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R-Cradio-illness > Stable Ischaemic Heart Disease and Angina Therapy > Flashcards

Stable Ischaemic Heart Disease and Angina Therapy Flashcards

1
Q

What are the risk factors for stable IHD and angina?

A 
Hypertension
Smoking 
Hyperlipidaemia
Hyperglycaemia
Male
Post-menopausal
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2
Q

What is hyperlipidaemia a disease of?

A

Muscular arteries - cerebral or coronary, not veins

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3
Q

From what age do fatty streaks appear?

A

Around 20

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4
Q

How does hyperlipidaemia affect the arteries?

A

Lesions start as fatty streaks
There is subendothelial accumulation of large foam cells derived from the macrophages and smooth muscles cells filled with lipids

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5
Q

How do fibrous plaques affect the arteries?

A

Develop from fatty streaks and project into the arterial lumen, reducing blood flow

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6
Q

Where do most of the changes to the artery in IHD occur?

A

In the intimal layer

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7
Q

What changes occur in the intimal layer in IHD?

A

Accumulation of monocytes, lymphocytes, foam cells and connective tissue

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8
Q

What are the usual features of foam cells?

A

Most are of smooth muscle origin

Necrotic core and fibrous cap

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9
Q

What does stable ischaemic heart disease result from?

A

Mismatch between myocardial blood and oxygen supply and demand

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10
Q

What are episodes of angina precipitated by?

A

Any activity which causes cardiovascular stress

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11
Q

How can drugs help to correct the imbalance in stable IHD?

A

Decrease myocardial oxygen demand by reducing cardiac workload
Increase supply of oxygen to ischaemic myocardium

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12
Q

What are the purposes of drug treatment of stable IHD?

A 
Relieve symptoms
Halt disease process
Regress disease process
Prevent MI 
Prevent death
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13
Q

What drugs can be used in the treatment of stable IHD?

A 
Beta blockers 
Ivabradine 
CCBs - rate limiting and vasodilation 
Nitrates
Potassium channel openers
Aspirin 
Clopidogrel
Tigagrelor
Cholesterol lowering agents e.g. HMG CoA reductase inhibitors
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14
Q

Give an example of a beta blocker used in the treatment of stable IHD

A

Atenolol

Bisoprolol

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15
Q

How do beta blockers work to treat stable IHD?

A

Reversible antagonists of beta-1 and beta-2 receptors (newer drugs are cardioselective and act primarily on beta-1 receptors)
Block the physiological responses to adrenaline and noradrenaline and so decrease 3 major determinants of myocardial oxygen demand - HR, contractility and systolic wall tension
Also allow improved perfusion of subendocardium by increasing diastolic perfusion time

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16
Q

What effect do beta blockers have on HR, force of myocardial contraction, CO, velocity of contraction and BP?

A

Decrease all of these

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17
Q

What do beta blockers protect the caardiomyocytes from?

A

Oxygen free radicals formed during ischaemic episodes

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18
Q

By reducing HR, force of contraction and BP, beta blockers increase what?

A

Exercise threshold at which angina occurs and so move the balance point at which demand for oxygen outweighs the supply of oxygenated blood

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19
Q

What is rebound phenomena?

A

When sudden cessation of beta-blocker therapy may precipitate MI, those at risk include patients with angina and males over 50 years old who are receiving beta blockers for other reasons

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20
Q

What are the contraindications to beta blocker use?

A 
Asthma
Peripheral vascular disease (relative contraindication) 
Reynaud's 
Heart failure 
Bradycardia
Heart block
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21
Q

What are the potential adverse drug reactions from beta blocker use?

A 
Tiredness/fatigue 
Lethargy 
Impotence
Bradycardia 
Bronchospasm
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22
Q

What are the possible drug-drug interactions with beta blockers?

A

Hypotension when used with other hypotensive agents
Bradycardia when used with other rate limiting drugs
Cardiac failure when used with negatively inotropic agents
NSAIDs antagonise antihypertensive actions
Exaggeration and masking of hypoglycaemic actions of insulin or oral hypoglycaemics

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23
Q

Give an example of a calcium channel blocker used in treatment of stable IHD

A

Diltiazem
Verapamil
Amlodipine

24
Q

How do CCBs work?

A

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

25
Q

How do rate-limiting CCBs treat stable IHD?

A

Reduce HR and force of contraction which reduces myocardial oxygen requirements

26
Q

How do vasodilation CCBs treat stable IHD?

A

Reduce vascular tone and so produce vasodilatation and reduce afterload, reducing myocardial workload

27
Q

What are the contraindications for CCBs use?

A

Evidence that use of rapid acting vasodilatory CCB may precipitate acute MI or stroke
Post-MI patients
Unstable angina

28
Q

What are the possible adverse drug reactions from CCB use?

A

Ankle oedema
Headache
Flushing
Palpitations

29
Q

What percentage of patients on CCBs will experience ankle oedema?

A

15-20%

30
Q

Give an example of a nitrovasodilator used in treatment of stable IHD

A

Glyceryl trinitrate
Isosorbide mononitrate
Isosorbide dinitrate

31
Q

What routes can GTN be given via?

A

Sublingual
Buccal
Transdermal

32
Q

What routes can isosorbide mono and dinitrate be given via?

A

Sustained release formula

Oral tablets

33
Q

How do nitrovasodilators work?

A

Relax almost all smooth muscle by releasing NO which then stimulates the release of cGMP which produces smooth muscle relaxation

34
Q

How do nitrovasodilators treat IHD?

A

Reduce preload and afterload so reduce myocardial oxygen consumption

35
Q

How do nitrates relieve angina?

A

Arteriolar dilatation - reducing cardiac afterload and myocardial work and oxygen demand
Peripheral venodilatation - reducing venous return, cardiac preload and myocardial workload
Relieve coronary vasospasm
Redistribute myocardial blood flow to ischaemic areas of the myocardium

36
Q

What are the benefits of GTN use?

A

Rapid treatment of angina pain
Avoid first pass metabolism - given via sublingual route
May be used frequently and prophylactically

37
Q

How are oral nitrates used?

A

As once-a-day sustained release formulation

Used for prophylaxis

38
Q

How are IV nitrates used?

A

Mainstay of treatment of unstable angina, used in combination with heparin

39
Q

What is the problem associated with nitrate therapy? How can this be overcome?

A

Tolerance to effects of nitrate therapy can develop rapidly
Can be overcome by giving an asymmetric dose of nitrate at 8am and 2pm and by using a sustained release preparation which incorporates a nitrate-free period

40
Q

What are the potential adverse drug reactions from nitrate use?

A

Headache

Hypotension

41
Q

Give an example of a potassium channel opener used in stable IHD treatment

A

Nicorandil

42
Q

How do potassium channel openers work?

A

Activate silent potassium channels, allows entry of potassium into the cardiac myocyctes which inhibits the calcium influx so has a negative inotropic action

43
Q

Why are potassium channel openers third line therapy?

A

Due to risk of bowel ulceration

44
Q

How does Ivabradine work?

A

Selective sinus node If channel inhibitor
Slows the diastolic depolarisation slope of the sinoatrial node
Results in reduction in HR which reduces myocardial oxygen demand

45
Q

What is the standard dose of aspirin used for treatment of stable IHD?

A

Low dose 75-100mg

46
Q

How does aspirin treat stable IHD?

A

Formation of platelet aggregates are important in the pathogenesis of angina, unstable angina and acute MI
Thromboxane stimulates platelet aggregation and vasoconstriction
Aspirin is a potent inhibitor of platelet thromboxane production

47
Q

When is aspirin useful as a treatment of IHD?

A

For the symptomatic treatment of chronic stable angina in adults with normal sinus rhythm and heart rate of 70bpm or greater
Only effective to reduce incidence of coronary artery disease outcomes in patients with heart rate of 70bpm or greater

48
Q

What are the indications for aspirin use?

A

Adults unable to tolerate or who have contraindications to beta blockers
Use in combination with beta blockers in patients with inadequately controlled stable angina at an optimal beta blocker dose

49
Q

What is the effect of aspirin on mortality of acute MI in stable angina patients?

A

Regular daily use of aspirin can reduce mortality of acute MI by 23%
In combination with streptokinase it can reduce mortality by 42% and re-infarction by 52%

50
Q

What is the effect of aspirin on mortality of acute MI in unstable angina patients?

A

Can reduce MI and death by 50%

In secondary prevention is can reduce re-infarction by 32% and combined vascular events by 25%

51
Q

Low dose aspirin is the most common cause of what hospital admission?

A

Admission due to GI bleed

52
Q

How does clopidogrel work?

A

Inhibits ADP receptor activated platelet aggregation

Prevention of atherosclerotic events in PVD

53
Q

Give an example of a cholesterol lowering agent used in treatment of IHD

A

Simvastatin
Pravastatin
Atorvastatin

54
Q

What cholesterol lowering agents are the most effective?

A

HMG CoA reductase inhibitors e.g. simvastatin

55
Q

What effect does cholesterol lowering have on cardiovascular mortality and total mortality in post-MI patients?

A

Can reduce cardiovascular mortality by 42% and total mortality by 30%

56
Q

What is the typical progression of a treatment regime of stable IHD?

A 
Beta blocker
Aspirin
Statin
CCB
Nitrate
Nicorandil
Refer for cardiology work up for possible stenting

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