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Cardiovascular System > Clinical pharmacology of stable coronary artery disease > Flashcards

Clinical pharmacology of stable coronary artery disease Flashcards

1
Q

Features of ischaemic heart disease

A
  • It is the most common cause of death in pre-retirement males
  • Acute coronary syndromes
  • Stable coronary disease
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2
Q

Acute coronary syndromes

A
  • Myocardial syndromes: STEMI or NSTEMI

- Unstable angina pectoris

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3
Q

Stable coronary artery disease examples

A
  • Angina pectoris

- Silent ischaemia

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4
Q

Risk factors of ischaemic heart disease

A
  • Hypertension
  • Smoking
  • Hyperlipidaemia
  • Being male
  • Post-menopausal females
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5
Q

Features of Stable coronary artery disease

A
  • SCAD arises as a result of a mismatch between myocardial blood/oxygen supply and demand
  • Attacks of angina (chest pain) may be precipitated by any stress which increases cardiac work and myocardial oxygen demand
  • Anything which increases heart rate, stroke volume or blood pressure
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6
Q

What are determinants of demand ischaemia (ischaemia during stress)?

A
  • Heart rate
  • Systolic blood pressure
  • Myocardial wall stress
  • Myocardial contractility
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7
Q

What are determinants of supply ischaemia (ischaemia at rest)?

A
  • Coronary artery diameter and tone
  • Collateral blood flow
  • Perfusion pressure
  • Heart rate (duration of diastole)
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8
Q

Features of Hyperlipidaemia

A
  • Atherosclerosis at the start
  • Disease of the muscular arteries (not veins)
  • Progressive deposition of cholesterol esters
  • Accounts indirectly for half of annual mortality
  • Lesions start as fatty streaks (aged 20)
  • Fibrous plaque
  • Most of the changes are in the intimal layer
  • Most of the foam cells are of smooth muscle origin
  • Necrotic core
  • Fibrous cap
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9
Q

How can drugs help to correct imbalance?

A
  • Decreasing myocardial oxygen demand by reducing cardiac workload:
    Reduce heart rate
    Reduce myocardial contractility
    Reduce afterload
  • Increasing the supply of oxygen to ischaemic 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

Definition of stable angina

A

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

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12
Q

Types of drugs used in drug therapy of angina

A
  • Rate limiting
  • Vasodilators
  • Anti-platelet
  • Potassium channel openers
  • Cholesterol lowering agents
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13
Q

Rate limiting drugs used in drug therapy

A
  • Beta-adrenoreceptor antagonists
  • Ivabradine
  • Calcium channel blockers
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14
Q

Vasodilators used in drug therapy

A
  • Calcium channel blockers: reduce afterload on the heart

- Nitrates e.g. GTN: oral, sublingual

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15
Q

What is the main potassium channel opener used in angina?

A

Nicorandil

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16
Q

Nitrates used in angina

A
  • Short duration: sublingual nitroglycerin
  • Intermediate: oral nitroglycerin
  • Long duration: transdermal nitroglycerin
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17
Q

Anti-platelet drugs used in angina

A
  • Aspirin
  • Clopidogrel
  • Tigagrelor
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18
Q

Cholesterol lowering agents used in angina

A
  • HMG CoA reductase inhibitors

- Fibrates

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19
Q

Beta blockers used in angina and features

A

Bisoprolol, Atenolol

  • Beta blockers are reversible antagonists of the Beta1 and Beta2 receptors
  • Newer drugs are cardioselective acting primarily on the beta1 receptors
  • Block the sympathetic system
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20
Q

What do beta blockers actually do?

A
  • Decrease three major determinants of myocardial oxygen demand: heart rate, contractility, systolic wall tension
  • Also allow improved perfusion of the subendocardium by increasing diastolic perfusion time
  • Decrease the force of myocardial contraction
  • Decrease the cardiac output
  • Decrease the velocity of contraction
  • Decrease blood pressure
  • Protect cardiomyocytes from oxygen free radicals formed during ischaemic episodes
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21
Q

What is the rebound phenomena of beta blockers?

A
  • Sudden cessation of beta blocker therapy may precipitate myocardial infarction
  • Those at risk include patients with angina and men over 50 years receiving beta blockers for other reasons
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22
Q

Contraindications of beta blockers

A
  • Asthma
  • Peripheral vascular disease
  • Raynauds syndrome
  • Heart failure: those patients that are dependent on sympathetic drive
  • Bradycardia/Heart block
23
Q

Adverse drug reactions of beta blockers

A
  • Tiredness/fatigue
  • Lethargy
  • Impotence
  • Bradycardia
  • Bronchospasm
  • Rebound: sudden cessation of beta blocker may precipitate MI
24
Q

Features of Drug-Drug interactions

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 or disopyramide
  • NSAIDs antagonise antihypertensive actions

Exaggerate and mask hypoglycaemic actions of insulin or oral hypoglycaemics

25
Q

Examples of Calcium channel blockers for angina

A
  • Diltiazem
  • Verapamil
  • Amlodipine
26
Q

Features of calcium channel blockers

A
  • Prevent calcium influx into myocytes and smooth muscle lining arteries and arterioles by blocking the L-type calcium channel.
  • Rate limiting CCB’s like diltiazem and verapamil also reduce heart rate and force of contraction
  • Vasodilating CCBs like nifedipine or amlodipine may produce a reflex tachycardia
27
Q

Further features of CCBs

A
  • CCBs reduce vascular tone and produce vasodilatation and reduce afterload: reduce myocardial work load
  • Rate limiting CCBs reduce the heart rate and the force of myocardial contractility: reduce myocardial oxygen requirements
  • CCBs may also produce coronary vasodilatation but of little importance
28
Q

Contraindications of CCBs (Nifedipine)

A
  • Never use nifedipine immediate release
  • Evidence that the use of rapidly acting vasodilatatory-CCBs (nifedipine) 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 patient
29
Q

Adverse drug reactions of CCBs

A
  • Ankle oedema: affects 15-20% of patients and does not respond to diuretics
  • Headache
  • Flushing
  • Palpitation
30
Q

Examples of Nitrovasodilators for angina

A
  • Glyceryl trinitrate (GTN): sublingual, buccal, transdermal
  • Isosorbide mononitrate: sustained release formulation, tablets
  • Isosorbide dinitrate: sustained release formulation, tablets
31
Q

Why is GTN administered sublingually?

A

Triglyceryl trinitrate undergoes high first pass metabolism in liver so the drug will be broken down and not work if given orally

  • So, sublingual administration bypasses this portal circulation and GTN can directly act on Large vessels
32
Q

Pharmacology of nitrovasodilators

A
  • Nitrovasodilators relax almost all smooth muscle by releasing NO which then stimulates the release of cGMP which produces smooth muscle relaxation.
  • Reduce preload and afterload so reduce myocardial oxygen consumption.
33
Q

How do 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
  • Redistributing myocardial blood flow to ischaemic areas of the myocardium
  • No evidence that nitrates reduce mortality
34
Q

What are the uses of GTN?

A
  • Used for rapid treatment of angina pain
  • To avoid first pass metabolism is given by the sublingual route
  • May be used frequently and prophylactically
35
Q

What are the uses of oral nitrates?

A
  • Commonly given as a once a day sustained release formulation
  • Used for prophylaxis
36
Q

What are the uses of intravenous nitrates?

A

The main stay in the treatment of unstable angina where they are used in combination with heparin

37
Q

Tolerance to nitrate therapy and how do you overcome it?

A
  • Tolerance to the effects nitrate therapy can develop rapidly.

Overcome this problem by:

  • Giving asymmetric doses of nitrate 8am and 2pm
  • Using a sustained release preparation which incorporates a “nitrate free period”
38
Q

Adverse drug reactions of nitrate therapy

A
  • Headache: increase dose slowly

- Hypotension: GTN syncope

39
Q

What are new approaches to myocardial ischaemia?

A
  • Metabolic modulation (trimetazidine)
  • Sinus node inhibition (ivabradine)
  • Late Na+ current inhibition (ranolazine)
  • Preconditioning (nicorandil)
40
Q

Action of Nicorandil - IPC

A
  • Activate “ATP sensitive potassium channels”

- The entry of potassium into cardiac myocytes inhibits calcium influx and so has a negative inotropic action.

41
Q

Preconditioning: Nicorandil

A

Activation of ATP-sensitive K+ channels:

  • Ischaemic preconditioning
  • Dilation of coronary resistance arterioles

Nitrate-associated effects:
- Vasodilation of coronary epicardial arteries

42
Q

What is the nitrate moiety of Nicorandil

A

The nitrate moiety produces relaxation of vascular smooth muscle with dilation of systemic venous circulation and epicardial coronary arteries

43
Q

Features of Ivabradine

A
  • It is a sinus node If channel inhibitor
  • Slows the diastolic depolarisation slope of the SA-node
  • Results in a reduction in heart rate: reduces heart rate and myocardial oxygen demand.
44
Q

What does Ivabradine reduce?

A
  • It reduces primary end point in angina patients

- It reduces myocardial infarction in patients with angina

45
Q

Features of Ranolazine

A
  • Ranolazine inhibits persistent or late inward sodium current (INa) in heart muscle in a variety of voltage gated sodium channels.
  • Inhibiting that current leads to reductions in intracellular calcium levels.
  • This in turn leads to reduced tension in the heart wall, leading to reduced oxygen requirements for the muscle.
46
Q

Antiplatelet agents and features

A
  • Low dose Aspirin (75-150mg)
  • The formation of platelet aggregates are important in the pathogenesis of angina, unstable angina and acute MI.
  • Aspirin is a potent inhibitor of platelet thromboxane production.
  • Thromboxane stimulates platelet aggregation and vasoconstriction.
47
Q

What can the regular daily use of aspirin do?

A
  • In acute MI: reduce mortality by 23%, in combination with streptokinase reduce mortality by 42% and reinfarction by 52%.
  • In unstable angina: reduce MI and death by 50%.
  • In secondary prevention: reduce reinfarction by 32% and combined vascular events by 25%.
48
Q

Features of Clopidogrel

A
  • Inhibits ADP receptor activated platelet aggregation.
  • Prevention of atherosclerotic events in PVD.
  • Acute coronary syndrome
  • Same incidence of bleeding as aspirin but possibly lower GI bleeding!
  • Newer agents such as prasugrel and ticagrelor. Possible advantages.
49
Q

Examples of Cholesterol lowering agents

A
  • Simvastatin
  • Pravastatin
  • Atorvastatin
50
Q

Features of cholesterol lowering agents

A
  • These are HMG CoA Reductase inhibitors which are the most effective cholesterol lowering agents.
  • Studies have demonstrated that aggressive cholesterol lowering post MI can reduce cardiovascular mortality by 42% and total mortality by 30%.
51
Q

What is the NICE guidance treatment regimen?

A
  • Beta blockers should be used for the relief of symptoms of stable angina.
  • When adequate control of anginal symptoms is not achieved with beta-blockade a calcium channel blocker should be added.
  • If the person’s symptoms are not satisfactorily controlled consider either switching to the other option or using a combination of the two.
52
Q

What should all patients with stable angina receive?

A
  • All patients with stable angina should be considered for treatment with ACEi.
53
Q

Drugs for secondary prevention of cardiovascular disease?

A
  • Aspirin 75mg daily taking into account the risk of bleeding and comorbidities.
  • ACE inhibitors for people with stable angina and diabetes.
  • Statin treatment
  • Treatment for high blood pressure

Cardiovascular System (36 decks)

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