Lecture 22-Cardiovascular disease Flashcards
Cardiovascular disease
what is cardiovascular disease (CVD)
general term for all diseases of heart and blood vessels
what is coronary heart disease (CHD) - what is it also referred to as
also referred to as coronary artery disease (CAD) or Ischemic heart disease (IHD)
damage that occurs when blood vessels carrying blood to heart become narrow and blocked
what is cerebrovascular disease (stroke)
damage to arteries to the brain
what is peripheral vascular disease
narrowing of the arteries other than those supply the heart or brain
what is hypertension
high blood pressure
what is atherosclerosis
characterised by plaques along inner walls of arteries
why are rates of death from heart disease decreasing
- better control of major risk factors
- better evidence based treatments
Heart disease reached a peak in the …. and has come back down from then
60s
The major risk factors that we have better control over now
- cholesterol
- systolic blood pressure
- smoking prevalence
The evidence based treatments that we now having which decrease the death from heart dieseas
diagnostic and therapeutic procedures
e.g phramacological treatment of hypertension, hypertension screening, bypass surgery, access to healthcare
what is the leading cause of death globally
coronary heart disease
what is the CVD mortality in maori compared to non maori
much higher in maori than non maori
Men vs women CVD
higher in men, but CVD is still the leading cause of death in women worldwide
1 in how many women die of heart disease or stroke compared to die of breast cancer
1 in 2 women will die of heart disease or stroke
1 in 25 women will die with breast cancer
age specific risk of CVD is lower in what gender
lower in women
How much longer after do women present with CVD than men
7-15 years later compared to men
Atherosclerosis process
We start with blood vessels and blood is flowing quite nicely
- We have the endothelium layer which acts as a nice barrier to the blood vessel and the blood going through produces protein which stops the build up of material
- We have irritation toward the blood vessels which allows things to get in that should be in
- Once they are in the blood vessel wall they start to oxidise
- It send signals to the immune system and itywill gobbel it up that they then die and they become foam cells and these are known as the dead macrophages
- So then the immune system will then be sent to get rid of the macrophages which will then end up in an inflammation
- Smooth muscle cell will produce which makes blood flow slow (increases blood pressure)
what are some examples of irritants to blood vessels that can lead to the process of atherosclerosis and what do these do
high levels of LDL cholesterol, high blood pressure or toxins from smoking damages the blood vessel allows things to get in, once they are in the wall they start to be oxidised
what happens if all the inflammation covered in the blood vessel ruptures
all this inflammation and mess will enter the blood vessel
LDL cholesterol is an
irritant to start the atherosclerosis process
chylomicrons are full of
triglycerides
what is the function of chylomicrons
transport dietary lipids from intestine to peripheral tissues
what is the function of VLDL
transports lipids from liver to peripheral tissues
what is the function of intermediate density lipoprotein
precursor of LDL
what is the function of LDL
transports cholesterol to peripheral tissues and liver
what is the function of lipoprotein a (Lpa)
associated with CHD risk, similar to LDL
what is the function of HDL
removes cholesterol from tissues and transfers it to the liver or other lipoproteins
what is the function of albumin
transports free fatty acids from adipose tissue to peripheral tissues
low density lipoprotein cholesterol is associated with what risk of
increased risk of CVD
Apo B containing lipoproteins are associated with what risk of
increased risk of CVD
high density lipoprotein cholesterol is associated with what
unsure, it wasn’t found that increasing this reduced risk
Lpa is associated with increased risk of what
increased risk of CVD
triglycerides is associated with increased risk of what
increased risk of CVD
why is it important to keep cholesterol levels low when you are young
its like smoking in your 20s isnt going to give you heart disease in your 30s, its about the long term effects that is important
what types of saturated fat increase our LDL cholesterol
- lauric acid : main fatty acid in coconut
- myristic : high in some dairy products
- palmitic acid : found in palm oil
what saturated fat has a neutral affect on our LDL cholesterol
steric acid seems to have a neutral affect : main fat found in dark chocolate
what monounsaturated fat reduces our LDL cholesterol
Oleic (cis)
what monounsaturated fat increases our LDL cholesterol
elaidic (trans)
what type of fats really reduce our cholesterol
polyunsaturated fats
how does omega 3 reduce our cholesterol, what is it found in
reducing triglycerides like VLDL
found in things like fatty fish
what does omega 6 reduce
reduce LDL
what did the keys equation look at
how much would our blood cholesterol change if we changed the amount of polyunsaturated fat, saturated fat and dietary cholesterol in our diets
for a given amount of saturated fat, it will raise our blood cholesterol levels …… as much as given polyunsaturated fat would decrease it
raise it twice as much
what is the keys equation
change in cholesterol = 2.74 x change in sat fat - 1.13 x change in polyunsat fat
what fat is highest in saturated fat
coconut oil
what oils are high in monounsaturated fats
olive, canola, peanut oil
what oils are high in polyunsaturated fats
safflower, flaxseed, walnut, sunflower oil
If you are changing one thing in someones diet then …
Something else is going to higher or lower
The meta analysis is to asses the affects of reducing saturated fat intake and replacing it with ..
-Carbohydrate
-PUFA
-MUFA
-Protein
a meta analysis found that reducing saturated fat intake had a what reduction in CVD risk
17% reduction in CVD risk
what was found from the meta analysis if the reduction in saturated fat was replaced with polyunsaturated fat
27% reduction
what was found in the meta analysis if reduction in saturated fat was replaced with carbohydrates or protein
not statistically significant
in studies that achieved at least a 0.2 mmol/L reduction of total cholesterol, events of CVD reduced by
26%
the reduction in CVD events was related to the degree of reduction in
serum total cholesterol
how does saturated fat increase cholesterol
- decrease LDL receptor activity
- suppress ACAT (rate limiting enzyme of cholesterol esterification) : resulting in greater proportion remaining in the regulatory pool
how does N-6 polyunsaturated fat decrease cholesterol
increase LDL receptor activity
increase CYP7 (rate limiting enzyme in converting cholesterol to bile acids)
what did the early studies of cholesterol do and what did they find (BUT and SO)
fed large amounts of cholesterol to rabbits
this induced atherosclerosis
BUT …. rabbits are herbivores, who are hypersensitive to cholesterol and were fed large amounts of cholesterol
SO …. useful between the link of blood cholesterol and atherosclerosis but not useful for dietary cholesterol for humans
why do some people say that seed oils are toxic and are going to kill us, why are these claims not true
they say they will be oxidised and cause problems in the body……. but in the body vitamin E is often associated with it which helps prevent oxidation
Regardless of the mechanism they are looking at the people with the most seed oil in their diet and they were the least likely to get heart disease -its associated with some inflammatory effects
what is not true about the claims saying we shouldnt have too much omega 6
its not about having too much omega 6 its about not having enough omega 3
what are the omega 3 recommendations from the American Heart Association
1.0 g/day of EPA + DHA to reduce risk of death from coronary heart disease in a secondary prevention setting
at least 2 serves of (preferably oily) fish per week (500mg of EPA + DHA) in a primary prevention setting
