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Arthrosclerosis and Ischemia > Risk factors for Atherosclerosis and principles of primary and secondary prevention > Flashcards

Risk factors for Atherosclerosis and principles of primary and secondary prevention Flashcards

1
Q

Contributions of INTERHEART study

A
  1. identifies/confirms risk factors
  2. identified daily consumption of fruits and vegetables, regular physical activity and regular alcohol intake as protective
  3. study across genders and ethnic races, and different ages
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2
Q

What did interheart conclude about risk factors

A

That known moifiable risk factors account for 90% of the population attributable risk in men and 94% in women for mi

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3
Q

Non modifiable risk factors for atherosclerosis

A

1) Age
2) Gender
3) Genetic predisposition (as indicated by family hx)

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4
Q

Age as a risk factor

A

-over a lifetime individuals bv are exposed to a variety of fators that damage the endothelium –> initiating inflammatory process that leads to formation of atherosclerotic plaques over time

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5
Q

Gender as a risk factor

A
  • men have earlier onset of CHD
  • difference probably due to protective effects of estrogen on bv wall and endothelium (protective effect lost at menopause)
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6
Q

In what type of premenaupausal women is the protective effect of estrogen lost

A 
-mainly if they are diabetic
and to lesser extent if they
-smoke
-genetic dyslipidemia 
** although protective effect is reduced
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7
Q

What can early vascular disease in men be attributed to

A

1) Lack of estrogen
2) lower HDL-C
3) Increased abdominal (visceral) fat

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8
Q

Family history of vascular disease

A

1) early onset in first degree male (father, brother or son) before age 55 or female (mother sister or duaghter) before 65

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9
Q

Genetic predictors of heart disease (that are inherited in some)

A
  • elevated LDL cholesterol
  • low HDL cholesterol
  • high bp
  • diabetes
  • elevated lipoprotein a
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10
Q

Modifiable risk factors for atherosclerosis

A
  • diet
  • exercise
  • elevated LDL-C
  • low HDL-C
  • smoking
  • stress
  • hypertension
  • abdominal obesity
  • inflammation
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11
Q

Dietary factors increasing risk atherosclerosis

A

-both indirect and direct increase risk atherosclerosis
Direct:
-trans and sat fats and high cholesterol in diet –> directly cause endothelial damage and plaque development
Indirect:
-calorie excess –> weight gain, abdominal obesity and hypertension related to weight gain
-diabetes

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12
Q

Dietary factors reducing risk coronary events

A

-higher levels of fruit/vegetable intake

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13
Q

Sedentary lifestyle as risk factor

A

-being sedentary = predictor of increased risk of vascular events (heart attack, stroke, tia, coronary bypass surgery, death due to mi)

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14
Q

Benefits of exercise

A
  • reduced bp
  • reduced LDL_C
  • reduced triglycerides
  • reduced progression of impaired glucose tolerance to type 2 diabetes mellitus
  • increased HLD-C
  • improved heart function
  • *benefits even in absence of weight loss
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15
Q

Harmful role of lipoproteins including LDL

A
  • elevated LDL particles (also indicated by elevated LDL and apolipprtein B)
  • accumulate in artery wall and taken up either as aggregated LDL or oxidized LDL by macrophages or smooth muscle cells in the artery
  • leads to foam cell formation and atherosclerotic lesions (plaques)
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16
Q

LDL and other risk factors

A

In the presence of other risk factors that damage the bv endothelium even lower levels of LDL can pass through the endothelium more easily and accumulate and cause harm

17
Q

triglycerides as risk factor

A
  • increased triglycerides on LDL make LDL more likely to be digested to smaller and denser particle
  • making LDL more hamful
    i. e. high triglycerides can be atherogenic if LDL or apoB levels are also elevated
18
Q

HDL and apolipoprotein A-I

A

-HDL and its main protein component apoA-I correlate with protection against heart disease

19
Q

Potential protective actions of HDL

A

-ability to remove excess cholesterol delivered to arterial cels by LDL (reverse cholesterol transport) and to induce relaxation of the artery wall

20
Q

Strongest modifiable predictor of risk for mi as identified in INTERHEART

A

the ratio of apoB/apoA-I
-highlights the importance of the balance between delivery of cholesterol into the arteries by LDL and its removal by HDL

21
Q

Assessment of someones cholesterol profile

A

-determine whether high cholesterol due to environmental factors (diet & exercise) or is genetic

22
Q

Cholesterol levels likely due to genetic factors

A
  • total cholesterol levels > 6.5 mmol/l
  • or HDL < 0.7 mmol/l
  • or LDL > 4.5 mmol/l
  • or triglycerides >3 mmol/l
23
Q

Why smoking is a risk factor for atherosclerosis + benefit of quitting

A
  • inhaled chemicals dissolve in blood and damage endothelium
  • damage leads to constriction of bv and reduction of flow to tissue including the heart
  • harm is reduced immediately upon stopping smoking and long term risk mainly gone after 2 years of quitting
24
Q

Why physochological stress is a risk factor for atherosclerosis

A

-something to do with stress resulting in increased blood cortisol and adrenaline levels and increased inflammatory cytokine levels and damage to the blood vessel endothelium

25
Q

Why hypertension is a risk factor for atherosclerosis

A
  • damage to the endothelium

- thickening of artery wall further impairing relaxation of arteries (putting more stress on heart)

26
Q

Why diabetes is a risk factor for atherosclerosis

A
  • something to do with abnormal lipid levels
  • increased LDL and decreased HDL (reducing LDL-C in people with diabetes appears to have as much or more effect in reducing coronary events as does maintaining low blood sugar)
  • glycosylation of proteins due to chronic high proteins also related to risk
27
Q

Why abdominal obesity is a risk factor for atherosclerosis

A

visceral fat releases more inflammatory factors –> damages blood vessel endothelium –> atherosclerosis
-waist circumference has become a standard tool for assessing an individuals overall risk vascular disease

28
Q

Lipoprotein a

a) structure
b) origin
c) why is a risk

A

a) One molecule LDL + an additional protein apo(a) attached to the apoB portion of LDL via disulfide linkage
b) liver, an individuals Lp(a) leve iss determined by inherited factors (one cause of inherited high bp)
c) may be due to it increasing leakiness of endothelium or increasing the tendency to form blood clots

29
Q

What is the treatment to lower Lpa

A

Statins work against LDL but no Lpa

  • only treatment is niacin (vitamin B3) in high doses
  • also the risk of high Lp(a) is markedly reduced if plasma LDL levels are lowered
30
Q

C-reactive protein

A
  • marker of inflammation in the body
  • produced by liver in response to increased levels of inflammatory molecules
  • will not tell you about the source or site of inflammation however has been shown to be an independent predictor of a persons risk of cornary heart disease (may contribute to atherosclerosis or blood clotting by itself)
31
Q

Framingham risk score -who to use in, who not to use in

A

Not for people with these conditions (already considered high risk of a vascular event)

  • already had a cardiovascular event (heart attack, stroke, TIA)
  • known to have ischemic heart disease or peripheral vascular disease
  • diabetes
  • chronic kidney disease and GFR <30 ml/min/m2
  • for people without these conditions and who are in primary prevention cateogory main tool used to calculate 10 year risk of non-fatal mi or coronary death is based on Framingham Risk Score
32
Q

Basis of Framingham Risk score

A

Assigns points based on:

a) individuals age
b) total cholesterol level
c) smoking status
d) HDL cholesterol
e) systolic blood pressure (depending on whether they are treated or untreated for high bp)

33
Q

Primary prevention

A
  • the process of inhibiting the development of disease before it happens
  • includes diet, exercise, stress reduction and medications
34
Q

Secondary prevention

A
  • preventing complications of established disease
  • treatment of heart attack or stroke that has occured, prevention of vascular events after the presence of disease is detected

Arthrosclerosis and Ischemia (6 decks)

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