We Finally Know How To Remove Plaque From Arteries

We didn't know that this was possible. We'd hypothesized about it, but to actually see it in the clinical trial gives people so much hope that we actually are ending heart disease. Because for a long time, the school of thought was that if arterial plaque had started developing in your blood vessels, it was just a one-way path. We could hopefully slow it down, possibly even stop it, and stabilize that plaque by having more calcium come down on top of it so that it doesn't rupture. But we didn't know that we could actually significantly reduce that existing plaque. Yes, there was some evidence of marginal benefits, but drastic reductions were more speculative. And even if this was possible, we didn't necessarily know how to get there. Well, now a new study from Denmark has shown that we can remove plaque. Not just stop new plaque from forming, but actually take some of that plaque away that's already in our blood vessels. But it takes a specific strategy. So, why does plaque develop in our blood vessels? Well, you'll know this already. It's usually things like high blood sugar levels, not being insulin sensitive, high inflammation, and high blood pressure. All of those just pour fuel on the fire. They speed up plaque formation. And that plaque can then rupture and then cause a heart attack. Now, one of the concerning things is that even if we control those risk factors, we can still see plaque developing. So, in the PESA study, which is spelled p e s a, researchers took middle-aged bank employees in Spain who didn't smoke. They had a normal weight, normal blood pressure, and normal blood sugar levels. They scanned the arteries in their neck, their belly, and in the legs. And then they checked their heart arteries for calcium and plaque. Half of them already had plaque somewhere. And even among those with ideal numbers, about a third of those people did. And the higher, get this, the higher their LDL cholesterol, the more likely they were to have it. About one in 10 people with an LDL of 60 to 70, rising to nearly two in three at 150 to 160 mg per deciliter of LDL cholesterol. Now, because of the PESA study and many other lines of evidence, including Mendelian randomization studies, where people are born with genes that lower their LDL cholesterol for life, and in clinical trials where we actively lower LDL cholesterol and apoB to see if we can lower heart disease rates, we can say with confidence that LDL cholesterol and apoB, which is a count of the particles that carry cholesterol into the artery wall, are causal risk factors for heart disease. So, it's not to say that it's the only risk factor. We still, of course, have to look after our blood pressure and insulin sensitivity, but we do have to look after our apoB as well. So, how do we lower apoB? We start with diet, but that can only go so far. We've entered a world where we can enhance the body beyond just diet and exercise and sleep. The first enhancement that we can reach for is statin medications, which reduce the amount of cholesterol that the liver produces. But is it safe to push blood cholesterol levels down to these levels, down so low? Well, on this point, nearly every cell in our body can produce its own cholesterol. The liver and the gut make most of it, and they send that extra around the body in case other tissues need a temporary top So, the amount of cholesterol in the blood is a tiny fraction of the body's total cholesterol. So, lowering the cholesterol in your blood does not starve your cells of it. But it is the cholesterol in the blood that can wreak havoc with our blood vessels, as I've already explained. But surely lowering cholesterol will destroy natural hormone production and our memory. Real quick before I answer that, I've put together a free health roadmap built around one idea: maximum health for minimum effort. It covers the numbers worth knowing, like your blood pressure, cholesterol, and blood sugar. Which screening tests come up at which age, and what the evidence suggests doing about each. It's free, and the link is in the pinned comment. So, back to that question. A trial of 1,200 people who were all on very strong cholesterol-lowering medications found no effect on memory. Another found no change in sex or adrenal hormones, even when LDL cholesterol was pushed very low. But one of the interesting findings is that when we use statins, in the short term, they actually seem to increase the amount of calcium that's in our blood vessels. So, let's explain that. This This where the body is trying to stabilize the plaque. It lays down calcium on top of that vulnerable soft plaque so that it's less likely to rupture. So, if you've had a coronary artery calcium scan, your score could actually look worse in the short term when you've just started statins, even though your chance of having a heart attack has gone down. And that brings us to the question, can we actually start to remove some of that plaque, not just stabilize it? Well, one of the big trials to show this came in 2006. It involved about 350 people with heart disease who took rosuvastatin 40 mg for 2 years. So, their LDL cholesterol fell to about 61. They then took ultrasound probes and threaded it inside their heart arteries, and they showed that the plaque had shrunk. The typical person lost about 8% of their plaque burden, and over the next decades, other trials have found similar findings. Plaque shrank in about six to seven people in 10 who were on intensive treatments, but only by about a few percent. And those studies looked at one stretch of one artery. Often in people who were already on a statin before they'd started. Meanwhile, other trials that were looking at heart attacks, they kept telling us the same thing. Lower LDL cholesterol is better. And earlier this year, a trial called the Ease Pave study, which was a randomized clinical trial involving over 3,000 people with heart disease. Half of them had an LDL target of under 55, and the other had a target of about 70. So, to get LDL cholesterol that low, a statin on its own often isn't enough. So, doctors added a second enhancement to the group that was targeting the LDL cholesterol of 55. And that second enhancement is a medication called ezetimibe. Ezetimibe works by telling the gut to not absorb as much cholesterol. So, because it works on a different pathway to statins, the two work really well together to lower LDL cholesterol and apoB. So, over the 3-year study follow-up period, 6.6% of the lower target group had a major cardiovascular event against 9.7%. So, if LDL cholesterol through this combination therapy means having fewer heart attacks, does it also mean plaque shrinking? Well, the new Danish trial called the flow promote trial gives us a look at exactly that. They took 104 people with newly diagnosed narrowing in their heart arteries and they weren't already on long-term statin treatment and they were randomly split into two groups. Half of them got atorvastatin 40 mg, which is a standard dose. The other half got a stronger combination therapy. So, rosuvastatin 40 mg on top of ezetimibe 10 mg. They then scanned everyone's heart arteries with a CT angiogram at the start and then at 9 months and then at 18 months using the same scanner settings each time. LDL cholesterol fell from about 120 to 70 mg per deciliter on the atorvastatin group and then for the combination group, it fell to 42. And the plaque shrank in both groups. On atorvastatin, the total plaque fell by about 14% but on the combination, it fell by a whopping 21% and this happened fast. So, on the combination treatment, much of that fall had already shown up at the 9-month scan but the crucial part is what that plaque is made of. So, the calcified plaque, it went the other way. It grew by about half in both of the groups. So, what's likely happening is that we're still trying to stabilize that plaque that I talked about earlier in the video. So, the calcium is being laid down on what's left but what matters more is the soft non-calcified plaque. This is the vulnerable plaque that can break away and cause heart attacks. The soft plaque, it fell even further by 20% in the atorvastatin group and then 28% in the combination group. And the lower that someone's LDL cholesterol went, the more their plaque tended to shrink. As the study's lead author puts it, the lower the LDL cholesterol, the greater the plaque regression. So, to put all of this into perspective, that 2006 ultrasound trial that I mentioned earlier in the video took 2 years to shrink plaque by about 7% but here in the combination treatment, it took off about 20% across the whole heart in over a year and a half. But can we really trust this trial? What is the whole picture and who funded it? Now, real quick before I answer those, most adults don't get enough potassium or fiber. So, I designed a potassium fiber drink that's a genuine upgrade from plain water. Each scoop has about 8 g of fiber, so 29% of the daily recommended intake, and 500 mg of potassium as potassium citrate. The fiber is acacia gum, so it doesn't turn into gel in the glass, and it dissolves easily. Check it out at potassiumfiber.com. So, back to the trial. The trial is small. It only involved 104 people, and the plaque wasn't actually the trial's main question. The main question was whether blood flow through the narrowed arteries would improve more on the stronger treatment. Unfortunately, for that primary outcome, it didn't reach statistical significance. There wasn't an improvement. The flow seemed to get a little bit better in both groups with no real differences between them. So, the authors themselves say that the plaque results should be treated as exploratory. And everyone in the study knew what tablets they were taking, so it wasn't a true double-blind trial. The person who was measuring the scans though, they didn't know which person was in each group. But, that brings me on to the next point. These measurements of the plaque is relatively rough. So, when the same team scanned the same patients twice an hour apart, one person's plaque reading could differ by up to 90 cubic millimeters out of a typical total of about 260. So, across the whole group, that noise it mostly averages out, and the gap between the two treatments still held. But, for any one person, a single reading going up or going down doesn't necessarily tell you much. And the gap between the two treatments depends on how you measure it. So, that 21% versus the 14% is the total amount of plaque. Overall though, I'm confident that the plaque shrank in both groups, and that is the really exciting part. I'm less sure exactly how much the extra combination therapy added though. But, overall it does make me glad that I myself am on combination therapy of rosuvastatin 5 mg and ezetimibe 10 mg. But, who funded this trial? Is it just big pharma trying to sell drugs? Well, was paid for by a Danish charitable organization called the Novo Nordisk Foundation, which had no role to play in this analysis. And the drugs are off-patent and extremely cheap. So, at costplusdrugs.com, rosuvastatin 5 mg and ezetimibe 10 mg, they each cost less than $10 a month. But what about side effects? Well, one in five people had their treatment changed during the trial, mostly for muscle aches or raised liver enzymes. Only two stopped their statin altogether. So, here is my take. We've known for about 20 years that plaque can shrink by a little bit, but this trial suggests how far it can go, and across all of the heart's main arteries, when LDL gets very low, we can start to shrink that plaque. And the lesson I take from this trial is that we do want to aim for lower LDL cholesterol levels for longer. So, here's what I do in the clinic. For most patients, we aim to get their apoB below 50. So, we generally start people, of course, in addition to diet and exercise, with rosuvastatin 5 mg. And if that's not enough to reach then we add on ezetimibe 10 mg. And if people are statin intolerant, which happens to about 1 to 2% of people, that's when we switch to PCSK9 inhibitors. But rosuvastatin 5 mg is a lot lower compared to the doses that was used in this new trial, where they used 40 mg of rosuvastatin. So, why do I advocate for low-dose statins? Well, rosuvastatin 5 mg on its own, it lowers LDL cholesterol by about 45%. But if we go all the way up to 40 mg, it only gets you to about 63%. So, overall, we've got diminishing returns as we increase the dose. And in a trial of 3,780 people with heart disease, a moderate dose of rosuvastatin plus ezetimibe prevented heart attacks and strokes just as well compared to the higher doses of rosuvastatin. And fewer people had to stop or cut back because of side effects. But hang on, what are PCSK9 inhibitors? Well, it's a class of medication that helps your liver to pull more of the LDL cholesterol out of the blood. They're very well tolerated, and they don't cause the muscle side effects that statins do in about 1 to 2% of people. But, what about coronary artery calcium scans? Cuz I've mentioned that in this video. Why not wait until a scan shows that plaque has developed before we start any of these enhancements? Well, to me, that misses the boat. We want to truly practice preventive care, which means intervening before problems start, before the plaque starts happening. Where I do use a scan in the clinic is for someone who's really reluctant to start any of these enhancements. Seeing calcium in their own arteries can be what convinces them to start these enhancements. So, finally, we know that plaque in your arteries is not necessarily a one-way street. We want to aim for low apoB, and we want to start early. If we do this, then we can truly end coronary artery heart disease. And to see all of the cholesterol-lowering options that we now have, and why I think heart attacks could become exceedingly rare in the future, make sure to check out this next video here. And I've put the full write-up of this video, so the transcript and every study that I've cited, over at drstenfield.com. Link is in the video's description.