Do Statins Prevent Heart Attacks?

This week’s blog explores a controversial topic: statins’ role in plaque reversal, reducing inflammation, and ultimately preventing heart attacks.

I was a statin hater from day one and delayed my own statin treatment for about three years. But after dealing with cardiovascular disease for several years, statins are significant to my treatment’s success. Dosing is essential. I do take low-dose statins and recommend low-dose statins if you have plaque.

If you have plaque, you have cardiovascular disease. I recommend that you take a low-dose statin.

Rarely will I recommend high-dose statin; I also recommend baby aspirin because you are in a different risk category.

We’ve reviewed how people can go from a 2% ten-year risk to somewhere between 2-40%, usually 10-20% risk. You can knock that down to 2% with lifestyle changes and several medications.

When and if you develop hot plaque, you won’t feel it. You won’t know it. If the hot plaque touches the bloodstream, it will increase the risk of clot formation; that’s when a heart attack happens.

There is something called pleiotropic mechanisms. The prefix “pleo” is used scientifically in astronomy and medicine; It means multiple. Statins have a pleiotropic mechanism. They decrease LDL. But they also reduce cardiovascular inflammation. It’s that latter mechanism, reduction of CV inflammation, that appears to be the bigger impact on the prevention of heart attacks.

Several researchers at Harvard discovered this. They found it with the Jupiter trial. They started noticing it in the WOSCOP studies as well. They found people where LDL was lower. Then it became higher, but they still had a decrease in heart attacks when they went on a statin.

These researchers (Paul Ridker & Gavin Blake) found statins also decreased cardiovascular inflammation. They deduced that part where your immune system starts attacking the plaque, creating clots.

They also found that certain statins are better than others in this space, and low-dose statins are necessary, not high-dose.

With the lower doses, we rarely have significant statin side effects. For example, we use Crestor (Rosuvastatin) five milligrams daily. Usually, we’ll use two and a half, or often we’ll do two and a half every other day or twice a week.

Livalo or Pitavastatin is a low-dose, kinder, gentler statin. We use a lot of it. Mostly what we use is very low-dose Rosuvastatin or Livalo.

We don’t recommend the use of Lipitor. Lipitor is good at decreasing LDL but not so good at inflammation. The reduced impact on CV inflammation is true, especially in several situations: if you’re a female- that’s half the population unless you consider that males are more likely to use statins at first.

And finally, the biggest problem is if you have pre-diabetes. Over 80% of the population has cardiovascular disease or pre-diabetes.

I will talk about a case from my “Prevention Myths” book. It’s an interesting case. It shows the value of a CT angiogram and the role of statins.

A patient, let’s call him Arnold, came to me and said, “Doc, I can’t believe you’re saying the same thing as all of the other doctors.” Wait a minute- lets’ see what that’s about. I had recommended that he consider using a low-dose statin.

Here’s how he came to me. He was 63 years old. He fainted while he was fishing with his son. He went to the nearest emergency department. The doctor in the ER said,” I can’t find anything wrong. Why don’t you take these statins”?

Arnold didn’t want to take statins. So he didn’t.

He went to an internist. The internist said the same thing. He did a stress test. Arnold passed the stress test-it was negative. But then the internist advised Arnold to take statins. Again, Arnold refused.

He knew a little bit about my YouTube channel. He knew I had a different perspective on statins. I don’t recommend them unless you already have plaque. When you have plaque, I recommend a very low dose instead of a high one.

When Arnold came to see me, we did a CIMT. The CIMT results were normal. They didn’t show anything. This raised some questions in terms of fainting. He did have some evidence of cardiovascular inflammation.

He had an elevated C-Reactive Protein, which means Arnold had some cardiovascular inflammation. He had a borderline oral glucose tolerance test and insulin response. We knew he had some of the underlying causes.

He had some evidence that those causes may be active. He had a borderline A1C. When you look at these results, especially in the baby boomer age group- folks 60 to 65, younger, and older- one of the most common causes of this problem is borderline or moderate pre-diabetes or even full-blown diabetes.

There are glucose metabolism problems that just have not been recognized. Professionals missed them.

His basal insulin was seven, a little bit high. The basal insulin that we would like to see is five or less.

For those worried about LDL, his LDL was 98. And he wasn’t on statins. So that wasn’t an issue.

I ordered a CTA (CT angiogram). It found that he had a plaque in the left anterior descending artery. That’s called the widow maker. The report made it clear that it wasn’t occlusive, meaning he didn’t have a blocked blood flow. That’s why his stress test was negative.

We did some more work, adjusted the CIMT, and found evidence of soft plaque. I told him that soft plaque could cause a heart attack even if it doesn’t block blood flow.

The fact that plaque was present indicated that Arnold had been through cycles of insulin resistance and inflammation, as I suspected. I see this time and time again when I see patients.

To continue with Arnold’s story, CIMT missed the plaque. You’d miss the diagnosis if you just looked at it without knowing Arnold’s story.

Here’s the rest of the story:

· his coronary calcium score began to show positive

· he agreed to take the statin

· he made some changes in his lifestyle

· he lost some weight

· he started to calcify the plaque

He knew this was a good result.

The small amount of soft plaque, which was challenging to find on the CT angiogram, had a risk of rupture. Once he reversed this situation and it calcified, he knew he had decreased heart attack and stroke risk.

He’s an anxious guy, but not nearly like he was in the past. He’s comfortable that we found the issue. We understood it. We dealt with it- we knew what to do. He increased his exercise regimen and doing it daily now.

Arnold feels confident that fainting spells were unrelated to any future cardiovascular event.

He hasn’t had any other fainting spells since then.

I rarely use high-dose statins because I don’t use statins for decreasing LDL. Usually, half the people that have a heart attack or stroke have normal LDL. So that’s evidence for me that LDL is not as important as most doctors think.

But let’s go back to that point about the pleiotropic effect. As a reminder, “pleio” means other; “tropic” means to go to. So pleiotropic result means that, as most docs are looking at dropping that LDL, I’m looking at something entirely different. I’m looking at decreasing cardiovascular inflammation. And it has been demonstrated that, and plenty of science shows that it does.

What was I taking for the longest time? First, I delayed taking a statin for a couple of years even though I was developing hypertension and some of those problems. I thought I had my lifestyle managed.

Bottom line: I used Crestor 5 milligrams. That’s what I tend to use now. You can use that every other day, three times a week, or even less often. There’s been research demonstrating you can get an improvement in cardiovascular inflammation from Rosuvastatin once a week. Now, I don’t routinely go there.

But again, we work very hard to accommodate a patient’s desires and concerns. And we don’t have a top-down type of approach. I don’t tell a patient, look, this is what you’re going to take. I don’t spend 7 minutes with a patient, write a script, and walk out the door. We talk a lot further. We have typical discussions, which will be between 30 and 60 minutes.

Even for myself, discussion and evidence have led me to try new ways. At one point, I switched to Pivasta. What is Pivasta? It’s the generic version of Livalo or Pitavastatin, 1 milligram once a day.

There’s nothing like a community. We saw that in the Louisville event. People got together and started talking about how they’ve had challenges and successes in preventing their heart attack, stroke, or chronic disease. It became clear that you don’t have to be a doc with a full-time, 30-year career in preventive medicine to understand this and successfully prevent heart attack and stroke – the number one killer and disablers of people.

You don’t have to be a physician to prevent eye or kidney disease. But you do have to listen, learn, think, & act with discipline.

People on statins will typically come to me with doses that are too high. Recently a patient came to me on 80 mg of Lipitor. It was a big dose, and he didn’t like it.

He had many muscle problems, so he stopped it; he’d been off it for a few months before coming to see me. His LDL was 130 to 140; it was more than most doctors accept.

The CIMT showed an arterial age of 35; this individual was 61. He had no discrete plaque. So he and I talked. He said one of the reasons he came to me was to see my perspective. He wanted to know if I thought he needed this medicine.

Well, I mean, most of you know my perspective. I don’t believe that just an LDL level of 130 with no plaque is dangerous and the reason to put somebody on a statin. I don’t think Framingham is the reason to put somebody on a statin.

I don’t use stress tests. I look at whether you have plaque. If you don’t have plaque, you won’t have a heart attack.

Believe it or not, the impact of statins on cardiovascular inflammation is taking some tiny steps into the mainstream of medicine. Here’s one of the first ones, the department of cardiovascular medicine at Oxford in current pharmaceutical designs was back in 2012.

Again, the evidence has been building for statins as anti-inflammatory agents in atherogenesis.

The molecular mechanisms and lessons from recent clinical trials so a couple of points that they made in here plaque generation is an inflammatory process yes we’ve been saying that 3-hydroxy3-methylglutaryl-CoA; the enzyme that these things impact, it’s HMG CoA reductase inhibitors that’s what statins, they do some other stuff too, but that enzyme is what has gotten the medical community initially focused on it because it had an impact of decreasing LDL.

Doctors have used statins for primary and secondary prevention of cardiovascular disease for a long time.

Primary prevention – for primary prevention, there are no signs or symptoms;

Secondary prevention – for secondary prevention, there are clear signs or symptoms.

If you want to get a little bit more understanding about primary versus secondary prevention and cardiovascular disease, see our article on the use of baby aspirin for primary vs secondary CV prevention. (We always recommended it for secondary, not primary prevention. The standards committees have now adopted that same stance. )

They do recommend it as well as we do. So again, this item of primary and secondary prevention sounds very simple. Still, once you start digging underneath, it has a significant impact and efficient implications, and it’s a little bit more confusing. Even most doctors don’t understand the difference between primary and secondary prevention, especially for cardiovascular disease.

STATINS – OUR EVOLVING UNDERSTANDING

When statins were initially developed, it was thought, “it’s all about LDL, the ‘bad’ cholesterol”. Since 2012, we have seen that statins reduce circulating C-Reactive Protein, a key marker for CV inflammation.

They also induce favorable effects on vascular redox; a mash-up of reduction-oxidation; remember oxidation? It is probably the most important underlying mechanism for inflammation, so it impacts the reduction-oxidation state of the redox strain and improves vascular reactive oxygen species.

So, let’s go to the following study: this was a critical study, the PRINCE study. This one came from investigators in Boston, Massachusetts. It’s a crucial study that addressed the anti-inflammatory effect again called the PRINCE trials – PRavastatin INflammation Crp Evaluation. It demonstrated that 40 milligrams of pravastatin given orally for 24 weeks reduced c-reactive protein levels in subjects without cardiovascular disease independently of the LDL cholesterol.

So again, let me repeat what Paul Ridker, Gavin Blake, and many others began to see. It didn’t matter whether LDL was involved. What was being impacted was CV inflammation; now, statins and nitric oxide (NO) are critical to maintaining endothelial homeostasis balance of the metabolic processes in the endothelium, the lining of the artery wall.

Endothelial homeostasis means the balance of the metabolic processes of the all-important lining of the artery wall. A healthy status increases nitric oxide bioavailability, increases gene expression for this activity, promotes endothelial healing, and inhibits isoprenoids (which are a problem in that space)

Cardiovascular inflammation is a big deal. It drives injury to that all-important endothelial lining. It’s called the intima.

The number one and two significant causes are too much insulin in the blood and too much glucose for too long.

Other inflammatory disease drivers are also rheumatoid arthritis and psoriatic arthritis.

Statins also inhibit endothelial cell activation, which is the first step in atherogenesis (plaque formation), damaging those endothelial cells; people looking at this space had always thought there were holes in the endothelial lining of the artery wall.

The evidence has shown that it’s not holes in that lining. Instead, it’s called transcytosis; in other words, the cell gets injured through inflammation, and these processes oxidize the LDL, and those particles could penetrate through the lining of those artery walls.

Here’s an article from the scientific journal Neurology. Neurologists have a significant stake in this area. It’s called stroke. There are two types of stroke; the first one is a clot or ischemic stroke causing loss of blood supply; the second one is bleeding into an area.

https://pubmed.ncbi.nlm.nih.gov/17724294/

By far, the most common is ischemic stroke. It’s also classified as part of cardiovascular disease because it’s the very same mechanism if you have this cardiovascular inflammation from inflamed liquid plaque seeps back through that injured endothelial or intimal cell into the blowing into the flowing bloodstream, causing a clot.

If that clock breaks off and goes to the heart, it’s a heart attack. If it breaks off and goes to the brain, it’s a stroke, so again very, very same causes the instrument, so back to this article, and again this was another article back to 2012.

LET’S DIGRESS BRIEFLY ABOUT STATIN SELECTION

I don’t use atorvastatin; it was the first one out of the blocks. It had the most prominent advertisements, it got the medical community hooked, and it’s been by far the biggest drug ever in terms of drug spending. If you look at the information we’re talking about and dig deeper into the impact of atorvastatin or Lipitor on cardiovascular inflammation; you’ll see evidence that it does have some. Still, it’s not nearly as good as other statins like simvastatin, Rosuvastatin, and Pitavastatin.

All those statins except Pitavastatin push you a little down this diabetes highway, so you ask why you would take something that causes the problem. Because it’s a benefits risk issue, as I said, I don’t recommend statins for people that don’t have plaque.

BACK TO THE NEUROLOGY ARTICLE

So, going back to the neurology article from 2012 about simvastatin withdrawal during acute myocardial infarction associated with C-Reactive Protein increased levels and pro-inflammatory effects. According to this article and a couple others, they’re beginning to see pro-inflammatory effects that might induce plaque instability and subsequent adverse events.

You’ve been hearing it from me for years. This information has been researched and demonstrated, and the medical community is beginning to adopt it. Another study on stroke found that stopping statins for three days was associated with an increased risk of death or disability dependency, so the conclusion from these studies is fascinating.

The anti-inflammatory effects of statins on the vascular wall are now widely accepted. At this point, cardiologists acknowledge that CV inflammation is the key; they’re just not clear yet what to do about it.

Some other drivers of cardiovascular inflammation statins suppress vascular and myocardial inflammation. They modulate vascular and myocardial redox states, the reduction-oxidation state, the inflammation state, and the improved nitric oxide bioavailability.

I mentioned before that I’ve been on five milligrams of Rosuvastatin for a couple of years. I’ve been experiencing terrible burning and stinging in my toes and lousy numbness in both hands in the middle of the night. I work out intensely, and I’m on my feet; there’s a significant focus on and a major fear associated with the impact of statins on muscle pains, the perception that it causes intense muscle pain.

Many researchers and most doctors ignore statin intolerance. That’s wrong. It’s dangerous.

There’s a significant concern and confusion about the placebo effect. People often have this problem and feel better when they have a placebo. Several excellent blinded studies compared placebo to statins and proved that the vast majority of this association was more of a placebo effect than an actual statin effect. But here’s the thing: if you go into the significant responsible standards committees who talk about this, they warn not to ignore statin problems.

I had my own regular, predictable episodes of calf pain.

I kept taking five milligrams of Rosuvastatin. That went on for about a year. It was something that I could live with. I would stretch the muscle back out and continue to work through it. I didn’t stop the statin. There are patients that I’ve had where we stopped or changed the statin. If you’ve got plaque, you need a statin. It’s not a great idea to stop the statin if you can push through it.

When the information about statin intolerance started coming out, there was a battle between the two major medical journals in England, the Lancet and the British Medical Journal. One of them was pro-statin, and the other one was anti-statin.

As a result, people began stopping their statins in droves. Some studies demonstrated the number of deaths climbing associated with decreased statin use.

I will tell you this. Please think twice before stopping statins if you have plaque. A lot of people have done it. Many deaths have demonstrated the real danger of stopping your statin when you have plaque and CV inflammation.

But if you don’t have plaque, I think you need to think twice about actually taking that statin. You probably don’t need it.

If you found this article helpful and want to start taking steps toward reversing your chronic disease, Dr. Brewer and the PrevMed staff are ready to serve you no matter where you’re located.

To find out more, schedule a consult here: prevmedhealth.com

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Do Statins Prevent Heart Attacks?

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