxide, arteries become harder and stiffer. Insulin resistance also causes inflammation in blood vessels, which can attract white blood cells and begin the process that leads to atherosclerotic plaques.

Plus, insulin resistance changes how the body breaks down lipids (by decreasing the activity of certain enzymes), which can elevate triglycerides, reduce HDL, and increase small dense LDL. This type of LDL is more likely to enter the blood vessel walls, become oxidized, and contribute to atherosclerosis. This trio of changes creates a combined risk greater than any single abnormality.

Standard ranges:

• Fasting insulin:

  • Optimal: 2 to 6 μIU/mL
  • Insulin resistance likely: >12 μIU/mL

• HbA1c:

  • Normal: <5.7%
  • Prediabetes: 5.7 to 6.4%
  • Diabetes: >6.5%

Cardiac damage markers

Troponin and NT-proBNP

Damaged cardiac muscle cells release troponin proteins (troponin I and troponin T), and the heart increases production of N-terminal pro-B-type natriuretic peptide (NT-proBNP) when under strain or experiencing failure.

Typically, only tested when a heart attack or heart failure is suspected, providers may also check troponin and NT-proBNP to determine cardiovascular risk in people with atherosclerosis and uncover its consequences, including:

• heart muscle damage from lack of oxygen (ischemia)
• increased cardiac workload due to atherosclerotic narrowing of the coronary arteries

High levels of high-sensitivity cardiac troponin I are linked to more severe coronary artery disease and a more rapid progression of the disease (likely due to plaque buildup from atherosclerosis). And studies have found that even mild coronary atherosclerosis can lead to detectable levels of high-sensitivity cardiac troponin T. NT-proBNP reflects cardiac wall stress and heart failure risk; higher values are associated with adverse cardiovascular outcomes. Use age- and assay-specific cutoffs (e.g., many labs flag ≥125 pg/mL as elevated in adults <75), and interpret in clinical context.

Troponin and NT-proBNP typically become abnormal after years or decades of atherosclerotic progression driven by elevated lipids, inflammation, and metabolic dysfunction.

Standard ranges:

• Troponin:
  • Normal troponin I: ≤0.04 ng/mL
  • Normal troponin T: ≤0.01 ng/mL
  • High-sensitivity troponin targets vary on different manufacturer’s testing assay, so your lab will provide the reference ranges.
• NT-proBNP: <125 pg/mL for people <75 years

What's next if your cardiac test results show heart disease risk?

If your results show you may be at risk of heart disease, your doctor will recommend treatment based on your situation and needs. This may include:

• Lifestyle changes: Following a heart-healthy diet (such as the Mediterranean diet), exercising more regularly, losing weight, quitting smoking, and drinking less alcohol can slow the progression of atherosclerosis.
• Statins: These drugs, such as atorvastatin and rosuvastatin, block cholesterol production in the liver and lower LDL cholesterol in people with atherosclerosis or at risk of developing it.
• Antiplatelet medications: Aspirin and clopidogrel can reduce the risk of blood clots from atherosclerosis and lower inflammation in blood vessels.
• Anticoagulants: Medications such as heparin and warfarin can also lower the risk of blood clots.
• Diabetes medications: These can lower blood sugar levels and reduce the risk of atherosclerosis-related complications.

Your provider may also want to monitor how well your treatments are working by:

• Regularly checking your cholesterol and blood sugar levels
• Keeping an eye on your blood pressure (high blood pressure can damage artery walls and contribute to plaque development)
• Using imaging techniques such as MRIs to see if plaque buildup is slowing or progressing

Take control of your cardiac health

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