Lecture 18--coronary Heart disease and nutrition Flashcards

1
Q

What is coronary heart disease

A

Pathological changes in the walls of the coronary arteries that reduce blood flow to the cardiac muscle

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2
Q

Which organ has the highest Oxygen demand?

A

The HEART (even during exercise has higher consumption that skeletal muscle). The heart is a HIGHLY OXIDATIVE ORGAN.

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3
Q

coronary blood flow is PHASIC, how much blood flows during systole (contraction) and diastole (relaxation)?

A

SYSTOLE => 80-100mL/min

DIASTOLE => (=80% CBF) 200-300mL/min

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4
Q

What are the 2 factors influencing Cerebral Blood Flow (CBF)?

A

1) PERFUSION PRESSURE IN THE AORTA: coronary arteries open into aorta .: more pressure in aorta means more blood is pushed into CBF
2) EXTRAVASCULAR COMPRESSION FROM CONTRACTING MYOCYTES: Pressure on blood vessel…external (extravascular) compression from contracting myocytes causes the coronary vessels to close during systole .: limiting blood flow. In diastole this external pressure is removed as the heart relaxes, causing the vessels to open and blood to flow in.

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5
Q

What is happening to Coronary Blood flow during ISO-VOLUMETRIC CONTRACTION?

A

LOW blood flow, maybe even a REVERSAL of flow b/c of (1) contracting myocytes & (2) perfusion pressure in aorta has not increased yet.

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6
Q

What is happening to Coronary Blood flow during EJECTION phase of the heart cycle?

A

Small amount of flow
>Perfusion pressure in aorta is increased= more blood is forced into coronary circulation
>CBF remains low b/c of compression by contracting myocytes

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7
Q

What is happening to Coronary Blood flow during DIASTOLE?

A

MOST BLOOD FLOW (highest perfusion pressure in aorta, reduced compression from contracting myocytes)

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8
Q

What are the 3 mechanisms that cause CHD?

A

(1) Vascular spasm
(2) Atherosclerosis
(3) Other complications (thrombosis)

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9
Q

What is the effect of exercise on a patient with coronary obstruction compared to a healthy period?

A

During exercise the period of DIASTOLE is SHORTENED (as heart rate increases) to accommodate an increase in heart rate.
In a patient with coronary obstruction the magnitude of CBF remains unchanged (vs. in a healthy person where an increase in blood flow compensates for reduced period of diastole). Thus the perfusion is dramatically reduced.

During Systole there can be a REVERSAL OF BLOOD FLOW due to cumulative effect of compression by contracting myocytes and resistance to flow due to the coronary obstruction.

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10
Q

Cardiac cells extract _____% of O2 from ______ at rest

A

…75%

haemoglobin

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11
Q

Tissue cells extract _____% of O2 from _____ at rest

A

…25%

Haemoglobin

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12
Q

during periods of high oxygen demand what strategy does the heart use to deliver more oxygen to the coronary circulation?

A

Increasing blood flow.

Can’t increase oxygen extraction (from haemoglobin) by much (already 75% saturated under normal conditons).

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13
Q

How can more oxygen be delivered to exercising tissue during periods of increased demand?

A

(1) Increasing extraction (at rest only 25% of bound O2 is used)
(2) Increasing blood flow

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14
Q

VASCULAR SPASM

A

Constriction that transiently narrows coronary vessels = increase resistance in vessel = reduced blood flow

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15
Q

What triggers vascular spasm?

A

Cold exposure
Physical exertion
Anxiety

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16
Q

Is vascular spasm reversion?

A

YES, usually no long term damage

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17
Q

Does vascular spasm only occur in patients of CHD?

A

NO, it can occur in the absence of CHD/atherosclerosis

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18
Q

What CAUSES VASCULAR SPASM?

A

(1) Increase in the ALPHA-VASOCONSTRICTOR EFFECT: increase sympathetic stimulation = more noradrenaline circulation = binds to a-receptors = constriction

(2) Deficient basal release of NITRIC OXIDE
* *NO=potent vasodilator
* *Released by endothelium
* *Unhealthy endothelium in CHD –> reduced release of NO

(3) Heightened VASOCONSTRICTOR RESPONSE TO ACh (only in patients with CHD)
* *normally ACh would cause vasodilation but in CHD instead causes vasoconstriction.

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19
Q

What cause for vascular spasm is unique to patients of coronary heart disease?

A

Heightened vasoconstrictor response to ACh (only in patients with CHD)
**normally ACh would cause vasodilation but in CHD instead causes vasoconstriction.

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20
Q

What is the main cause of CHD?

A

ATHEROSCLEROSIS

21
Q

What is involved in atherosclerosis?

A

Fatty deposits in walls of arteries (Atherosclerotic plaque) .= accumulate cholesterol, Ca2+ & other substances in the endothelium of arterial walls. Causes thickening of the vessels = narrowing of the lumen = restricts blood flow.

22
Q

What causes atherosclerosis?

A

Injury to blood vessels triggers INFLAMMATORY RESPONSE (movement of white blood cells to the area) –> ACCUMULATION of LDL, Ca2+ and other substances beneath the endothelium (atherosclerotic plaque).

23
Q

Atherosclerotic plaque

A

Fatty deposits in the walls of arteries that accumulate Cholesterol, Ca2+ & other substances. Lead to thickening of the vessel walls and narrowing of the lumen

24
Q

decreased blood flow to cardiac muscle (due to coronary obstruction) leads to…

A

(1) Chest pain (angina): pain associated with heart muscle shifting to ANAEROBIC METABOLISM in the face of reduced O2 supply which produces more H+ ions ==> acidic conditions ==> stimulates PAIN RECEPTORS

(2) shortness of breath
(3) heart attack

25
Q

What is THROMBOEMBOLISM

A

Plaque breaks through weak endothelial lining, revealing collagen to which blood platelets can stick, forming a blood clot.

26
Q

Thrombus vs. embolus

A

Thromus: the plaque is still attached to the endthelial lining

Embolus: the plaque detaches from the wall and moves ‘down stream’ blocking/lodging in a small vessel.

27
Q

What is the ‘failsafe’ for cardiac vessel blockage?

A

Anastomoses

Collateral circulation

28
Q

What is collateral circulation?

A

Can double size in 2-3 days, and can reach the size of a normal vessel in a few months. However, problems arise when these collateral vessels also develop plaques. = CHD is a ‘silent killer’

29
Q

CHD is a ‘silent killer’ what does that mean?

A

You remain symptom free while you have collateral circulation bypassing the blockages. Problems arise when the collateral vessels develop plaques and block themselves. By this stage it may be too late to treat

30
Q

What are the complications of thromboembolism?

A

complete blockage –> cardiac tissue supply by that vessel becomes ISCHEMIC & NECROTIC =tissue death

–> effects pumping of heart (reduced cardiac output) ==> less coronary blood flow ==> more tissue death (=VISCOUS CYCLE)

COLLATERAL CIRCULATION is used to combat this cycle.

31
Q

What are the uncontrollable risk factors of CHD?

A

(1) Age (older = more sedentary + increased weight)
(2) Gender (men age 45+, women age 55+ (due to protective effect of oestrogen in women)
(3) Heredity

32
Q

What mutation is present in HOMOZYGOUS FAMILIAL HYPERCHOLESTEROLEMIA?

A
  • *Mutation in the LDL GENE (which usually removes LDL from circulation)–> causes excessively high cholesterol
  • *XANTHOMA: High cholesterol causes subcutaneous fatty deposits
  • *Causes death by 20 years old.
33
Q

What are some controllable risk factors for CHD?

A

(1) High blood pressure (hypertension)
(2) High blood cholesterol
(3) Smoking
(4) Obesity
(5) Physical inactivity
(6) Diabetes
(7) Stress

34
Q

What are the complications of HYPERTENSION in relation to development of CHD?

A

hypertension ==>
> ENDOTHELIAL DYSFUNCTION = contributes to exacerbating atherosclerosis & causes plaques to become more unstable (by breaking endothelial lining)
>LEFT VENTRICULAR HYPERTROPHY (b/c heart pumps against higher resistance circulation = INCREASES MYOCARDIAL O2 DEMANDS
>Is associated with METABOLIC (insulin resistance, hyperinsulinaemia, hyperlipidaemia

35
Q

What are the complications of OBESITY & DIABETES in relation to development of CHD?

A

Abdominal adiposity => insulin resistance => HYPERGLYCAEMIA (+hyperlipidaemia)

(1) => GLYCOSYLATION of proteins in arterial walls –> atherosclerosis
(2) => Increases the formation of REACTIVE O2 SPECIES (react with LDL, exacerbate atherosclerosis)

36
Q

What are the complications of SMOKING in relation to development of CHD?

A

> Lower HDL LEVELS = more prone to atherosclerosis (HDL=protective)
NICOTINE causes vasoconstriction
CO (carbon monoxide) = reduces O2 carrying capacity of blood (competes for binding sites on harm)
Increases CIRCULATING FIBRINOGEN = promotes clot formation

37
Q

What are the complications of HIGH CHOLESTEROL in relation to development of CHD?

A

Plaques are made up of cholesterol, thus high levels of LDL cholesterol in the blood increase the build up of deposits in plaques

38
Q

What are the 2 main ways we can prevent CVD?

A

Diet/nutrition

Exercise

39
Q

What are the national heart foundation guidelines for reducing heart disease?

A

(1) Eat VARIETY (veg, whole grains, fruit, nuts, seeds)
(2) Healthier fats/oils
(3) Limit sugary/fatty/salt
(4) Drink mainly water
(5) Limit sat/trans fats + cholesterol
(6) Limit salt (

40
Q

What does exercise do for the body

A

(1) Increases HDL
(2) Lowers LDL & total cholesterol
(3) Helps control diabetes & hypertension

41
Q

Why should a person at risk of CHD consume Seafood?

A

> Seafood ==> OMEGA 3 = reduces levels of ENDOTHELIAL LIPASE (associated with atherosclerosis and inflammation)

42
Q

What is the recommendation about fats and protein consumption for prevention of CHD?

A

High protein: fat ratio

43
Q

how much salt should you consume per day according to the dietary guidelines? Why?

A
44
Q

A diet high in saturated fat will lead to..?

A

High levels of ENDOTHELIAL LIPASE (enzyme associated with atherosclerosis & inflammation)

45
Q

Treatment for CHD?

A

Lifestyle changes (dietary intervention, exercise, mediterranean diet?)

Medications (nitroglycerin)

Surgery (by-pass)

46
Q

What medications can be used to treat CHD?

A

NITROGLYCERIN

47
Q

Benefits of Olive oil (component of Mediterranean diet) in lowering CHD risk

A

> > High levels of MONOUNSATURATED FATS (oleic acid) = Reduces CHD

> > Also contains PHENOLS: potent inhibitors for reactive oxygen species

> > Reduce thrombogenesis (reduce clot formation)

> > Anti-inflammatory

> > Anti-hypertensive

48
Q

What are the characteristics of the Mediterranean diet?

A
> Lots of fruits/veggies/breads/grains/beans/nuts/seeds
>Olive oil = main fat source
>Dairy products, poultry, fish
>Little red meat 
>Red wine in moderation