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B2. 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
What are the fatty streaks that lesions start as composed of?
Sub endothelial accumulation of large foam cells (derived from macrophages plus smooth muscle cells) filled with lipid
26
How does fibrous plaque reduce blood flow?
Projects into the lumen of the vessel
27
Where in the blood vessel are most of the changes during atherosclerosis?
In the intimal layer
28
What is a fibrous plaque composed of?
Fibrous cap Necrotic core
29
What is the common pathology of stable ischaemic heart disease?
Atherosclerosis
30
What does therapy of stable ischaemic heart disease target?
Atherosclerosis
31
What treatment can help correct the imbalance of supply and demand?
Drug treatment
32
How can drug treatment help to correct the imbalance between supply and demand?
Decreasing the myocardial oxygen demand by reducing cardiac workload Increasing the supply of oxygen to ischaemic myocardium
33
How can drugs reduce the cardiac workload?
Reduce heart rate Reduce myocardial contractility Reduce afterload
34
What is the purpose of drug treatment for stable ischaemic heart disease?
Relieve symptoms Halt the disease process Regression of the disease process Prevent myocardial infarction Prevent death
35
What are examples of different drug therapies for angina?
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
36
What are examples of cholesterol lowering agents?
HMG CoA reductase inhibitors Fibrates
37
What are examples of drugs that improve the supply of blood to the heart?
Vasodilators such as nitrates and calcium channel blockers
38
What are examples of drugs that reduce the demand of the heart?
Rate limiting drugs such as beta blockers and calcium channel blockers
39
What are examples of beta blockers?
Bisoprolol Atenolol
40
What are beta blockers?
Reversible antagonists of the B1 and B2 receptors
41
What 3 major determinants of myocardial oxygen demand do beta blockers decrease
Heart rate Contractility Systolic wall tension
42
What do beta blockers allow greater perfusion of?
Subendocardium by increasing diastolic perfusion time
43
How do beta blockers increase diastolic perfusion time?
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
44
How do beta blockers change the relationship between exercise and angina?
Increase the exercise threshold at which angina occurs
45
What is a concern for beta blockers?
Rebound phenomena
46
What is beta blockers rebound phenomena?
Sudden cessation of beta blocker therapy may precipitate myocardial infarction
47
Who is at risk of beta blocker rebound phenomena?
Patients with angina and men over 50 years recieving beta blockers for other reasons
48
What are some contraindications for beta blockers?
Asthma Peripheral vascular disease (and relative contraindications) Raynauds syndrome Heart failure (patients are dependent on sympathetic drive) Bradycardia/heart block
49
What are some adverse drug reactions with beta blockers?
Tiredness/fatigue Lethargy Impotence Bradycardia Bronchospasm
50
What is lethargy?
Lack of energy and enthusiasm
51
What is lack of energy and enthusiasm?
Lethargy
52
What are sime drug-drug interactions with beta blockers?
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
What are examples of rate limiting drugs other than beta blockers?
Verapamil Diltiazem
54
What are examples of negatively inotropic agents?
Verapamil Diltiazem Disopyramide
55
What are examples of calcium channel blockers?
Diltiazem Verapamil Amlodipine
56
How do calcium channel blockers work?
Prevent calcium influx into myocytes and smooth muscle lining arteries and arterioles by blocking the L-type calcium channel
57
What are the 2 types of calcium channel blockers?
Rate limiting Vasodilating
58
How do rate limiting calcium channel blockers work?
Reduced heart rate and force of contraction
59
How do vasodilating calcium channel blockers work?
Produce a reflex tachycardia
60
What are examples of rate limiting calcium channel blockers?
Diltiazem Verapamil
61
What are examples of vasodilating calcium channel blockers?
Nifedipine Amlodipine
62
What does CCB stand for?
Calcium channel blockers
63
What are contraindications for calcium channel blockers?
Post myocardial infarction Unstable angina
64
Why is post myocardial infarction a contraindication for calcium channel blockers?
May increase morbidity and mortality in patients with impaired liver function
65
Why is unstable angina a contraindication for calcium channel blockers?
May increase infarction rate and death in the unstable patient
66
What are some adverse drug reactions of calcium channel blockers?
Oedema Headache Flushing Palpation
67
What are nitrovasodilators also known as?
Nitrates
68
What are examples of nitrovasodilators?
Glyceryl trinitrate (GTN) Isosorbide mononitrate Isosorbide dinitrate
69
What does GTN stand for?
Glyceryl trinitrate
70
How can glyceryl trinitrate (GTN) be given?
Sublinguinal Buccal Transdermal
71
How can isosorbide mononitrate be given?
Sustained release formulation in tablets
72
How can isosorbide dinitrate be given?
Sustained release formulation in tablets
73
How do nitrovasodilators work?
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
How do nitrovasodilators relieve angina?
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
What is GTN used for?
Rapid treatment of angina pain
76
How can GTN avoid first pass metabolism?
Given by the sublinguinal route
77
How are oral nitrates commonly used?
Once a day sustained release formulation
78
What are oral nitrates used for?
Prophylaxis
79
What are intravenous nitrates used for?
Treatment of unstable angina where they are used in combination with heparin
80
What is intravenous nitrates used with to treat unstable angina?
Heparin
81
What can develop to the effects of nitrate therapy rapidly?
Tolerance
82
How can tolerance to nitrate therapy be overcame?
Giving asymmetric doses of nitrate at 8am and 2pm Using sustained release preparation which incorporates a nitrate free period
83
What are potential adverse drug reactions of nitrates?
Headaches Hypotension
84
What does hypotension due to nitrates lead to?
GTN syncope
85
How can headaches due to nitrates be avoided?
Increase dose slowly
86
What are some new approaches to myocardial ischaemia treatment?
Preconditioning Late sodium current inhibition Sinus node inhibition Metabolic modulation
87
What drug is used for preconditioning?
Nicorandil
88
What drug is used for late sodium current inhibition?
Ranolazine
89
What drug is used for sinus node inhibition?
Ivabradine
90
What drug is used for metabolic modulation?
Trimetazidine
91
What is preconditioning?
An experimental technique for producing resistance to the loss of blood supply and thus oxygen
92
How does preconditioning work?
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
What does activation of ATP-sensitive potassium channels in preconditioning cause?
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
What is ivabradine?
Selective sinus node If channel inhibitor
95
What is nicorandil used for?
Preconditioning
96
What is ivabradine used for?
Sinus node inhibition
97
How does ivabradine work?
Slows the diastolic depolarisation slope of the SA node which results in reduction in heart rate (so reduces myocardial oxygen demand)
98
What is randolazine used for?
Inhibit late sodium current
99
How does ranolazine work?
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
What are examples of antiplatelet agents?
Low dose aspirin (75-150mg) Clopidogrel
101
What is considered to be low dose aspirin?
75-150mg
102
What is the formation of platelet aggregates important in the pathogenesis of?
Angina Unstable angina Acute myocardial infarction
103
What is aspirin a potent inhibitor of?
Platelet thromboxane production
104
What does thromboxane do?
Stimulates platelet aggregation and vasoconstriction
105
Who is low dose aspirin effective in?
Patients with a heart rate greater than 70
106
What are indications of low dose aspirin?
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
How does clopidogrel work?
Inhibits ADP receptor activated platelet aggregation
108
What are potential side effects of aspirin and clopidogrel?
Bleeding, such as lower GI tract bleeding
109
What can regular daily use of aspirin do?
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
What are examples of cholesterol lowering agents?
Simvastatin Pravastatin Atorvastatin
111
How do cholesterol lowering agents work?
HMG CoA reductase inhibitors
112
What does aggressive cholesterol lowering post myocardial infarction reduce?
Cardiovascular mortality by 42% and total mortality by 30%
113
What are the NICE guidelines for treatment of angina?
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
What should all patients with stable angina due to atherosclerotic disease recieve?
Long term standard aspirin and statin therapy
115
What are some drugs for secondary prevention of cardiovascular disease?
Aspirin 75mg daily ACE inhibitors for people with stable angina and diabetes Statin treatment Treatment for high blood pressure
116
What drugs should people with stable angina and diabetes recieve?
ACE inhibitors
117

B2. Cardiovascular System (41 decks)

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