Loading summary
A
Welcome to Healthier World with Quest Diagnostics. Our goal is to prompt action from Insight as we keep you up to date on current clinical and diagnostic topics in cardiovascular, metabolic, endocrine and wellness medicine. Most people recognize that our bodies produce inflammation when fighting a viral infection. But what many people may not realize is that this inflammation can raise the risk for cardiometabolic events. I'm Dr. Mason Latsko, and today on the podcast, I have Dr. Mark Penn, founder and chief medical Officer for Cleveland Heart Lab. We're going to talk today about how viral infections can accelerate atherosclerotic burden and increase the likelihood of a major Cardiovascular event. Welcome, Dr. Penn. Thank you for joining me today.
B
Pleasure to be here. Thank you.
A
So I want to first start by setting the foundation for the audience. Can you tell us, from a high level, what is known with regards to the link between cardiovascular events and a patient's experience with an increased viral load or the amount of virus present in the body during an infection?
B
Yeah. Long before we measured viral loads and viral titers in patients to say, you have influenza, you have echovirus, you have whatever you have. The CDC used to classify a flu outbreak as an excess in myocardial infarction, death in the elderly in a region, because what they recognized was if there's a flu outbreak, the elderly will die more commonly of a heart attack. So the concepts here are incredibly old.
A
Wow, that's really interesting. And arguably, in the last several decades, our understanding of this relationship has evolved quite a bit. Can you talk a little bit about the research that underlies why having an increased viral load after an infection can increase your risk for cardiovascular events?
B
So, you know what we've learned in the last 20, 25 years? We used to think people developed a vulnerable plaque, that plaque ruptured, they had heart attack. And it was a one to one kind of correlation. What we now recognize is a lot of people have a lot of vulnerable plaque throughout their life. But what we've come to realize is that when you have acute inflammation or elevated chronic inflammation like rheumatoid arthritis, the probability of that plaque you may have of healing goes way down, and the chance of it going on to rupture and causing a heart attack goes up. Right. And what we now are starting to see in the literature are some really exciting papers that demonstrate that the risk of having a heart attack is highest within the seven days of having influenza. And that paper was out in the New England Journal in 2018, before COVID and thus it should never have been a surprise that Covid caused heart attacks because Covid is a respiratory virus. Respiratory viruses increase cytokine load, inflammation, and most respiratory viruses can cause heart attacks. In recent literature, it's now been validated in JAMA by Kauai and colleagues that showed that, and then they extended that to show that several other viruses also are associated with an increased risk of myocardial infarction. So acute inflammation's bad, chronic inflammation, psoriatic arthritis, rheumatoid arthritis, paral bad. And the best way we can really prevent all this, besides vaccines to prevent the viral infection, is to minimize our risk of having vulnerable plaques, which is minimizing cardiometabolic risk, minimizing ldl, minimizing sugars, and frankly, measuring inflammation along this so that if and when the patient gets influenza respiratory virus, there aren't any plaques to go on to rupture.
A
Yeah, that's a really great point. And I like a quote that you had said in a previous talk, which is, cholesterol doesn't drive heart attacks. Right. It drives vascular inflammation, which leads to heart attacks, as does other chronic conditions such as hypertension, diabetes, stress, anxiety, as well as respiratory infections. Now, I want to kind of zoom in on this a little bit when we talk about inflammation. In your vast experience, what are you describing as important inflammatory markers that connect an elevated viral load with an increased risk for cardiovascular events?
B
Yeah. So the goal of any prevention program is to mitigate all the risks we can mitigate. Right. Given that, in general, inflammation is the final common pathway for a myocardial event with plaque rupture, what we want to do is lower the inflammatory markers as much as we can. So the three that are most commonly used are HSCRP, MPO, myeloperoxidase, or Lppla2 activity. CRP is more of a general marker. MPO is more specific to vascular on the luminal surface, and LPPOA2 is about activation of the necrotic core. If we get an LDL to 90, an A1C down to 5, 2, and their MPO, LP, PLA2, and CRP are normal, I don't know that that patient needs much more aggressive care. Conversely, if you get them down to 70 of an LDL and their A1C is, you know, 5, 3, and their MPO is elevated, their LP, PLA2 is elevated, their HSCRP is still elevated, we haven't mitigated all the risk. Now we have to ask ourselves, what's the risk? It could be gum disease. Right. Which really went way up during COVID because people didn't visit the dentist, it could be that rheumatoid arthritis, that's not well controlled in the vasculopathy that we know is associated with that. What we know, if the patient has residual inflammatory marker elevation, we have not mitigated all the risk. And if we haven't mitigated all the risk, then a viral infection, respiratory virus, could put that patient at a greater risk risk of having an mi.
A
So LDL has always been something that we know is linked to cardiovascular risk. And now we've highlighted how inflammation can play a role. But you bring up a 1C as being another key contributor to cardiovascular events. Can you speak a little bit more about your view on how metabolic dysfunction is related to cardiovascular risk and also how it plays a role in the relationship between cardiovascular events and. And an increased viral load?
B
So cardiometabolic disease obviously increases the probability of having vulnerable plaque form and therefore probabilistically increases your risk of an MI and having a clinical event. Metabolic dysfunction is what's driving the underlying vascular disease that is ultimately impacted by the respiratory virus. So if you have somebody who has diabetes, elevated insulin resistance, hyperglycemia, hypertriglyceridemia, elevated inflammatory markers. We've already discussed those patients are at increased risk when they get a viral infection. A recent study out of Diabetes Care really nicely showed that not all diabetics or pre diabetics are the same. Right. They identified four distinct clusters of patients, and what they found was that the differences are whether they have insulin resistance or not, and the difference is whether they have albuminuria or not. And, you know, those allow us to distinguish which of our patients we really have to worry about in very meaningful ways. We really now have, from a cardiometabolic point of view, the ability to individualize care in a way we haven't had in years or ever. And by doing so, going into cold and flu season as we are, we can really figure out who do we have to worry about getting a respiratory virus and who's well cared for and ready for it. And it determines whether they, you know, at some level, whether they live or die through the experience.
A
Yeah, and that's sobering, but it's. It's very true and a good point. So the next thing I want to talk about is I want to walk through first which labs should even be ordered in a patient to get a better sense of their vasculature and their risk. And then what is a classic lab readout that a provider should be concerned about?
B
Yeah. So anybody who has heart disease you should be worried about, right? Classic board question. You have a patient who has had a prior MI and you get to do one thing. You can lower their blood pressure, lower their lipids, continue aspirin, quit smoking, or give them a flu shot. The answer is flu shot. A little bit more than quitting smoking. So it's why certainly in the CCU I work in, and many of us work in, patients come in, they get a flu shot. It's the reason why even though you get a flu shot, you might still get the flu. A lesser viral load, a lesser inflammatory response is a very good thing. So again, no question about that. Same is true with COVID vaccines. It's a very effective way to minimize risk in the setting of the respiratory virus. Beyond that, patients who have real risk that hasn't been mitigated, they too need to have that risk mitigated. A1C insulin resistance score, LDL, APOB, MPO, LPPLA2 and HSCRP. That's going to give you a sense of the status of that patient's vasculature. And if those inflammatory markers are abnormal, what might be driving it. If the A1C is decent, the LDL is good and the inflammation's elevated. Again, the mouth is a really good place to go to the biome through TMAO in that setting is reasonable. If you have a high APOB and relatively controlled ldl, you have small dense LDL particles. Those are pro inflammatory. We have data submitted now that shows that those two link in a biomarker analysis. And if you have an elevated APOB but a controlled ldl, you need to target the LDL lower. Things like that, we have to think a little bit harder and that's where we individualize patients. But that's the approach I would take.
A
And what are your thoughts about bringing some of these biomarkers like APOB and hscrp, mpo, IR score to primary care in order to really help patients better mitigate their risk and help providers identify those high risk patients?
B
You know what we had talked about back in early Covid was the idea that now's the time to really up our game in prevention so that the milieu necessary for a heart attack in the setting of a virus isn't present.
A
Absolutely. Well put. We have the tools to really take the reins on prevention and it's time to do so so that we can help patients. Any final thoughts before we round out today?
B
Get your flu shots.
A
Excellent. Thank you so much for joining. Till next time. That's a wrap on this episode of Healthier World with Quest Diagnostics. Please follow us on your favorite podcast app and be sure to check out Quest Diagnostics Clinical Education center for more resources, including educational webinars and research publications. Publications thank you for joining us today as we work to create a healthier world, one life at a time.
Episode Title: Viral infections and cardiometabolic complications
Air Date: December 11, 2025
Host: Dr. Mason Latsko (Quest Diagnostics)
Guest: Dr. Mark Penn, Founder and Chief Medical Officer, Cleveland Heart Lab
Duration: 12 minutes
This episode delves into the critical connection between viral infections and cardiometabolic complications. Dr. Mason Latsko and Dr. Mark Penn discuss how inflammation from viral infections can escalate the risk of serious cardiovascular events, such as heart attacks, particularly in vulnerable populations. The episode emphasizes the role of inflammation, metabolic health, and preventative care—including vaccines and advanced biomarkers—to minimize these risks.
“Cholesterol doesn't drive heart attacks. Right. It drives vascular inflammation, which leads to heart attacks, as does other chronic conditions such as hypertension, diabetes, stress, anxiety, as well as respiratory infections.”
– Dr. Latsko [04:07]
“If the patient has residual inflammatory marker elevation, we have not mitigated all the risk.”
– Dr. Penn [05:45]
“Now's the time to really up our game in prevention so that the milieu necessary for a heart attack in the setting of a virus isn't present.”
– Dr. Penn [11:13]
Final Takeaway:
[11:40] Dr. Penn: “Get your flu shots.”
Tone: Clear, authoritative, and pragmatic, emphasizing scientific evidence and actionable prevention.