Ischaemic heart disease Flashcards

1
Q

Define what is meant by ischaemic heart disease

A

Known as coronary heart disease

Atherosclerosis within coronary artery which leads to impaired blood flow/thromboembolic occlusion

Coronary blood flow does not match demand leading to ischaemia (restriction of blood supply to tissues)

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2
Q

Describe the clinical features of stable and unstable angina

A

Stable: atherosclerotic disease, which limits the heart’s ability to respond to increased demand - symptoms on exertion but are relieved by rest.

Unstable: generally due to plaque rupture and the formation of a non-occlusive thromboembolism, or less commonly vasospasm (Prinzmetal angina) - symptoms at rest.

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3
Q

How to diagnose IHD

A

History

GTN

ECG - ST segment depression

In stable angina, pain is indujced by exercised (+ relieved by rest)

Angiography of coronary arteries

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4
Q

What are the lifestyle changes to manage IHD?

A

Smoking cessation

Exercise

Diet

Weight

  • Coronary artery bypass grafting*
  • Angiopasty + stenting*
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5
Q

Describe the mode of action of nitrates in IHD

A

Via release of NO

Venodilatation, leading to decrease in preload + a reduction in cardiac work

Coronary vasodilatation

Prolonged exposure can reduce effectiveness

  • must have nitrate free period (2 doses rather than 3 per day)
  • sustained release preparations: given once daily but do not give 24 hr coverage
  • patches: leave off for hours
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6
Q

Describe the mode of action of beta-blockers in IHD

A

1st choice drugs for prevention

-ve inotropic + chronotropic

reduced cardiac work + prevent symptoms

coronary flow occurs during diastole; slowing heart increases diastolic period + increases time for blood flow

anti-arrhymthmic effects decrease MI risk

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7
Q

Describe the mode of action of calcium channel inhibitors in IHD

A

Rate-limiting: verapamil and diltiazem

DHPs: amlodipine, nifedipine

Vasodilatation and improve coronary blood flow, so preventing symptoms.

Verapamil (and to a lesser extent diltiazem) also have myocardial depressant and bradycardic actions, so reducing cardiac work.

Verapamil also exerts Class IV anti-arrhythmic activity.

Rate-limiting CCBs > DHPs - do not cause reflex tachycardia

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8
Q

What was the outcome of the HOPE trial?

A

Indicated that ramipril reduced mortality in patients with IHD

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9
Q

Name an example of a potassium channel activator

What is its mode of action?

A

Nicorandil

Combined NO donor and activator of ATP-sensitive K-channels.

The target is the ATP-sensitive K+-channel (KATP)

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10
Q

What is the mode of action of Ivabradine?

A

Inhibits If channels (pacemaker Na/K currents in the SAN)

Reduces heart rate

INITIATIVE trial indicated that it was equally effective as atenolol but without beta-blocker side effects

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11
Q

Describe the role of antiplatelet drugs and statins in IHD

Discuss aspirin resistance

Is there any side effects?

A

e.g. low dose aspirin and/or clopidogrel

Ibuprofen can oppose beneficial actions of aspirin

Clopidogrel = ADP receptor antagonist

  • Equally effective
  • Used in pts who can not receive aspirin
  • can be used with aspirin
  • Interacts w/ omeprazole
  • Quarter of pts resistant to aspirin - not related to COX*
  • At an increased risk of CVD*
  • Other anti-platelets do not substitute for aspirin*

Hypercholesterolaemia is a side effect

For symptomatic relief/occasional treatment, a GTN spray/sublingual tablets would be appropriate

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12
Q

State how a patient with stable angina might be managed pharmacologically

Why in refractory disease verapamil cannot be taken with beta-blocker?

A

In refractory disease…

a beta-blocker plus DHP but NOT with verapamil.

Interaction between beta-blockers and verapamil (and to a less extent diltiazem) substantial risk of fatal aystole.

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13
Q

What should be used for unstable angina?

A

Low moleular weight heparin

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