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Cardio > Stable ischaemic heart disease and angina therapy > Flashcards

Stable ischaemic heart disease and angina therapy Flashcards

1
Q

Acute coronary syndromes are a type of Ischaemic heart disease

What are the different types of acute coronary syndromes?

A

Myocardial infarction:

  • STEMI
  • NSTEMI

Unstable angina pectoris

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2
Q

Stable coronary artery diseases are a type of Ischaemic heart disease

What are the different stable coronary artery diseases?

A

Stable angina pectoris

Silent ischaemia

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3
Q

What are the risk factors for ischaemic heart diseases?

A 
Hypertension 
Smoking 
Male 
Hyperlipidaemia 
Hyperglycaemia (diabetic) 
Previous CAD 
Peripheral vascular disease 
Post-menopausal females
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4
Q

What causes Stable coronary artery disease (SCAD)?

A

Mismatch between myocardial demand for/supply of oxygen

Attacks of angina (chest pain) are due to any factor that increases cardiac work and thus it’s oxygen demand:
- ie - factor that increases HR, BP or SV

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5
Q

The mismatch between supply and demand of oxygen for the heart in myocardial ischaemia can be thought of as ‘supply ischaemia’ & ‘demand ischaemia’

What factors determine the supply of oxygen to the myocardium?

A

Coronary artery demand & tone

Collateral blood flow

Perfusion pressure

Heart rate (duration of diastole)

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6
Q

Heart rate is one of the determinants of myocardial oxygen supply

How does heart rate (duration of diastole) affect the amount of oxygen reaching the muscle?

A

Blood can only flow through the coronary arteries during diastole

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7
Q

The mismatch between supply and demand of oxygen for the heart in myocardial ischaemia can be thought of as ‘supply ischaemia’ & ‘demand ischaemia’

What are the determinants of demand of oxygen for the myocardium?

A

Heart rate

Systolic blood pressure

Myocardial wall stress

Myocardial wall contractility

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8
Q

What are the problems posed by hyperlipidaemia?

A

Atherosclerosis of muscular, narrow arteries

Accounts indirectly for half of annual mortality:

  • In coronary arteries, it causes IHD which causes MI
  • Leads to stroke
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9
Q

Drugs can help reduce the imbalance between supply of/demand for oxygen in the myocardium

How do they do this?

A

Drugs usually aim to reduce DEMAND for oxygen by either:

1) Reduce heart rate
2) Reduce myocardial contractility
3) Reduce afterload

Some aim to increase oxygen supply to myocardium

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10
Q

What is the purpose of treating heart disease (applies to lots of diseases) with drugs?

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

What drugs for IHD aim to reduce heart rate?

rate limiting

A

Beta-adrenoceptor antagonists (blockers):
- Atenolol or Bisoprolol

Ivabradine:
- Used as alternative to B blockers

Calcium channel blockers (rate limiting CCBs):
- Diltiazem or Verapamil

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12
Q

What drugs for IHD are vasodilators?

A

Calcium channel blockers (vasodilating CCBs):
- Amlodipine or Felodipine

Nitrates:

  • Oral
  • Sublingual (GTN)
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13
Q

Aside from drugs aimed to reduce heart rate, or cause vasodilation…

What other drugs are prescribed to people with IHD?

A

Potassium channel openers

Aspirin/Clopidogrel/Tigagrelor

Cholesterol lowering agents (Statins):

  • HMG CoA reductase inhibitors
  • Fibrates
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14
Q

Explain the action of Beta blockers

A

Eg Atenolol, Bisoprolol

Reversibly inhibit B1 & B2 receptors thus blocking effects of sympathetic stimulation

Newer agents are cardioselective and act primarily on the Beta 1 receptors

Reduced demand:

  • Decreases HR
  • Decreases Contractility
  • Decreases systolic wall tension

Increases supply:
- Longer diastole period so longer time for blood to pass through coronary arteries

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15
Q

There is a medical risk associated with prescribed beta blockers

What is this risk?

A

Rebound phenomena

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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16
Q

Summarise the contraindications associated with Beta blockers such as Atenolol or Bisoprolol

A

Asthma

Peripheral vascular disease

Raynauds syndrome

Heart failure

Bradycardia / heart block

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17
Q

Why is there a contraindication with beta blockers and Raynauld’s syndrome?

A

Those with Raynaud’s suffer decreased blood flow to their fingers (digits)

Beta blockers can make this worse and increase the risk of digital infarcts

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18
Q

Explain the link/contraindication between beta blockers and heart failure?

A

Can cause heart failure in patients who rely on sympathetic drive (which BBs stop)

Beta blockers should only be prescribed to those who have stable angina, not unstable angina

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19
Q

What are the adverse drug reactions associated with beta blockers?

A

Tiredness / fatigue

Lethargy

Impotence

Bradycardia

Bronchospasm

Rebound phenomena:
- Sudden cessation of BB’s can precipitate to myocardial infarction

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20
Q

Summarise the Drug-drug interactions that Beta blockers can undergo

A

Hypotension:
- If used with other hypotensives

Bradycardia:
- If used with other rate limiting agents such a verapamil or diltiazem

Cardiac failure:
- If used with negatively inotropic agents such as Verapamil, diltiazem or Disopyramide

Exaggerate and mask hypoglycaemic actions of insulin or oral hypoglycaemics

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21
Q

What is the effect of drug-drug interactions that NSAIDs such as Aspirin, ibuprofen undergo?

A

NSAIDs antagonise anti-hypertensive actions

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22
Q

What is the general effect of Calcium channel blockers?

A

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

23
Q

What are the 2 types of calcium channel blockers, and examples of each?

A

Rate limiting:

  • Verapamil
  • Diltiazem

Vasodilators (dihydropyridines):

  • Amlodipine
  • Nifedipine
24
Q

What is the effect, on the heart, of Rate limiting CCBs?

A

Reduce heart rate & force of contraction

Therefore, reduce the cardiac work & oxygen demand

25
Q

What effect may be caused by vasodilating CCBs?

A

Reduce vascular tone
Produce vasodilation
Reduce afterload

Overall, reduce myocardial workload so oxygen demand decreases

26
Q

If a patient is on a beta blocker for angina, but they require a Calcium channel blocker as well…

What type of calcium channel blocker do you prescribe first?

A

Vasodilating CCBs such as Amlodipine or Nifedipine

If the patient took Beta blockers & rate limiting CCBs, then there is a risk that their HR would drop too low

27
Q

What is the danger associated with Nifedipine?

A

The CCB, Nifedipine, must only be given as a gradual release medication

There is evidence that the use of rapidly acting vasodilatatory-CCBs (nifedipine) may precipitate acute MI or stroke

28
Q

What are the contraindications of Calcium channel blockers?

A

Nifedipine may precipitate acute MI or stroke

CCBs may increase morbidity & mortality in post MI patients, who have impaired LV function

Unstable angina:
- Evidence that dihydropyridines may increase infarction rate and death

29
Q

What adverse drug reactions are associated with calcium channel blockers?

A

Ankle oedema

  • Affects 15-20% of patients
  • Does not respond to diuretics

Headache

Flushing

Palpitation

30
Q

What are the 3 main Nitrovasodilators?

A

Glyceryl Trinitrate (GTN)

Isosorbide Mononitrate

Isosorbide Dinitrate

31
Q

How can GTN be administered?

A

Sublingual, buccal, transdermal

Most commonly a spray under the tongue

32
Q

How is isosorbide mononitrate administered?

A

Sustained release formulation, tablets

Metabolised to active form in liver

33
Q

How is Isosorbide dinitrate administered?

A

Sustained release formulation, tablets

Metabolised to active form in liver

34
Q

How do nitrovasodilators work?

A

Release NO which stimulates release of cGMP which produces smooth muscle relaxation…

Arteriolar dilation:
- Reduces cardiac afterload

Peripheral venodilation:
- Reduces venous return ∴ reduces preload

Relieve coronary vasospasm

Redistribute myocardial blood flow to ischaemic areas of the myocardium

35
Q

Nitrovasodilators seem all spicy and good but are they medically useful?

A

Relieve symptoms

Don’t reduce mortality though

36
Q

Summarise the uses of Nitrovasodilators

A

GTN:

  • Rapid relief of angina pain or
  • Pre-cardiac stress prophylaxis

Oral nitrovasodilators:

  • One per day sustained release formulation
  • Prophylaxis
37
Q

When are intravenous nitrates used?

A

To treat unstable angina

Used in combination with heparin (anticoagulant)

38
Q

What problem may develop over a long time of taking nitrates?

A

Patient may develop tolerance

To stop this:

  • Asymmetric doses
  • Sustained release tablets means there is a free period from nitrates before they are metabolised
39
Q

When nitrates are first prescribed, the dosage is increased slowly

Why is this?

A

Avoid headaches

adverse drug reaction from nitrates

40
Q

A patient has a GTN spray for her angina:
She has an episode of pain and decides to sit down, take her spray and rest.
When she stands up again, she faints.

Why is this?

A

GTN spray has an adverse drug reactions of causing hypotension

The hypotension can cause ‘GTN syncope’

41
Q

“The effect of Short acting nitrates is ______”

A

Vasodilation

42
Q

“Beta blockers decrease ______ & ______”

A

Decrease heart rate & decrease myocardial contractility

43
Q

“Long acting nitrates cause ________”

A

Vasodilation

44
Q

What is the effect of DHP Calcium channel blockers?

A

Vasodilation

45
Q

What is the effect of Non-DHP calcium channel blockers?

A

Decrease heart rate & myocardial contractility

46
Q

What are the newer types of treatments for myocardial ischaemia?

A

Metabolic modulation - (Trimetazidine)
- Primarily inhibition of FA oxidation in myocytes

Sinus node inhibition - (Ivabridine)

Late Na+ current inhibition - (Ranolazine)

Ischaemic preconditioning - (Nicorandil)

47
Q

How does Nicorandil work?

A

Nicorandil works by:

1)
- Activating ATP sensitive potassium channels
- Entry of potassium into cardiac myocytes inhibits calcium influx and so has a negative inotropic action
- This also causes dilation of coronary resistance arterioles

2)
Nicorandil forms* nitrate moiety produces relaxation of vascular smooth muscle with dilation of systemic venous circulation and epicardial coronary arteries.

48
Q

What is Ivabridine used for, and with who?

A

Selective sinus node If channel inhibitor:

  • Slows the diastolic depolarisation slope of the SA-node
  • Reduction in heart rate

It is only used in patients with HR 70 or above

(Not used on patients with Afib)

49
Q

What is Ranolazine?

A

Late Na+ current inhibition by acting on a variety of Sodium channels in myocardium

Inhibiting current reduces intracellular calcium levels

This in turn leads to reduced tension in the heart wall, leading to reduced oxygen requirements for the muscle.

50
Q

What is the main antiplatelet agent that we used for IHD?

A

Low dose Aspirin (75-150mg)

Aspirin is a potent inhibitor of platelet thromboxane production
Thromboxane stimulates platelet aggregation and vasoconstriction

51
Q

In acute MI, what is Aspirin given with?

A

Streptokinase

52
Q

What is the risk with Aspirin?

A

GI bleeding

Low dose aspirin is the most common cause of admission with GI bleed
- Risky with the elderly

Clopidogrel is alternative if patient does not tolerate it well, however it has the same risk of bleeding (but not GI bleeding)

53
Q

How does Clopidogrel work?

A

Inhibits ADP receptor activated platelet aggregation

(anti-platelet basically)

Used to prevent atherosclerotic events in PVD & to treat acute coronary syndromes

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