Oct 16, 2026 · 10 min · 6 segments
In this #europcr 2026 interview, Davide Capodanno and Peter Libby discuss the role of inflammation in atherosclerosis and why many high-risk coronary plaques remain undetected by angiography. Advances…
Peter LibbyGuest
Davide CapodannoHost
So, uh, we have a, a- an important conversation here, I think, uh, particularly in this, uh, environment because we are learning a lot about, uh, the biology of plaques.
We treat, uh, as interventionists, uh, focal lesions, but atherosclerosis at large, of course, is a systemic, uh, disease.
Well, you know, lifestyle and lipid-lowering control of traditional risk factors like hypertension and diabetes is fundamental in all of preventive cardiology.
But what we've learned in a time when we have excellent ways of approaching those traditional risk factors is that inflammation has emerged as a major factor in residual risk in the current pharmacologic era.
So my laboratory's been interested in inflammation, uh, experimentally and clinically for many years, and we were very interested in the concept of the high-risk plaque, the so-called vulnerable plaque.
And so we spent several decades actually working on the biology, understanding the cell and molecular processes that contribute to the creation of the thin-capped fibroatheroma.
And what we found was when we have inflammation in the intima, in the plaque, that there's a conversation between the inflammatory cells that congregate there.
The T lymphocytes can send a messenger to the smooth muscle cells that are the guardians of the integrity of the plaque's fibrous cap because they synthesize the interstitial collagen, the same collagen that lends strength to our sinew-
And the smooth muscle cell, when stimulated by these inflammatory mediators, has a brake on new collagen synthesis that you need to repair and maintain that all-important extracellular matrix.
We also worked out that there are inflammatory mediators, mostly elaborated by macrophages in the plaque, that can turn on the enzymes that chew up collagen.
And also, inflammation can control the expression of the gene that encodes tissue factor, the potent procoagulant that makes it so dangerous for the blood with its coagulation factors contact with the lipidic core of the plaque that is filled with inflammatory cells that can trigger acute events.
Now, in the current era, we've come to believe that superficial erosion may be on the rise because we're better at controlling lipids and traditional risk factors.
So, uh, we have a, a- an important conversation here, I think, uh, particularly in this, uh, environment because we are learning a lot about, uh, the biology of plaques.
We treat, uh, as interventionists, uh, focal lesions, but atherosclerosis at large, of course, is a systemic, uh, disease.
Well, you know, lifestyle and lipid-lowering control of traditional risk factors like hypertension and diabetes is fundamental in all of preventive cardiology.
But what we've learned in a time when we have excellent ways of approaching those traditional risk factors is that inflammation has emerged as a major factor in residual risk in the current pharmacologic era.
So my laboratory's been interested in inflammation, uh, experimentally and clinically for many years, and we were very interested in the concept of the high-risk plaque, the so-called vulnerable plaque.
And so we spent several decades actually working on the biology, understanding the cell and molecular processes that contribute to the creation of the thin-capped fibroatheroma.
And what we found was when we have inflammation in the intima, in the plaque, that there's a conversation between the inflammatory cells that congregate there.
The T lymphocytes can send a messenger to the smooth muscle cells that are the guardians of the integrity of the plaque's fibrous cap because they synthesize the interstitial collagen, the same collagen that lends strength to our sinew-
And the smooth muscle cell, when stimulated by these inflammatory mediators, has a brake on new collagen synthesis that you need to repair and maintain that all-important extracellular matrix.
We also worked out that there are inflammatory mediators, mostly elaborated by macrophages in the plaque, that can turn on the enzymes that chew up collagen.
And also, inflammation can control the expression of the gene that encodes tissue factor, the potent procoagulant that makes it so dangerous for the blood with its coagulation factors contact with the lipidic core of the plaque that is filled with inflammatory cells that can trigger acute events.
Now, in the current era, we've come to believe that superficial erosion may be on the rise because we're better at controlling lipids and traditional risk factors.
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