The Coronary Calcium Score (CCS) or Heart Calcium Score is an effective way to quantify the amount of calcium in the coronary arteries. The average score is 0, especially in younger patients. (This is one of those times when it is good to be called a “Zero”!) However, the calcium score may increase as we age slowly. The report will provide a total calcium score and an age-related percentile of that score. These values show how patients stand compared to their age-related peers.

For at least 30 years, we have known that coronary artery disease (CAD) is inflammatory. We also know a positive correlation exists between the amount of calcium within the arteries and the risk of future cardiac events such as heart attacks. The Coronary Calcium Score is a frequent screening test used by physicians to quantify the amount of calcification within the coronary arteries. It has a dualistic purpose as a diagnostic and predictive tool for patients at risk for coronary artery disease (CAD). The test can also serve as a motivating factor to encourage patients to engage in lifestyle changes. If the test is abnormal, it may lead to the initiation of statin therapy. With this background in mind, I would like to address some critical factors related to the Calcium Score and its role in diagnosing and treating CAD.

Metaphorically, I equate calcium in the arteries to the scar that develops after an infection on our skin. Imagine a bacterial infection that forms on your arm. Like the arteries in our heart, the skin has three primary layers (epidermis, dermis, and hypodermis). When the surface barrier layer (epidermis) allows foreign invaders to enter the inner layers, this event triggers an inflammatory response in the epidermis and dermis. The area turns red, and inflammatory cells rush to the site to engage and neutralize the invading organism. Bacteria are the usual pathologic agents in the skin, while small dense LDL cholesterol particles are the culprits in the arteries. The inflammatory reaction leads to swelling as chemicals and more cells enter the “arena.” Both processes lead to the development of a boil that weakens the thin epidermis (or endothelium in the artery). This abscess can either open and drain or gradually recede as the inflammatory cells get control of the process. The rupture of this soft liquified plaque in the artery results in acute clot formation and frequently leads to a heart attack. If a break does not occur, an ongoing oxidation process results in scar formation in the skin and calcification in the arterial segment. Calcium, therefore, is a marker of previous inflammation within the arterial wall.

Higher scores are generally associated with a greater risk of a future cardiac event such as a heart attack or need for a stent. However, the CCS cannot reveal the magnitude of any blockages in the heart because it is a static image rather than an angiographic one. Its value lies in its ability to identify higher-risk patients that need more careful attention and guidance regarding their risk. It is a good motivation tool for my cynical or unmotivated patients who need more convincing evidence of their trouble.

Some factors can alter the value of the CCS and diminish its value. Long-distance endurance exercise over many years may be associated with higher calcium scores. Although some patients have significant underlying CAD, the correlation with risk may need more accuracy. Chronic exposure to released oxidative metabolites during prolonged endurance exercise may play a role. These patients generally have high-performance levels on stress testing and may be less prone to acute cardiac events.

Lipoprotein (a), also identified as (Lp(a), is a type of LDL cholesterol particle that is genetically determined. Elevated Lp(a) levels greater than 50 are associated with an increased risk of coronary artery disease, aortic stenosis, and stroke. Patients with elevated levels frequently have coronary artery calcification and aortic valve calcification. All patients with abnormal coronary calcium scores and a family history of CAD or multiple risk factors need to obtain this blood test. Unfortunately, treatment options are minimal. Statin therapy may increase levels. Newer injectable cholesterol agents (PCSK9 inhibitors) appear to lower Lp(a) levels, but these agents are costly, and the insurance approval process can be tedious.

Long-term use of statin therapy is also known to be associated with higher calcium scores. This effect appears to be related to impairment in the synthesis of Vitamin K2. Vitamin K2 is a cofactor needed to activate proteins in the arteries and tissues (matrix GLA-protein) that reduce calcium deposition in the arteries. Vitamin K2 supplements in some studies may mitigate this risk, but these supplements should be used cautiously in patients on certain blood thinners like Warfarin. Patients on Warfarin therapy are known to have an increased risk of coronary artery calcification. Therefore, Warfarin’s effect of antagonizing Vitamin K factors may play a role.

I have been concerned about the valuable benefits that are supposed to occur with statin therapy in patients with high CCS. There is a paradox that exists here. How does a drug that increases coronary calcification reduce long-term cardiovascular risk when we know that the risk of a heart attack increases as the CCS increases? There is already enough controversy regarding statin therapy in the primary prevention of CAD. This “paradox” only further serves to confuse. This concern should raise valid arguments about the long-term prevention benefits of statin therapy. Do we ignore the data on the value of the CCS, or should we question the usefulness of statin therapy in patients with elevated scores? These questions are essential to discuss with your doctor. It allows for shared decision-making before agreeing to take a drug for the rest of your life.

What is my current approach to the utility of CCS in evaluating and treating my patient population? First, I must admit that my practice has changed as science has evolved. Initially, I felt compelled to treat patients with higher scores (greater than 100) with risk factor counseling and statin therapy. I no longer apply statin use to all these patients. Instead, I perform stress testing for patients complaining of chest discomfort and sedentary patients with higher scores who want to begin a regular exercise regimen. I also obtained advanced lipid parameters, including an Lp(a) level, apolipoprotein B measurement, and a high-sensitivity CRP to assess underlying inflammation. I also measure LDL particle size and numbers before considering lifestyle and drug therapy. I do not automatically begin statin therapy in patients with elevated scores. Everyone receives individualized treatment plans based on labs, lifestyle, and risk.

There is a valid criticism of mass screening for CAD with coronary calcium scoring studies. The predictive and treatment-directed value in the very young (40 years or younger) and the elderly (greater than 75 years) is minimal, in my opinion. There is a small radiation risk, which is acceptable in most patients. However, I do not obtain calcium testing in younger women, especially those of childbearing age. (I also avoid any nuclear imaging studies in this patient group.) Indiscriminate screening can also lead to further unnecessary testing. An abnormal score can also confuse and provoke anxiety in some patients if the true meaning of the results is not adequately explained. The initial cost of the study is usually low ($50). Still, any abnormality can lead to much more expensive testing, and much of this additional evaluation may be unnecessary in lower-risk patients.

I rarely perform serial studies, and they are only necessary if the patient is interested in the impact of various interventions that have been utilized. Statin therapy invariably leads to higher scores, which can be very discouraging for patients who genuinely try to lower their risk factors. I remind patients of this effect and almost always discourage them from additional scoring studies.

We can be confused by this paradox related to coronary calcium, statin therapy, and overall risk. There is a dichotomy between the effect of statins on calcium scoring (statins raise the score) versus the prediction of long-term risk (a higher calcium score is associated with a higher risk of cardiac events). Why do physicians recommend statin therapy in all patients with elevated scores? I suspect that most doctors are unaware of the effects of statins on the calcium/artery process. We have been under the assumption that calcium in the arteries only connotes previous arterial inflammation and plaque formation. Is it possible that calcium can independently deposit within the arterial wall without associated inflammatory activity? I don’t have a definitive answer, but I have cared for many patients with very high calcium scores (7000 in one case) who did not have significant coronary artery obstruction. This observation does not dismiss the possibility of obstructive disease in those patients with high scores. It simply raises the question of whether high calcium scores consistently predict disease. All patients with elevated calcium scores should have an Lp(a) blood level drawn to determine if this hereditary factor is linked to the presence of coronary calcification. Patients with high Lp(a) levels do not respond to statins, and their risk may be enhanced due to the negative effect of statin therapy on these values.

Doctors must be mindful of the calcium/statin/survival paradox conundrum. Imagine a 50-year-old healthy man with a modest cholesterol elevation arriving in the office with an abnormal coronary calcium score. After seeing a hospital marketing campaign, he decided to get the test independently. He is nervous and anxious because his score is 50. His primary care physician reviews the information and informs the patient that he has underlying CAD. A statin is prescribed, and a cardiology referral is made. The Cardiologist orders a stress test and agrees with the statin. The stress test is unremarkable, and he is sent on his merry way with a recommendation to get another calcium score in 5 years. Everyone feels better, but is this the correct approach? Would it be essential to notify the patient that reduction in cardiac events is not proven with calcium scores less than 100? Would it be helpful to obtain an Lp(a) level to ensure that statin therapy doesn’t make his risk potentially more significant? Would increasing his dietary Vitamin K or K2/K7 supplementation benefit the patient? Is there a discussion about statins’ potentially harmful side effects, including the risk of muscle discomfort and diabetes? Is it a good idea to get another scan when the higher score only discourages the patient further and leads to further testing?

We who have chosen the field of medicine must heal and not harm. Therefore, we must think first before we react. Our intentions are good, and our treatment protocols seem valid. And yet, we can come to the wrong conclusion that leads to damage rather than benefit for the patient. At times like this, it is perhaps helpful for us to reflect on some valuable words of wisdom that may open our minds and help us to change our approach:

“For every complex problem, there is an answer that is clear, simple, and wrong.”

H.L. Mencken