The coronary artery calcium (CAC) score is a noninvasive imaging technique that quantifies arterial calcification. Read on to learn the benefits of knowing a patient’s CAC score, why serial measurements are not advised, and how to treat arterial calcification.
Cardiovascular disease (CVD) is the leading cause of death in the developed world, accounting for one in every four deaths in the United States (1).One of the underlying mechanisms of CVD is often atherosclerosis, the buildup of plaque inside an artery. Atherosclerosis develops in the arteries as a series of events.
Lipoproteins constantly travel throughout the bloodstream, either as LDL to deliver cholesterol to cells, or as HDL to remove cholesterol from cells. Healthy blood vessel walls are lined with a single layer of endothelial cells, called the endothelium. When the endothelium is damaged or when too many LDL particles are present, LDL particles can deposit within the arterial wall. Once there, the particles can be oxidized, triggering a cascade of inflammation and plaque development.
At first, the vessel remodels and expands as the plaque develops, but over time the artery can narrow and restrict blood flow. A fibrous cap separates the plaque from the bloodstream. If the cap ruptures, the blood exposed to the plaque begins to clot. Clots can restrict blood flow locally or they can travel elsewhere to do the same. Plaques with thin fibrous caps and abundant inflammatory cells are more likely to rupture (2, 3, 4).
The CAC score
Arterial plaques calcify over time. The calcified portion of plaques occupies approximately 20 percent of the total plaque area, so we can estimate the total plaque/lesion area from its calcium content imaged by a CT scan.
The coronary artery calcium (CAC) score was developed in the 1980s to quantify coronary calcification. Using electron beam or multidetector computed tomography (EBCT or MDCT), serial three-millimeter sections from the aorta through the apex of the heart are x-rayed. The Agatston score, reported in Hounsfield units, is calculated by multiplying the lesion area by a stepwise density factor between 1 and 4 (5).
The Agatston score estimates the extent of coronary artery disease:
- 0: No plaque or evidence of coronary artery disease.
- 1–10: Minimal coronary artery disease.
- 11–100: Mild coronary artery disease. Mild or minimal coronary narrowing likely.
- 101–400: Moderate coronary artery disease. Significant narrowing possible.
- > 400: Severe coronary artery disease. High likelihood of at least one significant coronary narrowing.
CAC score can enhance prediction of CVD risk
The Framingham Risk Score predicts a person’s chance of developing CVD within the next 10 years, based on age, diabetes, smoking, blood pressure, total cholesterol, and HDL cholesterol. However, this model only identifies 70 percent of individuals at risk for CVD (5). What’s more, up to 60 percent of cardiovascular events occur in those who were classified as “low” or “intermediate” risk by the Framingham Risk Score (5). Adding the CAC to the risk calculation better predicts CVD and clinical outcomes (6, 7). The CAC score on its own is a verified independent predictor of cardiovascular events (8).
The CAC score has other benefits. The imaging procedure is noninvasive and does not require a contrast agent. Patients who know their CAC score tend to adhere better to treatment plans because they can “see” calcified plaques (9).
Some of the risks of the CAC score include the following:
- The radiation dose delivered is 50 percent more than a mammogram (5), which can increase cancer risk with repeat exposures (10).
- An increasing score over time could indicate an increase in plaque density rather than in size.
- The score does not give information about arterial stenosis (although someone without calcification is very unlikely to have arterial narrowing).
- The interscan variability is non-negligible (11).
Statins don’t lower CAC
The CAC score typically progresses 20 to 25 percent per year (5). Rapid increases have been associated with worse outcomes (12, 13, 14), but tracking the CAC over time is not validated as a way of assessing changes in CVD risk following treatment (15).
If you have been following my work for awhile, you probably know that I believe statins are overprescribed, have wildly overstated benefits, and are accompanied by an obscene list of side effects. In initial prospective studies, statins appeared to lower the CAC, at least in some patients (16, 17), but statins have failed to show any effect on CAC progression in controlled clinical trials.
In the BELLES trial, 615 postmenopausal women were treated with statin or placebo. LDL was lowered in the treatment group, but CAC progression was the same in both groups (18).
In the St. Francis Heart Study, 1,000 healthy men and women with very high CAC scores were treated with vitamin C, vitamin E, and a statin or matching placebos. CAC progression again was not different between groups (19). Of note, future cardiovascular events in this trial were best predicted by baseline CAC score.
Another study looked at high-dose versus low-dose statin treatment for 12 months in patients with a moderate CAC score. The high dose lowered LDL levels, but neither statin dose affected CAC progression (20).
Does calcification stabilize plaques?
With an advanced technique called radiofrequency ultrasonography, the lipid material, fibrous tissue, and calcification of arterial plaques can be distinguished from one another and quantified. In two studies that used this imaging technology, statin therapy did decrease overall plaque area, but the proportion of calcified plaque actually increased (21, 22).
A higher coronary calcium score could indicate more stabilized arterial plaques
Treatment for high CAC
What can we make of these seemingly contradicting results? One speculation is that dense calcium can stabilize a plaque, making it less likely to rupture (23). Treatment could also reduce inflammation, which may further stabilize an existing plaque.
This is one shortcoming of the CAC score—a patient with a few densely calcified, stable plaques and a patient with numerous spotty calcification lesions could have the same CAC score, while the person with fewer, denser plaques could be less likely to experience plaque rupture (24).
Some data support this idea. In one study, first acute cardiovascular events occurred more often in patients with mild and moderate CACs instead of a high CAC, indicating that dense calcium plaques could be more stable (25). Knowing the CAC score can certainly be valuable, but it is not the holy grail marker of CVD.
It remains unclear from the literature if a high CAC score can actually be reversed, or if lowering it is even beneficial. For these reasons, the American College of Cardiology Foundation and the American Heart Association do not recommend taking serial CAC measurements and/or basing treatments off it alone (26).
However, any CAC score indicates arterial plaque and inflammation, both of which should be addressed. Instead of tracking calcification for CVD risk, I evaluate measures such as:
- LDL particle number (LDL-P) and oxidized LDL. Read my post on why the number of cars on the road (LDL-P) is more telling than the number of total passengers carried (LDL-C).
- Blood pressure. Blood pressure can often be lowered without prescription meds.
- Thyroid function. The thyroid regulates lipid metabolism, so thyroid dysfunction should be investigated if lipid measures are out of whack.
- Gut health. A healthy gut supports a healthy heart. Recent data strongly suggest a gut–heart connection.
A diet that contains a variety of nutrient-dense, whole foods, including organ meats, vegetables, pastured meats, and fermented foods will reduce inflammation and help prevent disease. A few nutrients are especially relevant to cardiovascular health:
For an in-depth analysis, see my previous article on vitamin K2. In brief, vitamin K2 ensures that calcium goes where it should (bones, teeth) and prevents calcium from depositing where it shouldn’t (blood vessels, brain). Higher vitamin K2 intake is associated with lower risks of cardiovascular disease (27, 28, 29).
Without adequate vitamin K2, matrix GLA-protein (MGP) cannot be carboxylated and therefore cannot keep calcium out of the arteries. Circulating uncarboxylated MGP correlates well with cardiovascular calcification (30, 31).
Unfortunately, many patients are deficient in vitamin K2. The richest food sources include natto (Japanese fermented soybeans), pastured egg yolks, and goose liver. Cod liver oil is a great source of vitamins A and D, which synergize with vitamin K2.
Vitamin C is required to make collagen, a major constituent of the arterial wall. When vitamin C isn’t adequate to fix arterial wall damage, lipoproteins instead patch up the hole and begin the process of atherosclerosis. Humans cannot make vitamin C and must obtain it from diet.
Say no to calcium supplements. Yes, strong bones require calcium, along with adequate vitamin D, exercise, and vitamin K2, but calcium supplements are not the answer! Calcium supplements increase the risks of arterial stiffness and heart attack (37, 38, 39).
Although often understated, lifestyle changes hugely impact health. Not only are getting enough exercise and maintaining a healthy weight important, but overall, people need to sit less. One study found that sitting time, regardless of the amount of time spent exercising, correlated with heart disease risk (40). Reducing stress and getting adequate sleep will also support a healthy heart.
Now I’d like to hear from you. Do you have patients concerned with their CAC scores? What are your treatment strategies for preventing and treating atherosclerosis? Let us know in the comments!