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Cardiovascular System > SIHD & Angina - Therapy > Flashcards

SIHD & Angina - Therapy Flashcards

1
Q

What does SIHD stand for?

A

Stable ischaemic heart disease

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2
Q

What are acute coronary syndromes?

A

Sets of signs and symptoms due to decreased blood flow in the coronary arteries

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3
Q

What are some acute coronary syndromes?

A

Myocardial infarction

Unstable angina pectoris (angina which is irregular)

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4
Q

What are the 2 kinds of myocardial infarction?

A

STEMI

NSTEMI

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5
Q

What is stable coronary artery disease?

A

Set of signs and symptoms due to recurrent, tansient spisodes of chest pain representing demand-supply mismatch

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6
Q

What are examples of stable coronary artery disease?

A

Angina pectoris

Silent ischaemia

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7
Q

What is angina pectoris?

A

Chest pain due to coronary heart disease

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8
Q

What is chest pain due to coronary heart disease called?

A

Angina pectoris

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9
Q

What is silent ischaemia?

A

Ischaemic episodes with no symptoms so the patient is unaware

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10
Q

What are ischaemic episodes with no symptoms so the patient is unaware called?

A

Silent ischaemia

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11
Q

What are risk factors for stable coronary artery disease?

A

Hypertension

Smoking

Hyperlipidaemia

Hyperglycaemia

Male

Post-menopausal female

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12
Q

Are males or females more at risk of stable coronary artery disease?

A

Males

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13
Q

What does stable coronary artery disease arise due to?

A

Mismatch between myocardial blood/oxygen supply and demand

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14
Q

What does SCAD stand for?

A

Stable coronary artery disease

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15
Q

What may attacks of angina due to stable coronary artery disease be precipitated by?

A

Any stress which increases cardiac work and myocardial oxygen demand

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16
Q

What are the 2 kinds of ischaemia?

A

Demand ischaemia

Supply ischaemia

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17
Q

When does demand ischaemia occur?

A

During stress (physical/emotional)

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18
Q

When does supply ischaemia occur?

A

At rest

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19
Q

What are some determinants of demand ischaemia?

A

Heart rate

Systolic blood pressure

Myocardial wall stress

Myocardial contractility

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20
Q

What are some determinants of supply ischaemia?

A

Coronary artery diameter and tone

Collateral blood flow

Perfusion pressure

Heart rate (duration of diastole)

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21
Q

What is hyperlipidaemia a disease of?

A

Muscular arteries (not veins)

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22
Q

What is the process of hyperlipidaemia leading to atherosclerosis?

A

1) Progressive depositions of cholesterol esters
2) Lesions start as fatty streaks
3) Develop into fibrous plaque

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23
Q

What does ischaemic heart disease lead to?

A

Myocardial infarction

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24
Q

What does cerebrovascular disease lead to?

A

Stroke

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25
Q

What are the fatty streaks that lesions start as composed of?

A

Sub endothelial accumulation of large foam cells (derived from macrophages plus smooth muscle cells) filled with lipid

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26
Q

How does fibrous plaque reduce blood flow?

A

Projects into the lumen of the vessel

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27
Q

Where in the blood vessel are most of the changes during atherosclerosis?

A

In the intimal layer

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28
Q

What is a fibrous plaque composed of?

A

Fibrous cap

Necrotic core

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29
Q

What is the common pathology of stable ischaemic heart disease?

A

Atherosclerosis

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30
Q

What does therapy of stable ischaemic heart disease target?

A

Atherosclerosis

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31
Q

What treatment can help correct the imbalance of supply and demand?

A

Drug treatment

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32
Q

How can drug treatment help to correct the imbalance between supply and demand?

A

Decreasing the myocardial oxygen demand by reducing cardiac workload

Increasing the supply of oxygen to ischaemic myocardium

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33
Q

How can drugs reduce the cardiac workload?

A

Reduce heart rate

Reduce myocardial contractility

Reduce afterload

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34
Q

What is the purpose of drug treatment for stable ischaemic heart disease?

A

Relieve symptoms

Halt the disease process

Regression of the disease process

Prevent myocardial infarction

Prevent death

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35
Q

What are examples of different drug therapies for angina?

A

Beta-adrenoceptor antagonists (rate limiting)

Ivabradine (rate limiting)

Calcium channel blockers (rate limiting)

Calcium channel blockers (vasodilators)

Nitrates (vasodilators)

Potassium channel openers

Aspirin/clopidogrel/tigagrelor

Cholesterol lowering agents

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36
Q

What are examples of cholesterol lowering agents?

A

HMG CoA reductase inhibitors

Fibrates

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37
Q

What are examples of drugs that improve the supply of blood to the heart?

A

Vasodilators such as nitrates and calcium channel blockers

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38
Q

What are examples of drugs that reduce the demand of the heart?

A

Rate limiting drugs such as beta blockers and calcium channel blockers

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39
Q

What are examples of beta blockers?

A

Bisoprolol

Atenolol

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40
Q

What are beta blockers?

A

Reversible antagonists of the B1 and B2 receptors

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41
Q

What 3 major determinants of myocardial oxygen demand do beta blockers decrease

A

Heart rate

Contractility

Systolic wall tension

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42
Q

What do beta blockers allow greater perfusion of?

A

Subendocardium by increasing diastolic perfusion time

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43
Q

How do beta blockers increase diastolic perfusion time?

A

Decrease the heart rate

Decrease the force of myocardial contraction

Decrease cardiac output

Decrease velocity of contraction

Decrease blood pressure

Protect cardiomyocytes from oxygen free radicals formed during ischaemic episodes

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44
Q

How do beta blockers change the relationship between exercise and angina?

A

Increase the exercise threshold at which angina occurs

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45
Q

What is a concern for beta blockers?

A

Rebound phenomena

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46
Q

What is beta blockers rebound phenomena?

A

Sudden cessation of beta blocker therapy may precipitate myocardial infarction

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47
Q

Who is at risk of beta blocker rebound phenomena?

A

Patients with angina and men over 50 years recieving beta blockers for other reasons

48
Q

What are some contraindications for beta blockers?

A

Asthma

Peripheral vascular disease (and relative contraindications)

Raynauds syndrome

Heart failure (patients are dependent on sympathetic drive)

Bradycardia/heart block

49
Q

What are some adverse drug reactions with beta blockers?

A

Tiredness/fatigue

Lethargy

Impotence

Bradycardia

Bronchospasm

50
Q

What is lethargy?

A

Lack of energy and enthusiasm

51
Q

What is lack of energy and enthusiasm?

52
Q

What are sime drug-drug interactions with beta blockers?

A

Hypotension with other hypotensive agents

Bradycardia when used with other rate limiting drugs

Cardiac failure when used with negatively inotropic agents

NSAIDS antagonise antihypertensive actions

Exaggerate and mask hypoglycaemic actions of insulin or oral hypoglycaemics

53
Q

What are examples of rate limiting drugs other than beta blockers?

A

Verapamil

Diltiazem

54
Q

What are examples of negatively inotropic agents?

A

Verapamil

Diltiazem

Disopyramide

55
Q

What are examples of calcium channel blockers?

A

Diltiazem

Verapamil

Amlodipine

56
Q

How do calcium channel blockers work?

A

Prevent calcium influx into myocytes and smooth muscle lining arteries and arterioles by blocking the L-type calcium channel

57
Q

What are the 2 types of calcium channel blockers?

A

Rate limiting

Vasodilating

58
Q

How do rate limiting calcium channel blockers work?

A

Reduced heart rate and force of contraction

59
Q

How do vasodilating calcium channel blockers work?

A

Produce a reflex tachycardia

60
Q

What are examples of rate limiting calcium channel blockers?

A

Diltiazem

Verapamil

61
Q

What are examples of vasodilating calcium channel blockers?

A

Nifedipine

Amlodipine

62
Q

What does CCB stand for?

A

Calcium channel blockers

63
Q

What are contraindications for calcium channel blockers?

A

Post myocardial infarction

Unstable angina

64
Q

Why is post myocardial infarction a contraindication for calcium channel blockers?

A

May increase morbidity and mortality in patients with impaired liver function

65
Q

Why is unstable angina a contraindication for calcium channel blockers?

A

May increase infarction rate and death in the unstable patient

66
Q

What are some adverse drug reactions of calcium channel blockers?

A

Oedema

Headache

Flushing

Palpation

67
Q

What are nitrovasodilators also known as?

68
Q

What are examples of nitrovasodilators?

A

Glyceryl trinitrate (GTN)

Isosorbide mononitrate

Isosorbide dinitrate

69
Q

What does GTN stand for?

A

Glyceryl trinitrate

70
Q

How can glyceryl trinitrate (GTN) be given?

A

Sublinguinal

Buccal

Transdermal

71
Q

How can isosorbide mononitrate be given?

A

Sustained release formulation in tablets

72
Q

How can isosorbide dinitrate be given?

A

Sustained release formulation in tablets

73
Q

How do nitrovasodilators work?

A

Release NO which then stimulates the release of cGMP which produces smooth muscle relaxation, this preduces preload and afterload so reduces the myocardial oxygen consumption

74
Q

How do nitrovasodilators relieve angina?

A

Arteriolar dilation and so reducing cardiac afterload and thus myocardial work and oxygen demand

Peripheral venodilation so reducing venous return, cardiac preload and thus cardiac workload

Relieving coronary vasospasm

Redistributing myocardial blood flow to ischaemic areas of the myocardium

75
Q

What is GTN used for?

A

Rapid treatment of angina pain

76
Q

How can GTN avoid first pass metabolism?

A

Given by the sublinguinal route

77
Q

How are oral nitrates commonly used?

A

Once a day sustained release formulation

78
Q

What are oral nitrates used for?

A

Prophylaxis

79
Q

What are intravenous nitrates used for?

A

Treatment of unstable angina where they are used in combination with heparin

80
Q

What is intravenous nitrates used with to treat unstable angina?

81
Q

What can develop to the effects of nitrate therapy rapidly?

82
Q

How can tolerance to nitrate therapy be overcame?

A

Giving asymmetric doses of nitrate at 8am and 2pm

Using sustained release preparation which incorporates a nitrate free period

83
Q

What are potential adverse drug reactions of nitrates?

A

Headaches

Hypotension

84
Q

What does hypotension due to nitrates lead to?

A

GTN syncope

85
Q

How can headaches due to nitrates be avoided?

A

Increase dose slowly

86
Q

What are some new approaches to myocardial ischaemia treatment?

A

Preconditioning

Late sodium current inhibition

Sinus node inhibition

Metabolic modulation

87
Q

What drug is used for preconditioning?

A

Nicorandil

88
Q

What drug is used for late sodium current inhibition?

A

Ranolazine

89
Q

What drug is used for sinus node inhibition?

A

Ivabradine

90
Q

What drug is used for metabolic modulation?

A

Trimetazidine

91
Q

What is preconditioning?

A

An experimental technique for producing resistance to the loss of blood supply and thus oxygen

92
Q

How does preconditioning work?

A

1) Activate ATP sensitive potassium channels
2) Entry of potassium into cardiac myocytes inhibits calcium influx and so had a negative inotropic action (decreases force of speed of contraction of muscles)

93
Q

What does activation of ATP-sensitive potassium channels in preconditioning cause?

A

1) Potassium efflux and hyperpolarisation of the smooth muscle membrane and closure of voltage gated calcium channels
2) Closure of calcium gated channels reduces intracellular levels of calcium, resulting in relaxation of vascular smooth muscle and dilation of systemic and coronary arterioles

94
Q

What is ivabradine?

A

Selective sinus node If channel inhibitor

95
Q

What is nicorandil used for?

A

Preconditioning

96
Q

What is ivabradine used for?

A

Sinus node inhibition

97
Q

How does ivabradine work?

A

Slows the diastolic depolarisation slope of the SA node which results in reduction in heart rate (so reduces myocardial oxygen demand)

98
Q

What is randolazine used for?

A

Inhibit late sodium current

99
Q

How does ranolazine work?

A

1) Inhibits persistent or late inward sodium current (INa) in heart muscle in a variety of voltage gated sodium channels
2) Inhibiting that current leads to reduction in intracellular calcium levels, this in tern leads to reduced tension in the heart wall leading to reduced oxygen demand

100
Q

What are examples of antiplatelet agents?

A

Low dose aspirin (75-150mg)

Clopidogrel

101
Q

What is considered to be low dose aspirin?

102
Q

What is the formation of platelet aggregates important in the pathogenesis of?

A

Angina

Unstable angina

Acute myocardial infarction

103
Q

What is aspirin a potent inhibitor of?

A

Platelet thromboxane production

104
Q

What does thromboxane do?

A

Stimulates platelet aggregation and vasoconstriction

105
Q

Who is low dose aspirin effective in?

A

Patients with a heart rate greater than 70

106
Q

What are indications of low dose aspirin?

A

Adults unable to tolerate or with a contraindication to beta blockers

Or in combination with beta blockers in patients inadequately controlled with an optimal beta blocker dose

107
Q

How does clopidogrel work?

A

Inhibits ADP receptor activated platelet aggregation

108
Q

What are potential side effects of aspirin and clopidogrel?

A

Bleeding, such as lower GI tract bleeding

109
Q

What can regular daily use of aspirin do?

A

Reduce mortality of acute myocardial infarction (by 23%)

Reduce unstable angina leading to myocardial infarction and death (by 50%)

In secondary prevention reduce reinfarction by 32% and combined vascular events by 25%

110
Q

What are examples of cholesterol lowering agents?

A

Simvastatin

Pravastatin

Atorvastatin

111
Q

How do cholesterol lowering agents work?

A

HMG CoA reductase inhibitors

112
Q

What does aggressive cholesterol lowering post myocardial infarction reduce?

A

Cardiovascular mortality by 42% and total mortality by 30%

113
Q

What are the NICE guidelines for treatment of angina?

A

1) Beta blockers should be used as first line therapy for the relief of symptoms of stable angina
2) If adequate control of angina not achieved add a calcium channel blocker
3) If still not control consider switching to other options or using a combination of the 2
4) All patients with stable angina due to atherosclerotic disease should recieve longh term standard aspirin and statin therapy
5) All patients with stable angina should be considered for treatment with ACEi

114
Q

What should all patients with stable angina due to atherosclerotic disease recieve?

A

Long term standard aspirin and statin therapy

115
Q

What are some drugs for secondary prevention of cardiovascular disease?

A

Aspirin 75mg daily

ACE inhibitors for people with stable angina and diabetes

Statin treatment

Treatment for high blood pressure

116
Q

What drugs should people with stable angina and diabetes recieve?

A

ACE inhibitors

Cardiovascular System (41 decks)

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