Instalab ResearchThe CAC score is measured in Agatston Units using CT imaging. A score of 0 indicates no visible calcified plaque and corresponds to extremely low risk of a heart attack in the next 10 years. Scores of 1 to 100 suggest mild plaque buildup, scores of 101 to 400 indicate moderate disease, and anything above 400 reflects significant plaque burden and very high cardiovascular risk. At the extreme end, some patients record scores above 1000, a finding that signals a substantial likelihood of major cardiac events within only a few years.
This test is uniquely predictive because it reflects total plaque burden. Cholesterol tests measure one risk factor, but calcium imaging reveals the cumulative effect of decades of biology, genetics, and lifestyle. Studies consistently demonstrate that higher CAC scores correlate with higher rates of heart attack, stroke, and need for interventions such as stents or bypass surgery. Unlike many other risk tools, CAC provides information that is directly linked to future outcomes and survival.
There is no therapy that dissolves or removes calcified plaque once it has formed. Calcium is a sign of past inflammation, a scar within the artery wall. Treatment does not target the calcium itself but rather the active processes that continue to build unstable, rupture-prone plaque. The goal is to slow progression, stabilize vulnerable areas, and dramatically reduce the chance of a sudden cardiovascular event.
This means that treatment is not about the number going down on repeat scans. In fact, calcification can increase even as risk goes down, because plaques harden and stabilize. The true success is not seen in the calcium score but in the prevention of heart attacks, strokes, and premature death.
Statins are the first line of defense for individuals with high CAC. They lower LDL cholesterol, reduce vascular inflammation, and stabilize plaques. In large clinical trials, statins have consistently lowered the risk of heart attacks and cardiovascular death, particularly in individuals at high risk. For those with CAC scores above 300, guidelines strongly recommend aggressive statin therapy regardless of baseline cholesterol levels. The evidence here is robust and statistically significant across multiple populations.
It is important to note that statins do not reduce calcium scores. In fact, scores often continue to rise because soft, unstable plaque becomes calcified and stable. This apparent paradox is actually protective. What matters most is that statins dramatically cut event rates in patients with high CAC.
Hypertension accelerates vascular injury and contributes to both the growth of plaque and the instability that can lead to rupture. CAC scoring is now being used in clinical practice to help personalize blood pressure treatment. Patients with high scores derive substantial benefit from more intensive blood pressure control, reducing cardiovascular risk even further. Large observational and interventional studies confirm that lowering blood pressure in this population improves outcomes, and the risks of modern blood pressure therapies are low.
Diet, exercise, and smoking cessation are the most powerful non-pharmacologic tools available. Patients with high CAC scores often feel a new urgency to commit to sustainable change. Diets that are rich in fruits, vegetables, whole grains, nuts, and fish consistently reduce LDL cholesterol and systemic inflammation. Exercise, particularly regular aerobic activity combined with resistance training, improves endothelial function, lowers blood pressure, and improves weight management. Smoking cessation is non-negotiable, as tobacco is one of the most potent accelerators of atherosclerosis.
Some studies combining intensive lifestyle change with statins and lipid-targeting therapies even show evidence of slowed or reversed plaque progression. These findings reinforce that while calcium itself may not regress, overall cardiovascular biology can improve significantly.
For some patients, statins alone are not enough to reach modern LDL targets. In such cases, non-statin therapies like ezetimibe or PCSK9 inhibitors are highly effective. These agents have demonstrated substantial reductions in LDL cholesterol and strong evidence for lowering cardiovascular events. Although there is less direct evidence specifically in high-CAC populations, the consistency of benefit across risk groups supports their use. Patients with CAC above 400 who remain above LDL targets despite statins should be considered for these therapies.
Supplements such as omega-3 fatty acids, niacin, and vitamin D have been studied in the context of atherosclerosis. While some small studies suggest possible slowing of plaque progression, the evidence is inconsistent and often limited by small sample sizes or lack of statistical rigor. At present, these should not be considered primary therapies. They may play a supporting role in broader lifestyle patterns, but they are not substitutes for proven medical therapy.
One of the most important points to emphasize is that a high calcium score alone is not an indication for procedures such as stents or bypass surgery. These interventions are lifesaving in the presence of severe symptoms or acute events, but studies show they do not improve outcomes when used simply because of a high calcium number. For asymptomatic individuals, the focus should remain squarely on risk factor modification and prevention.
The optimal plan is individualized. Someone with a score of 0 may be spared medication and focus on lifestyle. Someone with a score of 800, even if cholesterol looks normal, should be treated as high risk and started on statins, have blood pressure tightly controlled, and be guided into lasting lifestyle change. The CAC score allows clinicians to match treatment intensity with actual disease burden, giving patients a clearer path forward.
