Clinical pharmacology of stable coronary artery disease

Question 1

What are acute coronary syndromes?

Answer 1

Myocardial infarction: STEMI or NSTEMI

Unstable angina pectoris (UAP)

Question 2

What are stable CA diseases?

Answer 2

Angina pectoris

Silent ischaemia

Question 3

Define stable angina

Answer 3

A clinical syndrome of predicable chest pain or pressure precipitated by activities such as exercise or emotional stress, which increases myocardial oxygen demand

Question 4

What does SCAD arise from?

Answer 4

A mismatch between myocardial blood/oxygen supply and demand

Question 5

What may attacks of angina be precipitated by?

Answer 5

Anything which increases HR, SV or BP

Question 6

What are the mechanisms in which drugs can correct the mismatch in the blood/oxygen supply?

Answer 6

reducing HR
Reducing Myocardial contractility
Reducing afterload
Increase supply of oxygen

Question 7

Name the 3 types of rate limiting drugs

Answer 7

• Beta adrenoceptor antagonists
• CCBs
• Ivabradine

Question 8

Name the 2 types of vasodilators

Answer 8

• CCBs

- Nitrates -> oral, sublingual

Question 9

What drug is a pottasium channel activator?

Answer 9

Nicrorandil

Question 10

What drug is a sodium current inhibitor?

Answer 10

Ranolazine

Question 11

What drugs are cholesterol lowering agents?

Answer 11

• HMG CoA reductase inhibitors

- Fibrates

Question 12

Name 2 beta blockers

Answer 12

Bisoprolol

Atenolol

Question 13

Describe the mechanism of the B blockers

Answer 13

• Beta blockers are reversible antagonists of the B1 and B2 receptors
• Newer drugs are cardioselective acting primarily on the B1 receptors
• Block the Sympathetic system

Question 14

What is the effect of B blockers

Answer 14

• Decrease three major determinants of myocardial oxygen demand(HR, Contractility and systolic wall tension)
• Also allow improved perfusion of the subednocardium by increasing diastolic perfusion time
• By reducing HR, Force of contraction and blood pressure. B 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

Question 15

What are the contraindications of B blockers

Answer 15

• Asthma
• Peripheral vascular disease
• Raynauds syndrome
• HF
• Existing bradycardia/Heart block

Question 16

ARDS of B blockers

Answer 16

• Tiredness/fatigue
• Lethargy
• Impotence
• Bradycardia
• Bronchospasm
• Rebound
  (sudden cessation of B blocker therapy may precipitate myocardial infarction)

Question 17

Describe the drug-drug interactions of b blockers when used when other hypotensive agents

Answer 17

Causes increased hypotension

Question 18

Describe the drug-drug interactions of b blockers when used with other rate limiting drugs(verapamil or diltiazem)

Answer 18

Bradycardia

Question 19

Describe the drug-drug interactions when used with negatively ionotropic agents (verapamil or diltiazem)

Answer 19

Cardiac failure

Question 20

Describe the drug-drug interactions when b blockers are used with insulin or oral hypoglycaemics

Answer 20

Exaggerate and mask hypoglycaemic actions

Question 21

Name 3 common CCBs

Answer 21

Diltiazem, Verapamil, Amlodpinine

Question 22

Describe the mechanism of CCBs’

Answer 22

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

Question 23

What type of CCB is Diltiazem?

Answer 23

Rate limiting CCB

Question 24

What type of CCB is Amlodipine?

Answer 24

Vasodilating CCB

Question 25

What type of CCB is Verapamil?

Answer 25

Rate limitng CCB

Question 26

What is the effect of Rate liming CCBs

Answer 26

Reduce HR and force of contraction

Question 27

What is the effect of vasodilating CCBs

Answer 27

Reduce BP and afterload

Question 28

What are the contraindications of CCBs

Answer 28

• Never use nifediping immediate release as could 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 dath in the unstable patient

Question 29

ADRs of CCBs

Answer 29

• Ankle oedema (Affects 15-20% of patients and does not respond to diuretics)
• Headache
  Flushing
  Plapitation

Question 30

What are the 3 types of nitrovasodilators?

Answer 30

GTN
Isosorbide mononitrate
Isosorbide dinitrate

Question 31

What is the administration route of each of the nitrovasodilators?

Answer 31

GTN - Sublingual, baccual and transdermal
Isosorbide mononitrate - Sustained release formation, tablets
Isosorbide dinitrate - Sustained release formation, tablets

Question 32

Describe the pharmacological mechanism of nitrovasodilators

Answer 32

The nitro-vasodilators relax almost all smooth muscle by releasing NO which then stimulates the production of cGMP which produces smooth muscle relaxation

Question 33

How do nitrovasodilatorsreduce myocardial consumption

Answer 33

Reduce preload and afterload

Question 34

How do nitrates relieve angina?

Answer 34

• Arteriolar dilation and so reducing cardiac after load and thus myocardial work and oxygen demand
• Perpiheral venodilation and so reducing vneous return, cardiac preload and thus myocardial workload
• Relieves coronary vasospasm

Question 35

Describe how nitrate tolerance can be overome?

Answer 35

Giving asymmetric doses of nitrate at 8am and 2pm

Using a sustained release preparation which incorporates a ‘nitrate free period’

Question 36

What are the ADRs of nitrates?

Answer 36

Headache - if so increase dose slowly

Hypotension - GTN synocope