Nelson Vergel
Founder, ExcelMale.com
If you've been diligently taking your statin or PCSK9 inhibitor like Repatha, getting your LDL cholesterol down to target levels, and then your repeat coronary artery calcium (CAC) scan comes back higher than before—you're probably confused and maybe even alarmed. Wasn't the whole point of lowering cholesterol to reduce plaque in your arteries?
A new viewpoint article just published in JACC: Advances (January 2026) by Dr. Shaun Khanna and colleagues from Australia addresses this exact paradox and offers some reassuring insights that every man monitoring his cardiovascular health should understand.
How can medications that prevent heart attacks make your calcium score go up?
Think of it this way:
In untreated disease, calcification represents cumulative injury, inflammation, and necrosis—it's a marker of damage accumulating over years.
In treated disease, calcification may actually represent healing and stabilization—your body is essentially sealing off dangerous plaques.
The authors describe what they call the "healing hypothesis." When you aggressively lower LDL cholesterol, several beneficial things happen inside your arteries:
Lipid pools inside plaques shrink
Inflammation decreases
Dense calcium deposits form that "cap" the dangerous necrotic cores
The fibrous cap covering the plaque thickens and becomes more stable
The plaques become less likely to rupture—which is what actually causes heart attacks. But all that healing and sealing involves laying down calcium, which shows up on your CT scan.
Reduces total atheroma (plaque) volume
Increases calcium density
Thickens the protective fibrous caps
The increase in calcium density—not volume—is particularly associated with greater stability and lower event rates. In other words, denser, more consolidated calcium indicates a more stable, "healed" plaque.
PCSK9 inhibitors appear to amplify these effects even further, thickening fibrous caps and reducing the lipid content of plaques without necessarily decreasing total CAC scores.
So if you start aggressive lipid-lowering therapy and get a repeat CAC scan 1-2 years later showing higher calcium, you may be catching your arteries in the middle of a healing process. The dangerous lipid-rich components have already shrunk, but the calcification that stabilizes the plaque is still being laid down.
Additionally, some of the apparent increase in calcium scores may be due to CT imaging artifacts. When plaque composition changes and becomes denser, technical factors like "blooming" can make calcium appear larger than it actually is.
Don't panic over short-term CAC increases. If you've started statins or PCSK9 inhibitors and your repeat CAC scan shows progression, this should not automatically trigger alarm or changes in therapy—especially if you've achieved your LDL targets and remain asymptomatic.
Context matters. A rising CAC score accompanied by reduction in non-calcified plaque, improved vessel remodeling, or decreased inflammation is likely a favorable sign, not a negative one.
The goal is event reduction, not imaging regression. The ultimate measure of success is whether you have a heart attack or stroke—not what your calcium score looks like. The clinical trials consistently show reduced events with lipid-lowering therapy regardless of what happens to CAC.
CAC volume may be more informative than the Agatston score. If you're tracking your CAC over time while on statins, CAC volume (measured in mm³) is less affected by statin-induced plaque densification and may better reflect actual disease burden.
Very high scores still warrant aggressive treatment. Scores above 400 or 1,000 still indicate extensive atherosclerosis requiring maximum preventive efforts, regardless of what therapy you're already on.
Understanding this paradox prevents unnecessary anxiety and potentially harmful decisions—like stopping a medication that's actually helping because your calcium score went up.
The bottom line: A rising CAC score while on lipid-lowering therapy likely represents your plaques becoming more stable and less dangerous—a biological success that just happens to look like radiographic progression.
As the authors conclude, clinicians (and patients) should interpret CAC findings through a pathophysiologic lens, integrating plaque composition, clinical outcomes, and therapeutic context—not relying on calcium scores alone.
Reference:
Khanna S, Nerlekar N, Bhat A. Reconciling Coronary Artery Calcification in the Lipid-Lowering Era. JACC: Advances. 2026;5(1):102506. doi:10.1016/j.jacadv.2025.102506
Discussion: Have you experienced this situation—calcium score going up despite being on statins? Share your experience in the comments below.
A new viewpoint article just published in JACC: Advances (January 2026) by Dr. Shaun Khanna and colleagues from Australia addresses this exact paradox and offers some reassuring insights that every man monitoring his cardiovascular health should understand.
The Paradox Explained
Here's the situation that puzzles both patients and doctors: Statins and the newer PCSK9 inhibitors (like Repatha and Praluent) clearly reduce heart attacks and cardiovascular deaths. The clinical trial data is overwhelming. Yet when researchers follow patients on these medications with serial CT scans, their coronary calcium scores often increase over time—sometimes even faster than in people not taking these drugs.How can medications that prevent heart attacks make your calcium score go up?
It's About What the Calcium Represents
The key insight from this article is that coronary artery calcium is not a direct measure of how much plaque you have. Instead, it reflects the composition and stability of your plaques.Think of it this way:
In untreated disease, calcification represents cumulative injury, inflammation, and necrosis—it's a marker of damage accumulating over years.
In treated disease, calcification may actually represent healing and stabilization—your body is essentially sealing off dangerous plaques.
The authors describe what they call the "healing hypothesis." When you aggressively lower LDL cholesterol, several beneficial things happen inside your arteries:
Lipid pools inside plaques shrink
Inflammation decreases
Dense calcium deposits form that "cap" the dangerous necrotic cores
The fibrous cap covering the plaque thickens and becomes more stable
The plaques become less likely to rupture—which is what actually causes heart attacks. But all that healing and sealing involves laying down calcium, which shows up on your CT scan.
More Calcium Can Mean Less Danger
This sounds counterintuitive, but the research supports it. Studies using intravascular ultrasound and optical coherence tomography (which can look inside the arteries in detail) show that statin therapy:Reduces total atheroma (plaque) volume
Increases calcium density
Thickens the protective fibrous caps
The increase in calcium density—not volume—is particularly associated with greater stability and lower event rates. In other words, denser, more consolidated calcium indicates a more stable, "healed" plaque.
PCSK9 inhibitors appear to amplify these effects even further, thickening fibrous caps and reducing the lipid content of plaques without necessarily decreasing total CAC scores.
The Timing Factor
There's also a timing issue at play. Lipid and inflammatory components of plaques respond quickly to therapy—often within months. But calcification is a slower process that can lag by months to years.So if you start aggressive lipid-lowering therapy and get a repeat CAC scan 1-2 years later showing higher calcium, you may be catching your arteries in the middle of a healing process. The dangerous lipid-rich components have already shrunk, but the calcification that stabilizes the plaque is still being laid down.
Additionally, some of the apparent increase in calcium scores may be due to CT imaging artifacts. When plaque composition changes and becomes denser, technical factors like "blooming" can make calcium appear larger than it actually is.
What This Means for Your Clinical Care
Based on this understanding, the authors offer some practical guidance:Don't panic over short-term CAC increases. If you've started statins or PCSK9 inhibitors and your repeat CAC scan shows progression, this should not automatically trigger alarm or changes in therapy—especially if you've achieved your LDL targets and remain asymptomatic.
Context matters. A rising CAC score accompanied by reduction in non-calcified plaque, improved vessel remodeling, or decreased inflammation is likely a favorable sign, not a negative one.
The goal is event reduction, not imaging regression. The ultimate measure of success is whether you have a heart attack or stroke—not what your calcium score looks like. The clinical trials consistently show reduced events with lipid-lowering therapy regardless of what happens to CAC.
CAC volume may be more informative than the Agatston score. If you're tracking your CAC over time while on statins, CAC volume (measured in mm³) is less affected by statin-induced plaque densification and may better reflect actual disease burden.
Very high scores still warrant aggressive treatment. Scores above 400 or 1,000 still indicate extensive atherosclerosis requiring maximum preventive efforts, regardless of what therapy you're already on.
The Bigger Picture for Men's Health
For those of us in the men's health community, this is particularly relevant. Many men on testosterone replacement therapy are also managing cardiovascular risk factors and taking statins. CAC scoring has become a popular tool for risk assessment.Understanding this paradox prevents unnecessary anxiety and potentially harmful decisions—like stopping a medication that's actually helping because your calcium score went up.
The bottom line: A rising CAC score while on lipid-lowering therapy likely represents your plaques becoming more stable and less dangerous—a biological success that just happens to look like radiographic progression.
As the authors conclude, clinicians (and patients) should interpret CAC findings through a pathophysiologic lens, integrating plaque composition, clinical outcomes, and therapeutic context—not relying on calcium scores alone.
Reference:
Khanna S, Nerlekar N, Bhat A. Reconciling Coronary Artery Calcification in the Lipid-Lowering Era. JACC: Advances. 2026;5(1):102506. doi:10.1016/j.jacadv.2025.102506
Discussion: Have you experienced this situation—calcium score going up despite being on statins? Share your experience in the comments below.
