Cardiovascular Disease Flashcards
What cells are present in the heart for self-renewing?
The adult heart harbours a pool of resident endogenous cardiac stem and progenitor cells (eCSCs).
- The stem cells are clonogenic, self-renewing and multipotent
Explain what is meant by:
- stroke
- CHD
- MI
- heart failure
- Arrhythmia
- caused by blocked blood vessels to brain
- disease of blood vessels to heart, reducing blood supply
- cut off blood supply to heart
- when heart cannot pump properly, so not enough O2 blood to body
- abnormal heart beat
What are is the trend in mortality rates from CVD in the UK between 1969-2021?
Decline in mortality rates from CVD
- Education, improvements in treatment
- Decline in prevalence of smoking rates
CVD was responsible for 25% of deaths in the UK
How does exercise impact CVD?
What forms of exercise might this be?
- Individuals that exercise have a lower instance of CVD, live longer
- Higher occupational PA decreases chance of CVD compared to sedentary people
- Work exercise - Bus conductors (active) experienced roughly half the number of heart attacks as drivers (sedentary)
- Men engaged in light or moderate work were twice as likely to die from CHD as those whose work was classified as heavy.
- Leisure exercise - higher leisure PA less likely to develop CVD
- Sedentary individuals have highest risk of CVD(1)
- Individuals that do below PA guidelines (>1) - some activity better than none
- Meeting PA guidelines
- Extreme over PA recommendations, is not beneficial in regards to risk of CVD
What is the long-term effect of exercise on CVD?
A 1 MET increase in baseline cardiorespiratory fitness was associated with an 18% reduction in CVD deaths after adjustment for confounders
- Dose response association
What is the action of LPL on VLDL & chylomicrons?
- Triglyceride-rich lipoproteins are hydrolysed within the capillary beds of adipose tissue & skeletal muscle by the enzyme LPL. The hydrolysis of the triglyceride portion of these lipoproteins releases NEFA for uptake into the adipose tissue (for esterification and storage) & skeletal muscle (for oxidation/storage).
Why is high LDL associated with increased risk of CVD?
- Low HDL from diet leads to formation of smaller and denser LDL particles which can enter the endothelial lining, initiating the formation of atherosclerotic lesions. This is termed the ‘atherogenic lipoprotein phenotype’.
What associations are there between TG levels and risk of CVD?
- When triglycerides are high, blood is more likely to clot, increasing detrimental effects on endothelial function & systemic inflammation = contribution towards the formation of atherosclerotic plaque.
What is the most effective way to reduce post-prandial lypidemia?
- expending 400 kcal through exercise has a greater effect on postprandial lipid metabolism than reducing energy intake by 400 kcal.
Can genetics influence a persons risk of CVD?
- Physical activity (self-report), cardiorespiratory fitness (submaximal exercise test) and grip strength measured at baseline
- Genetic risk score calculated using 62 genetic variants associated with CHD - nature vs nurture
- PA could be a protective factor over their genetic disposition for CVD
- High genetic risk of CVD can lead to increased chance of developing it, however lifestyle changes can reduce this risk
Describe the development of atherosclerosis:
Intima is the part of the blood vessel that is in contact with the blood
- Once injury takes place, cholesterol accumulates in blood vessel wall(becomes permeable) - these are digested and accumulate, causing the fatty streak leading to a build up
- This leads to blood cloths and atherosclerosis
* Endothelial dysfunction increases permeability to lipoproteins and promotes adhesion of monocytes to endothelium(initial stages of atherosclerosis).
* Once plaques are formed they can rupture, increasing risk of adverse CV events. Plaques have a large lipid pool inside and thin fibrous cap, increasing apoptosis. This may then rupture and get stuck in a major artery, restricting blood flow to the heart
When do clinical endpoint emerge of atherosclerosis?
around 45% build up of plaque we see: MI, stroke, gangrene is feet, aneurysm.
Name some physiological factors which are associated with a person’s risk of CVD:
- insulin sensitivity
- lipid and lipoprotein metabolism
Adipokines can promote insulin resistance in blood vessels within adipose tissue/other vessels, causing endothelial dysfunction = increased cardiovascular risk - blood pressure
- vascular function
- inflammation
Describe the lipoprotein fractions:
- HDL protect from CVD by assisting transfer of excess cholesterol from the tissues to the liver(to be excreted as cholesterol & bile salts, termed ‘reverse cholesterol transport’) - Healthy to have higher concentration
- chylomicrons transport exogenous (dietary) triglyceride
- VLDLs transport endogenous triglyceride
- LPL(lipoprotein lipase) hydrolyses triglyceride portion of lipoproteins into non-esterified fatty acids(NEFA) for uptake into adipose tissue & skeletal muscle
- Leptin suppresses appetite and increasing energy expenditure. Leptin has proinflammatory actions in many immune cells: monocytes/macrophages, neutrophils, NK cells and T cells - linked to plaque vulnerability
Why are low LDL lipoprotein fractions important?
- LDL’s transport cholesterol in blood
- Depletion of cholesterol ester from LDL through reversed cholesterol transport results in smaller and denser LDL particles which may be particularly likely to penetrate the endothelial lining, thereby entering the sub-endothelial space to initiate the formation of atherosclerotic lesions.
