Atherosclerosis - Pathogenesis, risk factors and complications

In this video, Dr Matt explains the pathophysiology of atherosclerosis- which include the risk factors, pathogenesis and chronic complications.

[animaloverdani]

best explanation for clinicians. I love how you include the 2 pathways that lead to ischemia. thank you!

[stephengreenwood]

Very good, tell all my paramedic students to watch and take notes from these tutorials

[davidcooper]

I just do not understand the educational curriculum in USA in highschool and college did not teach the basic medical information so that people are aware to take preventive measures through diet and exercise, where they are applicable ahead of time. I fished my education in the 1990, and I had to take biology studying about other animals instead learning the basic medical information to understand how my body works first. Good video!

[TheJpepe]

The main problem are the sugars and carbohydrates which oxidize the LDL converting it from type A to type B which is the one that leaks thru the intima and get digested by macrophages and form the Foam cells.

[antov]

Thank you for answering my Pathophysiology exam questions Doc!

[giridhar]

Very good I really appreciate your work

[af_co]

Great video as always, thanks Dr. Matt!✨

[faithwambua]

Thank you so much. I'm sure by watching your tutorials I will become the next cardiologist.

[ericgokey]

Great video, it helped me study. I was wondering Dr. the cause was not really talked about, we know that LDL comes from our food and that our livers only produce HDL, HDL lowers and cleans out LDL and LDL is what collects along with calcium and other debris. So LDL is really the issue. Since is have stopped consuming LDL in total, my LDL went from 230 in 2013 to LDL of 90 in 2018. this is by simply eliminating LDL from my diet. So, I had Hyperlipidemia, and now I'm healthy.
Cholesterol LDL only exists in Animal products.
Fiber helps us with cholesterol levels. and fiber only exists in plant foods.
(Our liver produces ALL of the cholesterol we need of HDL.)
so why would we not put together a great video like this one and note the actual cause. NOT predisposition like genetics (the escape goat)
but the actual cause.
genetics is like the gun handed to us from our parents.
however, our diet rich in animal products are the bullet and the willfully pulled trigger.
so genetics gun
diet bullets and pulled trigger.
These are important notable facts.
-Eric R Gokey.
Author
Med student
veteran
Again, thank you for the video.

Dr. Michael Greger: 'The primary reason diseases tend to run in families may be that diets tend to run in families.',


Your genetics load the gun. Your lifestyle pulls the trigger.
-Mehmet Oz

[Eagle_Delta]

Lipid peroxidation is an important event in the pathogenesis of atherosclerosis?

Now what fatty acids are prone to lipid peroxidation unsaturated fatty acids?

[raghadtv]

thank u so much, this was very helpful

[s_g]

Ldl gets inside intima thru damaged endothelial lining and there causes oxidation. High blood sugar causes HPN.

[SarahKos]

When a person with calcified arteries is calcium deficient, will the body preferentially resorb calcium from the bones or the abnormally calcified arteries?

[nickbower]

It is a thrombogenic issue. LDL theory is incorrect, it cannot pass through the endothelium. The first step is the damage to the glycocalyx, then thrombogenic damage, then plaques etc

[Eagle_Delta]

Definition of atherosclerosis is the presence of a sterol in an arterial macrophage?

[ozb]

bad fat, good
theirs no such thing, our body's make all the lipids the body does not make anything that is bad, what matters is lipid ratio's and if our liver make more LDL or more HDL or VLDL or SDLDL it's do a response to something we are just not aware
you guy's make good video's and i normally watch them but today i don't feel it maybe i'll continue in a day or two

[dombarton]

Carbohydrates are the main cause....its never fat!. Age is not an excuse!!! If you eat a carnivore diet or at least a low carb diet you will ward off heart disease.

Saturated fats are extremely important. Cholesterol is also very important.. essential for life. LDLs can be good and can be bad. The process of turning good LDL into Bad LDL isnt driven by fat in the diet..its driven by carbohydrates. Sugars..enter the circulation and damage the LDL particles. VLDLs..then IDLs..then LDL..all have an apo b 100 marker on their surface. The LDL receptor binding site is crucial for the liver to accept and recognise an LDL particle..ITs sugar from both simple and complex carbs that damage these binding sites through a process called glycation. This stops the liver from recognising it. It also fractionally shrinks it..causing it to be termed as small LDLs. This leads to oxidation of the LDL particle. Sugar can also cause it to become glyco oxidised which causes oxidative stress to the liver which leads to fatty liver disease. This damages the apob100 protein..makes it impossible for the liver to remove it from the circulatory system. So in effect it accumulates in the blood. This is what we term as an increase LDL particle count. Its the particle count which is a much better predictor of cardio vascular risk. So for an oxidised LDL particle to enter into an atherosclerotic plaque it has to pass through the lining of the artery. It firstly needs to breach this brush like layer called the glycocalyx. High levels of blood sugar damage the glycocalyx. Lectins in foods also damage the glycocalyx. The loosening of the tight junction proteins holding the epithelial tissue together. This lets the oxidised LDLs and circulating monocytes to enter into the sub endothelial space. Once there these monocytes turn into a macrophage. These macrophages express scavenger receptors which can recognise and bind to the damaged LDL particles that the liver receptors could not. These engulfed macrophages leads to the formation of a foam cell..a macrophage packed with lipids. Its these foam cells that are contained within atherosclerotic plaque..end result a BLOCKAGE. This is process...remembering that SUGAR is the cause not FAT. Humans do not need to ingest a single gram of sugar..not a single gram...we can make all the necessary glucose from a process known as gluconeogenesis. So eating saturated fats will increase your LDL levels but its the SUGAR that makes it go bad. So make sure you understand this.and spread the word to everyone else who bad mouths cholesterol and LDLs. They are crucial for life.
As a medic Meta analysis studies have shown the higher LDLs in your body..the longer you LIVED.

SO STOP CARBS and LIVE LONGER and HEALTHIER!


Insulin resistance is the cause of so many illnesses...hyperinsulinemia .... obesity is caused by constant high amounts of insulin in the blood caused by CARBS, which increases insulin...and in turn stores FAT. FAT does not raise insulin levels at all. Insulin is the fat-storage hormone. This is why when you stop the carbs, you lose fat. It's very simple biochemistry. type 1 diabetics are often quite skinny, why because they don't produce enough insulin.

[nswhorse]

LDL is not the cause of atherosclerosis, nor is LDL-C (the cholesterol carried by LDL particles). This has to be one of the dumbest widely accepted errors in the history of science. Yes, there is an association between high LDL-C and atherosclerosis and CVD, but correlation is not causation, and there is literally zero evidence that it is causative. Nor is there any mechanistic model for how it could possibly be the cause. And there is also an association with low LDL-C, which has a stronger effect size than high LDL-C. If LDL-C is pathogenic, why would a low level be even more strongly associated with both all cause mortality and CVD? The reality is that both LDL and cholesterol are *protective* and both involved in the immune cascade that seeks to repair inflammatory damage. LDLs are also subject to both oxidative damage and glycation (which I note you neglected to mention), the same as the epithelium, and it is damaged LDLs that circulate and ultimately become stuck in plaques, because the liver receptors can't attach retrieve them from the bloodstream. This is why high LDL-C is *associated* with atherosclerosis and CVD. A combination of being present as part of the attempt to repair the damage, as well as the carrier LDL becoming damaged itself. Damaged epithelium + damaged LDL = atherosclerosis. The damage is caused primarily by oxidised polyunsaturated fatty acids (chiefly from so-called vegetable oils and their hydrogenated derivatives) and by glycation damage due to chronic high blood sugar from constant carbohydrate consumption.

The consequence of the false belief that high LDL-C is the cause of atherosclerosis is the associated false belief that saturated fatty acids and dietary cholesterol are dangerous and should stop being consumed since both cause an up-regulation of LDL production by the liver. Cutting these out of the diet is the second most stupid way to try to minimise the risk of atherosclerosis and CVD. Neither have anything to do with *causing* these diseases. The most stupid way to try to minimise the risk of atherosclerosis and CVD is to take a statin drug. This is because statins up-regulate the liver receptors for LDLs, which will only succeed in removing the healthy, undamaged LDLs and leave alone the small, dense, damaged LDLs, which are the actual problem, and which can't attach to the liver receptors. They can thus continue circulating and accreting to plaques.

[ernestovillarin]

I was disappointed because you did not provide any solution to the problem unlike almost all doctors posting what to do.