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Cardiovascular block > Clinical Pharmacology of Stable Coronary Artery Disease > Flashcards

Clinical Pharmacology of Stable Coronary Artery Disease Flashcards

1
Q

What is the most common cause of death in pre-retirement males ?

A 
Acute coronary syndrome:
	- MI- STEMI or NSTEMI
	- Unstable angina 
Stable coronary artery disease 
	- Angina
        - Silent ischaemia
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2
Q

What is the epidemiology of angina ?

A

ISD data suggests 34.3/1000 for men ages 65-74 and 59.7/1000 for men 7yrs and over live with angina
For women in the same age groups: 23.3 and 38.5/1000

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3
Q

What are the risk factors for angina ?

A 
Hypertension
Smoking
Hyperlipidaemia
Hyperglycaemia 
Previous CAD
Existing PVD
Male 
Post-menopausal females
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4
Q

How does stable coronary artery disease arise ?

A

As a result of a mismatch between myocardial blood/oxygen supply and demand

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5
Q

What is demand ischaemia ?

A

Ischaemia during stress (emotional or physical)

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6
Q

What is supply ischaemia ?

A

Ischaemia at rest

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7
Q

What are the determinants of demand ?

A

HR
Systolic BP
Myocardial wall stress
Myocardial contractility

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8
Q

What are the determinants of supply ?

A

Coronary artery diameter and tone
Collateral blood flow
Perfusion pressure
HR (duration of diastole)

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9
Q

How do drugs help correct the imbalance ?

A

Decreasing myocardial oxygen demand by reducing cardiac workload
Reduce HR
Reduces myocardial contractility
Reduce afterload
Increasing the supply of O2 to iscahemic myocardium

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10
Q

What is the purpose of drug treatment ?

A 
Relieve symptoms
Halt the disease process
Regression of the disease process
Prevent myocardial infarction
Prevent death
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11
Q

What rate limiting drugs can be used for SCAD ?

A

B-blockers
Ca channel blockers
Ivabradine

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12
Q

What are the vasodilating drugs used for SCAD ?

A

Ca channel blockers

Sodium current inhibitor

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13
Q

What other drugs are used ?

A 
Potassium channel activators - nicorandil 
Sodium current inhibitor - ranolazine 
Aspirin/clopidogrel/ticagrelor 
Cholesterol lowering agents:
- HMG CoA reductase inhibitors
- Fibrates
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14
Q

What are B-blockers ?

A

Beta blockers are reversible antagonists of the B1 and B2 receptors
Block the sympathetic system

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15
Q

What 3 determinants of myocardial O2 demand does B-blockers decrease ?

A

HR
Contractility
Systolic wall tension

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16
Q

What does B-blockers reduce ?

A

HR
Force of contraction
BP

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17
Q

What will B-blockers increase ?

A

Beta blockers increase the exercise threshold at which angina occurs and so move the balance point at which the demand for oxygen outstrips the supply of oxygenated blood

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18
Q

What are the contraindications of B-blockers ?

A 
Asthma
Peripheral Vascular Disease
 - Relative contraindication
Raynaud's Syndrome
Heart failure
Those patients who are dependent on sympathetic drive
Existing Bradycardia / Heart block
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19
Q

What are the adverse drug reactions to B-blockers ?

A 
Tiredness 
Fatigue
Lethargy
Impotence
Bradycardia
Bronchospasm
Rebound- sudden cessation of beta blocker therapy may precipitate MI
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20
Q

What are the drug-drug interactions of B-blockers ?

A

Primarily Pharmacodynamic
Hypotension when used with other hypotensive agents
Bradycardia when used with other rate limiting drugs such as verapamil or diltiazem
Cardiac failure when used with negatively inotropic agents such as verapamil, diltiazem
Exaggerate and mask hypoglycaemic actions of insulin or oral hypoglycaemics

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21
Q

What are examples of B-blockers ?

A

Bisoprolol

Atenolol

22
Q

What do calcium channel blockers do ?

A

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

23
Q

What do the rate limiting CCBs do ?

A

Reduce heart rate and force of contraction

24
Q

What are some examples of rate limiting CCBs ?

A

Diltiazem

Verapamil

25
Q

What do the vasodilating CCBs do ?

A

Reduce BP and afterload

26
Q

What is an example of vasodilating CCBs ?

A

Amlodipine

27
Q

What are the contraindications of CCBs ?

A

NEVER USE NIFEDIPINE IMMEDIATE RELEASE may precipitate acute MI or stroke
Post- MI- may increase morbidity and mortality in patients with impaired LV function
Unstable angina- Evidence that dihydropyridines may increase infarction rate and death in the unstable pateint

28
Q

What are the adverse drug reactions to CCBs ?

A

Ankle oedema
Headache
Flushing
Palpitations

29
Q

What nitro-vasodilators can be used for angina ?

A

Glyceryl trinitrate (GTN)
- Sublingual, buccal, transdermal
Isosorbide mononitrate
- Sustained release formulation, tablets
Isosorbide dinitrate
- Sustained release formulation, tablets

30
Q

What is the pharmacology of nitro-vasodilators ?

A

Relax almost all smooth muscle by releasing NO which stimulates the production of cGMP which produces smooth muscle relaxation
Reduce preload and afterload

31
Q

How can nitrates relieve angina ?

A

Arteriolar dilatation and so reducing cardiac afterload and thus myocardial work and oxygen demand
Peripheral venodilatation and so reducing venous return, cardiac preload and thus myocardial workload
Relieving coronary vasospasm

32
Q

How fast can a tolerance to nitrates develop ?

A

Rapidly

Overcome this by gibing asymmetric doses of nitrates 8am and 2pm

33
Q

What are the adverse drug reactions to nitrates ?

A

Headache- increase dose slowly

Hypotension- GTN syncope

34
Q

What is an example of a potassium channel activator ?

A

Nicorandil

35
Q

What is the mechanism of K channel activators ?

A

Activates ATP sensitive potassium channels allowing entry of potassium into cardiac myocytes and inhibiting calcium influx and so has a negative inotropic action
Induce relaxation of vascular smooth muscle and has coronary vasodilator properties

36
Q

What is an example of a selective sinus node If inhibitor ?

A

Ivabradine

37
Q

What is the mechanism of Ivabradine ?

A

Inhibits the If pacemaker current in the SAN and reduces HR
Reduced HR = reduced myocardial O2 demand
Used for the symptomatic treatment of chronic stable angina in adults with normal sinus rhythm and heart rate ≥ 70 bpm

38
Q

What are the indications for ivabradine ?

A

Adults unable to tolerate or with a contra-indication to the use of beta-blockers
in combination with beta-blockers in patients inadequately controlled with an optimal beta-blocker dose

39
Q

What does ivabradine reduce ?

A

Fatal and nonfatal MIs

40
Q

What is an example of late Na+ current inhibitor ?

A

Ranolazine

41
Q

What is the mechanism of Ranolazine ?

A

Inhibits persistent or late inward sodium current (INa) in heart muscle.
This leads to reduction in intracellular calcium levels
This results in reduced heart wall tension and reduced oxygen requirements

42
Q

What are the drug interactions of Ranolazine ?

A

Ranolazine is metabolised CYP3A4
It also inhibits CYP2D6
Do not use with clarithromycin, ketoconazole

43
Q

What antiplatelet therapy can be used ?

A

Aspirin
Clopidogrel
Ticagrelor
Prasugrel

44
Q

What do antiplatelets agents do ?

A

Prevent the formation of platelet aggregates which are important in the pathogenesis of angina, unstable angina and acute MI

45
Q

What does aspirin inhibit ?

A

Potent inhibitor of platelet thromboxane production which stimulates platelet aggregation

46
Q

What drugs belong to the P2Y12 inhibitors ?

A

Clopidogrel
Ticagrelor
Prasugrel

47
Q

What do the P2Y12 inhibitors block ?

A

Block the platelet P2Y12 receptor, which plays a key role in platelet activation and the amplification of arterial thrombus formation

48
Q

What should be used in pateints with a high or moderate risk of ischaemic events who do not have a high risk of bleeding ?

A

Dual antiplatelet therapy

49
Q

What is the most commonest cause of admission with GI bleed ?

A

Aspirin

50
Q

What are examples of cholesterol lowering agents- statins ?

A

Atorvastatin

Simvastatin

Cardiovascular block (28 decks)

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