Home Uncategorized What causes heart disease part 61 – strokes

What causes heart disease part 61 – strokes

15th January 2019

Within this never-ending story on cardiovascular disease, I’ve tended to use the terms”heart disease” and”cardiovascular disease” almost interchangeably. Well, everyone does it, so why not me? However, in this blog I will be splitting cardiovascular disease into its two main components, heart attacks and strokes, and concentrating mainly on strokes.

The first thing is that there are 3 chief causes of strokes.

  • Atrial Fibrillation (ischaemic)
  • A burst blood vessel in the brain (haemorrhagic)
  • A blood clot (ischaemic)

[There are also cryptogenic strokes (no known cause), strokes because of hole in the center, strokes because of antiphospholipid syndrome, strokes due to sickle cell disease etc. etc..)

Atrial Fibrillation (AF) is a condition where the upper chambers of the heart (atria) don’t contract and relax smoothly every second or so. Primarily because there is a disturbance in the electrical conduction system, causing the atria to spasm and twitch in a fashion that is highly irregular.

When this happens, blood clots can form in the left atrium then break off and head to the brain and become stuck. They’re also able to travel elsewhere in the body resulting in a blockage to an artery in the leg the uterus, the arm and suchlike. Should they form at the right atrium, they will end up stuck in the lungs.

These clots are usually quite small, about the size of a large grain of rice, but this is still big enough to do quite appreciable damage. The treatment for AF is to try and undo the fibrillation or, if this doesn’t work, to provide anticoagulants such as warfarin to stop the clots forming.

When a blood vessel in the brain bursts, A haemorrhagic stroke is. Blood is then forced to the mind and causes a good deal of damage — resulting in a stroke. As you can imagine haemorrhagic strokes are quite severe. The remedy is to NOT offer an anti-coagulant of any sort. Haemorrhagic strokes are often/usually brought on by a thinning of the artery wall, causing a ballooned area (aneurysm), which then bursts.

An interesting question, and I have seen different perspectives on this is whether a small blood clot travels to the brain where it gets trapped, but does not completely block the artery, so it does not cause a stroke, but it creates an area of damage — that is then repaired — which leaves a weakness in the artery that balloons out — an aneurysm.

Anyway, the most common cause of a stroke is that large atherosclerotic plaques form in the main arteries that supply blood to the brain (carotid arteries). These plaques form around the base of the neck. There forms then A blood clot along with the plaque , then breaks off and travels to the brain, where it gets stuck – as with atrial fibrillation — causing a stroke. The result is exactly the same as with AF, but the underlying causing is different.

According to the American Stroke Association 87% of strokes are ischaemic.

Which means that the majority of strokes are caused by atherosclerotic plaques in the throat. You would expect that the risk factors for stroke could be exactly the same as the risk factors for heart attacks, as the underlying process is the same.

Well, many of the risk factors that are standard will be the same. Smoking, high blood pressure diabetes and suchlike. However, there is most certainly a LDL not. There’s a research study called the Simon Broome registry, started in the UK, that monitors the health outcomes of individuals diagnosed with familial hypercholesterolaemia (FH).

It is. One on the Simon Broome registry’s findings, of the earlier papers in the BMJ, found that:

‘Familial hypercholesterolaemia is associated with a substantial excess mortality from coronary heart disease in young adults but might not be associated with a significant excess mortality in elderly patients. 1

For’may not be’, substitute,’isn’t’. In actuality, what the Simon Broome registry has found is that, after the age of, about fifty, FH doesn’t increase the risk of heart. LDL is a risk factor not, and before the age of fifty after? Which means that it cannot be a risk factor at all [the thing that kills young people before the age of fifty is currently clotting factor abnormalities — not elevated LDL]

2 Yes, as you may have guessed, I was a co-author.

If we move away from cardiovascular disease, to strokes. FH has never been found to be a risk factor for stroke — at any age. Here is a study done in Norway, and published in the Journal Stroke. It was called’Risk of ischaemic stroke and complete cerebrovascular disease in familial hypercholesterolaemia.’

A total of 46 cases (19 women and 27 men) of cerebrovascular disease were observed in the cohort of individuals with FH, with no increased risk of cerebrovascular disease compared with the general population (standardized incidence ratio, 1.0; 95% CI, 0.8–1.4). 3

They used the term population attributable risk factors (PAF), which’weights’ the variables, based on how widespread they are (i.e., how many people have got the a variety of risk factors). Their list of PARs for stroke was as follows:

  • 51.8percent – Hypertension (self-reported history of hypertension or blood pressure >160/90mmHg)
  • 18.9percent – Smoking status
  • 26.5% – Waist-to-hip ratio
  • 18.8percent – Diet hazard score
  • 28.5percent – Regular physical activity
  • 5% – Diabetes mellitus
  • 3.8percent – Alcohol intake
  • 4.6% – Psychosocial stress
  • 5.2% – Depression
  • 6.7% – Cardiac causes (atrial fibrillation, previous MI, rheumatic valve disease, prosthetic heart disease )
  • 24.9% – Ratio of ApoB to ApoA (reflecting cholesterol levels)

You will see that LDL is not in that list. ApoB to ApoA’s ratio is. However, this is primarily the proportion of VLDL (triglycerides) into HDL (‘good’ cholesterol), which can be an accurate reflection of’insulin resistance’ and bears no relationship to LDL. As I always say to people who ask me for information on reviewing clinical study…’the main thing to concentrate on is not what’s there, it’s what is not there.’

Any study on CVD will be analyzing LDL levels. It would be shouted from the rooftops if a relationship were discovered. That you hear nothing about LDL in this paper means that there was no correlation — at all.

You can, if you desire, try to find some evidence that a LDL level increases the risk of stroke. I must warn you you will look for quite a long time, because there is no evidence, anywhere. It has interested me for many years that this issue is simply swept under the carpet.

Now, write out one hundred times:

  • Raised LDL isn’t a risk factor for stroke
  • Raised LDL isn’t a risk factor for stroke
  • Raised LDL isn’t a risk factor for stroke….

Then, ask yourself the question. How can a elevated LDL be a risk factor for not stroke and cardiovascular disease — because the two states are, essentially , the same condition? Plaques in medium sized cells with the critical/final event being the formation of a blood clot.

Then, ask yourself another question. How can lowering the LDL level provide any advantage, if a raised LDL isn’t a risk factor for stroke? The right response is that… it can’t. Not by a wonderful amount in absolute terms, but the benefit does seem to exist).

‘A meta-analysis of randomized trials of statins in combination with other preventive strategies, involving 165,792 people, showed that each 1-mmol/l (39 mg/dl) reduction in LDL-cholesterol equates to a reduction in relative risk for stroke of 21.1 (95% CI: 6.3-33.5; p = 0.009)’ 4

Just to repeat the main purpose. A LDL is not, and hasn’t been, a risk factor for stroke. Yet it’s claimed that lowering the LDL level lowers the risk of stroke? In fact, the evidence from the statin trials prove, beyond any doubt, that any benefit achieved by statins cannot be through lowering the LDL level.

As follows, the logic stripped down is:

  • A raised level of variable A Doesn’t cause disease B
  • Thus lowering factor A cannot decrease the risk of disease B
  • Therefore, you cannot claim that lowering factor A can have any possible effect on disease B

However, every single cardiovascular pro appears delighted to inform us, in all seriousness, that lowering factor A does, indeed, reduce the risk of disease B. Despite this breaking the very fabric of logic in 2.

“Alice laughed: “There’s no use trying,” she explained; “you can’t believe impossible things. ”

I Would you harbor ’t had much practice,” said the Queen. ” Alice in Wonderland.

1: https://www.bmj.com/content/303/6807/893

4: https://www.ncbi.nlm.nih.gov/pubmed/19814666


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