Cause for concern. What steps to take next?
Already on a statin. Normal weight. Don’t smoke.
Taking BP meds.



Edited 1 time(s). Last edit at 09/10/2025 04:53PM by tibbar.

The usual advice is the same as for cardiac health in general. Lose weight, exercise, reduce alcohol, etc. How are your cholesterol numbers? Statins can help lower calcium levels.

Statins also tend to raise serum glucose levels. For the aged, those with metabolic syndrome, or those predisposed toward diabetes, this is not a 'good' side effect. If nothing else, it induces insulin activity and the associated weight gain.

It seems your dose of statin is too low, or you won't ever benefit much from a statin due to genetic risk factors (beyond your control). More and more physicians are beginning to question the dogma behind statins. When the analysis is done, something like 200 people would have to take a statin for 10 years to save one of them from a heart attack. Meanwhile, a lot of people are getting rich.

A calcium score is like a photograph. It shows an instant in time. It shows no linear progression or regression, no motion, no directionality. A CRP and one or two other scores might be better at pointing to the cause of the deposits. Remember, it's actually better for the deposits to be calcified. You WANT that. You don't want the plaque to be friable and liable to be dislodged and end up in the lungs, any coronary vessels, or in the brain. And that is one way statins help; they actually encourage calcium deposition in those plaque deposits.

But, why is the lesion happening...at all? The answer is well established and it points to inflammation. That can come from diabetes or other comorbidities that affect the endothelial linings of blood vessels. And this is where a CRP test can show an elevated score, and from there you might investigate other causal factors.

This is just my rudimentary and very inexpert understand from all that I have read and heard. Really, this discussion would be best held with a cardiologist.

I just talked to my brother in law last week. Unfortunately, he developed AFIB after a COVID infection months ago. An echo showed his right atrium was enlarged from the infection. He was talking about his treatment and the tests his cardiologist did. He had a CAC test which showed >90% 'blockage'. As you would imagine this put him under extreme stress. He then had an angiogram weeks later which showed no blockages.

I was thinking of maybe getting the CAC test but now I think I will pass.

Thanks for the responses. I am 79, 148 lbs, Never smoked. Moderate drinker. Take meds for a long history of high blood pressure. Taking a small statin dose for 2 years. Dr upping and switching me to Crestor.
My neck was x rayed for a mildly pinched nerve condition. It showed some calcification. So calcium test and Doppler test ordered.
Calcium test was 895. Is it always right?
Having Doppler tomorrow.
Had my every 6 years nuclear stress test 3 years ago following Bruce protocol. I stopped after about. 91/2 minutes. I replicate on the treadmill once a month and go to nine minutes…but walking on steep hills has me huffing and puffing.
I take Flec and have pacemaker.
No afib in recent year.
Thanks

Thank you very much for your insights.
Dr just switched from 40 mg of lovastatin to 20 mg of the stronger Crestor.
Cholesterol with drug was 151.
Bun, Creatine, and eGFR just outside the normal upper range by a point or two.
I have been on Flec and warafin for 16 years. Up until 2023 I had maybe 4-10 shortish episodes per year. I am very symtomoatic.
In 2023 I had a long episode 8 days. For heart function echo was greatly diminished, but came back. I had to be cardio converted. My pacemaker has shown no episodes since..knock on wood.
Thanks again for your inputs.
I exercise 3-4 days a week…mostly walking and treadmill. 4mPH for 15 minutes. On treadmill…longer if on street.



Edited 4 time(s). Last edit at 09/12/2025 12:38AM by tibbar.

Thanks for info. Hope he is feeling better.

As Gloaming wrote above. Let's not forget that statins also lower GLP1. What a business model - give one drug and then another one to and another one to deal with the unwanted direct (wouldn't call them euphemistically side effects) effects
It all seems to me more like akin to making a deal with the devil

I forgot to mention in my post that statins are also supposed to lower inflammation. I don't know much about that, but I did absolutely read it somewhere in the past eight months. Surprised me, and helped me to get over my distaste for them. I do take one on cardiologist's advice. He feared ischemia when I first presented with AF. All tests, including angiogram and Doppler, plus the dreaded MIBI nuclear stress test (X2 for me) came back with 'minor deposits'. It was sleep apnea. I'm still taking the statin because the medical establishment thinks it's a miracle drug.

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gloaming
I forgot to mention in my post that statins are also supposed to lower inflammation.

I've read there is thought that statins primary benefit come from lowering inflammation. Also that this benefit can be realized at low doses, which would reduce or avoid many side effects. I first read about this maybe 15 years ago, from the late Dr. Duane Graveline, a then retired astronaught (and MD) who got, among other things, transient global amnesia, from taking these meds. More from him can be read at [spacedoc.com]

Thanks, George.

Quote
GeorgeN

I forgot to mention in my post that statins are also supposed to lower inflammation.

I've read there is thought that statins primary benefit come from lowering inflammation. Also that this benefit can be realized at low doses, which would reduce or avoid many side effects. I first read about this maybe 15 years ag
o, from the late Dr. Duane Graveline, a then retired astronaught (and MD) who got, among other things, transient global amnesia, from taking these meds. More from him can be read at [spacedoc.com]

Also what Dr Brewer says? Wonder what his take on ‘his’ statins is on their lowering GLP 1 ?
[youtu.be]



Edited 1 time(s). Last edit at 09/13/2025 08:53PM by Joe.

This is from a post (not mine) in a FB group on heart disease & calcification. It specifically references the role of microbes and heart disease. I've pursued this for a number of years with oral hygiene. 12 years ago, cleanings took 90 minutes and I needed them 4x/year. Today it is twice a year and less than 30 minutes with no gum pockets over 2 mm. I also use other, off label, approaches to deal with biofilms and microbes throughout my body.

A New Paradigm: The Infectious Roots of Heart Disease

For generations, the narrative surrounding coronary heart disease has centered on a familiar cast of culprits: high cholesterol, hypertension, smoking, and diabetes. This traditional view posits that atherosclerosis, or the hardening of the arteries, is primarily a disease of lifestyle and metabolism. However, a compelling and rapidly growing body of evidence is forcing a paradigm shift, suggesting that this established view is incomplete. Research indicates that chronic, often hidden, infections may be a pivotal and previously underappreciated factor in the development, progression, and ultimate rupture of atherosclerotic plaques. This "infectious hypothesis" is not new, dating back to experiments in the 1970s, but it has been revitalized by advanced molecular techniques that reveal the hidden microbial world within our own arteries. This emerging understanding recasts heart disease, at least in part, as an infectious and inflammatory condition, opening the door to revolutionary new strategies for prevention and treatment.

Microbial Footprints in Diseased Arteries
A cornerstone of the infectious hypothesis is the direct detection of microbes within the very plaques that cause heart attacks. Using highly sensitive molecular tests, scientists have uncovered the genetic footprints—the DNA—of a wide array of bacteria and viruses inside arterial lesions. These microbes often originate from distant sites in the body, such as the mouth, gut, and respiratory tract, suggesting they travel through the bloodstream to colonize the vessel wall.

A landmark 2025 study published in the Journal of the American Heart Association provided a stunning piece of this puzzle. Researchers found that oral streptococci of the “viridans group” were the most common bacteria identified, present in approximately 42% of coronary plaque samples. These bacteria are ubiquitous in the human mouth, forming the basis of dental plaque, and are typically considered harmless. Their frequent presence deep inside the arteries of the heart was a revelatory finding, strongly reinforcing the long-observed epidemiological link between poor oral health, chronic gum disease (periodontitis), and an increased risk of heart attacks. Pathogens specifically associated with periodontitis, such as Porphyromonas gingivalis, have also been consistently identified in atheromas, further cementing the mouth-heart connection.

Beyond oral bacteria, other pathogens have been strongly implicated. Chlamydia pneumoniae, a bacterium that causes respiratory infections, was a primary focus of research in the 1990s. Multiple studies found its DNA and proteins within plaques, and animal models demonstrated that infection could accelerate atherosclerosis. Similarly, latent viruses, particularly herpesviruses like cytomegalovirus (CMV), have been found in arterial lesions. These viruses establish lifelong infections and are thought to contribute to chronic vascular inflammation over many years. This evidence collectively shows that atherosclerotic plaques are not sterile accumulations of fat but can be active, colonized microbial habitats.

Mechanisms: From Chronic Inflammation to Autoimmune Attack
Infectious agents contribute to heart disease through a sophisticated and multifaceted assault on the vascular system. Their mechanisms can be broadly categorized into several key pathways:

Chronic Inflammation: Persistent infections, whether in the gums, lungs, or elsewhere, create a state of chronic, low-grade systemic inflammation. This elevates inflammatory markers in the blood, such as C-reactive protein, which can damage the delicate inner lining of the arteries (the endothelium). More critically, when microbes directly colonize the arterial wall, their components (like lipids and proteins in their cell walls) are recognized by the immune system's frontline sensors, known as Toll-like receptors (TLRs). This triggers a powerful local inflammatory cascade within the plaque itself, recruiting immune cells that ingest cholesterol, transforming into "foam cells" and driving plaque growth.
Molecular Mimicry and Autoimmunity: One of the most elegant and insidious mechanisms is a process of mistaken identity. Certain bacterial proteins, most notably a class called Heat Shock Proteins (HSPs), bear a striking structural resemblance to human HSPs. During a chronic infection, the body produces antibodies to fight the bacterial HSP. However, when human arterial cells are stressed by traditional risk factors like high blood pressure, they display their own human HSP on their surface as a danger signal. The anti-bacterial antibodies can then cross-react and mistakenly attack the human arterial cells, initiating an autoimmune "friendly fire" that causes persistent vascular injury and inflammation.
Direct Pathogenic Effects: Infections can also directly worsen cardiovascular risk factors. Some viral and bacterial infections can alter lipid metabolism, leading to lower levels of "good" HDL cholesterol and higher triglycerides. Furthermore, bacterial toxins can impair endothelial function and promote a pro-clotting state, making the blood more likely to form a thrombus.

The Biofilm Breakthrough: A Hidden Bacterial Bunker
Perhaps the most significant recent discovery is that bacteria within plaques often organize themselves into biofilms. A biofilm is a resilient, structured community of microbes encased in a self-produced slimy matrix that glues them to a surface. The 2025 study on oral streptococci found that these bacteria formed distinct biofilm colonies within the necrotic, lipid-rich core of the plaques.
This biofilm formation is a game-changing insight for two reasons. First, inside the biofilm, bacteria enter a dormant, metabolically slow state, effectively hiding from the immune system. Macrophages circulating in the plaque do not recognize these dormant colonies, allowing a chronic infection to smolder for years without causing alarm. Second, the protective slime matrix makes the bacteria highly resistant to antibiotics, which cannot easily penetrate the biofilm or kill inactive cells.

This "hidden bunker" model provides a powerful explanation for the sudden and unpredictable nature of heart attacks. Researchers theorize that while the biofilm is stable, it is a silent threat. However, an external trigger—such as a systemic viral infection like the flu, a high fever, or even intense stress—can "awaken" the dormant bacteria. The activated bacteria begin to multiply and break out of the biofilm, suddenly becoming visible to the immune system. The immune system then launches a massive, localized inflammatory assault against the newly exposed invaders right in the most vulnerable part of the plaque. This intense inflammation releases enzymes that rapidly digest and weaken the plaque's protective fibrous cap, leading to its rupture. The exposed plaque contents trigger a blood clot (thrombus) that blocks the artery, causing a heart attack. This model explains not only why infections like the flu can trigger cardiac events but also why past clinical trials using short-term antibiotics failed—they were unable to eradicate the bacteria bunkered down in their resilient biofilm fortresses.

Clinical Implications and the Future of Cardiovascular Prevention
The recognition of infection's role in heart disease has profound implications for both current and future medical practice. It elevates the importance of managing chronic inflammation as a core component of cardiovascular health.

For prevention, the message is clear and actionable. Meticulous oral hygiene—including regular brushing, flossing, and professional dental care to treat periodontitis—is no longer just about preserving teeth; it is a critical strategy to reduce the load of bacteria entering the bloodstream and seeding the arteries. Likewise, staying up-to-date on vaccinations for influenza, COVID-19, and pneumonia is a vital protective measure, as preventing these acute infections can avert the trigger that might awaken a dormant plaque biofilm and cause a heart attack.
Looking forward, these discoveries are paving the way for revolutionary therapeutic approaches. While simple antibiotics have failed, future strategies might involve drugs that can specifically dismantle biofilms or targeted antimicrobials used for high-risk patients. The ultimate goal, however, may be vaccination. Researchers now speculate that a vaccine targeting key atherogenic bacteria, such as the viridans streptococci or P. gingivalis, could one day prevent a significant portion of heart attacks. This would represent a true paradigm shift, transforming the treatment of our leading killer from a chronic management problem into a preventable, infectious-style disease, much as the discovery of H. pylori transformed ulcer treatment decades ago. While heart disease remains a complex condition influenced by genetics, diet, and lifestyle, acknowledging its infectious component provides a powerful new lens through which to understand and, ultimately, conquer it.

Deep Dive: [docs.google.com]

I am positive I read about a suspected link between heart disease and gum disease at least 10 years ago. It rings true. I could even see a case for sinusitis, fungal infections, anything that raises the body's natural immune response and its attendant inflammation. The 'smarter' pathogens are at the stage in their evolution where they can suppress, fool, or co-opt the immune system to their own purposes. Had to happen sooner or later.

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gloaming
I am positive I read about a suspected link between heart disease and gum disease at least 10 years ago.

Absolutely true. It's been known for some time (although the insurance industry seems incapable of recognizing the evidence). And that's true both in an acute sense and a chronic sense. Chronic low-level gum disease produces inflammation and we all know that prolonged inflammation is damaging to the cardiovascular system. But it's' also true in the acute sense that infections in the teeth or gums can travel to the chest via lymph nodes and cause nasty things like endocarditis.

I had some personal experience with that as a young man. At 18 my dentist noted that all four of my wisdom teeth were completely impacted below the bone.

I asked, "What I should do about that?"

He said "Nothing unless they begin to bother you." So I happily did nothing for the next six years.

He was wrong. When I was 24, I went to a routine dental checkup and the dentist brought in an x-ray to show me. There was this faint but plainly visible circular shadow directly below one of my wisdom teeth. "That's an abscess," he said, and then wrote me a prescription for antibiotics and referred me to an oral surgeon for immediate removal of the wisdom teeth. He explained that that abscess was a direct threat to my heart. The antibiotics weren't to treat the abscess, they were to prevent it from killing me.

To all….thank you. Interesting info.

Cause for action. My high calcium score led to an angiogram and, shortly after, six stents. Life saver.

I don't know the details of your case and history, but I probably would want a cardiac CT angiography (CTA) scan with Fractional Flow Reserve (FFR-CT Analysis) on a high-resolution CT scanner, typically found at major cardiac hospitals. This will show exactly what is going on inside your arteries, as opposed to your calcium scan, which is just an indirect marker.

Alternative approaches are optimal medical therapy (OMT) with statins, etc, and then only act on symptoms. In my opinion, this approach is just asking for trouble when the technology now exists to find out what is actually happening right now. And FWIW I was on the usual meds and passed the usual tests (echo and stress) and still needed the stents.

Jim



Edited 1 time(s). Last edit at 09/25/2025 02:18PM by mjamesone.

Jim,
Thank you so much for taking the time to inform me. I am due to meet with a cardiologist in about 2 weeks.

Joe H

I met with a cardiologist who works in the same hospital as my EP. Because I had gone 9 minutes plus on the Bruce nuclear stress test 2 years ago, he wanted to think more about whether to do further testing. I had relayed Jim’s experience to him. It made an impression on him, but he seemed to be of a mind to settle on Crestor at least in the short term. At the moment he is not recommending more tests and then a potential angiogram because I can currently exercise pretty well for a 79 year old. But the Dr was open minded and wanted to think on the whole situation…wants to meet again 3 months.

They've had good luck at the Cleveland Clinic with a whole food, plant-based diet, no oil. Dr. Caldwell Esselstyn has lots of videos on youtube on the subject of reversing heart disease. They show amazing changes on angiograms! His wife Anne and daughter Jane have nice cooking videos. Read about the "China Study."

Libby,
Thank you. I was surprised at score. I eat a pretty healthy diet, normal weight, etc.
Since the score, the EP thinks it best to switch off Flecainide ( on it for 16 years with a typical year being 5-10 short episodes a year…but one year 2023 I had a long episode that needed to get cardio converted.and/ or get an ablation in Boston.