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Cardiovascular > Pharmacological Treatment of Angina > Flashcards

Pharmacological Treatment of Angina Flashcards

1
Q

What is angina pectoris?

A
  • Chest pain due to inadequate supply of oxygen to the heart.
    • Typically severe and crushing.
    • Feeling of pressure and suffocation behind the breastbone.
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2
Q

Describe the characteristics of pain distribution in angina.

A
  • Chest
  • Arm
  • Neck
  • Jaw
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3
Q

What brings on angina?

A
  • Exertion
  • Cold
  • Excitement
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4
Q

What is thought to cause the pain associated with angina?

A
  • It is thought that chemical factors that cause pain in skeletal muscle (i.e K+, H+​ and adenosine) are responsible.
  • Angina can accompany or be a precursor to MI.
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5
Q

List the treatments used to reduce chest pain symptoms associated with angina.

A
  • Beta-blockers
  • Nitrates
  • Calcium channel antagonists
  • Nicorandil
  • Ivabradine
  • Ranolazine
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6
Q

List the treatments used to prolong survival in patients with angina.

A
  • Beta-blockers
  • Aspirin
  • Statins
  • Angiotensin converting enzyme inhibitors
  • Angiotensin II receptor blockers
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7
Q

Describe the coronary blood flow through the left vetricle.

A
  • Left and right coronary arteries feed the blood supply to the heart.
  • Most tissues are perfused when the heart contracts.
  • Anything that changes the duration of diastole (window for coronary flow) changes the opportunity for perfusion and causes a change in diastolic pressure.
    • If the window is short enough, the base diastolic level rises as the level of blood in the ventricle rises.
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8
Q

What factors shrink the window for perfusion?

A
  • Shortening diastole
    • Eg. increased heart rate.
  • Increased ventricular end diastolic pressure
    • Eg. a progressive decline in ventricular emptying; aortic valve stenosis.
  • Reduced diastolic arterial pressure
    • Eg. mitral or aortic vlve incompetence; heart failure.
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9
Q

Describe the issues with coronary blood flow.

A
  • Myocardium cannot function anaerobically
    • Anaerobic glycolysis increases in lactic acid production.
  • Arterioles close mechanically during systole.
  • Decreased diastolic filling period during exercise.
  • Increased oxygen demand and increased metabolic demand during exercise.
  • Work output of the heart increases by 6-9x during strenuous exercise
    • ​Uses 70-80% of coronary blood flow oxygen at rest
      • Increased demand must be met by increased flow
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10
Q

Describe the autoregulation of arteriolar radius.

A
  • It matches the demand to blood flow by altering flow at arteriolar level.
  • Metabolic control:
    • ​Muscle cell produces byproducts (eg. adenosine) which trigger vascular smooth muscle cells to relax (potentially via an intermediate produced by endothelial cells).
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11
Q

Describe what causes coronary ischaemia.

A
  • Coronary ischaemia is usually the result of atherosclerosis.
  • This causes angina.
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12
Q

Describe what causes sudden ischaemia.

A
  • Sudden ischaemia is usually caused by thrombosis.
  • This may result in cardiac infarction.
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13
Q

What is variant angina?

A
  • Angina caused by coronary spasms.
    • This is the smooth muscle of the heart spontaneously contracting and relaxing.
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14
Q

What is the cellular effect of ischaemia?

A
  • Cellular calcium overload results from ischaemia.
    • This may cause cell death and dysrhythmias.
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15
Q

Describe the progression of atherosclerosis.

A
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16
Q

What are the classes of angina?

A
  1. Chronic stable angina
    • Fixed stenosis
      • Demand ischaemia
  2. Unstable angina
    • Thrombus
      • Supply ischaemia
  3. Printzmetal’s variant angina
    • Vasospasm
      • Supply ischaemia
17
Q

Describe stable angina.

A
  • Predictable chest pain on exertion.
  • Caused by a fixed narrowing of the coronary arteries.
  • Treated by decreased workload of the heart and therefore decreased oxygen requirement.
  • Also use drugs to prolong survival (eg. aspirin, statins, ACE inhibitors).
18
Q

Describe unstable angina.

A
  • Occurs at rest and with less exertion than stable angina.
  • Associated with a thrombus around a ruptured atheromatous plaque but without complete occlusion of the vessel (similar to MI).
19
Q

Describe variant (Prinzmetal) angina.

A
  • Uncommon
  • Caused by coronary artery spasm
  • Not completely understood, but sometimes associated with atherosclerosis.
20
Q

Describe the main mechanism of action of antianginal drugs.

A

Mainly work by reducing the metabolic demand of the heart.

21
Q

Which antianginal drugs are vasodilators?

Describe their mechanism of action.

A
  • Organic nitrates
  • Nicorandil
  • Calcium antagonists
  • These are vasodilators!
  • They work by reducing preload or afterload of the heart.
22
Q

Which antianginal drugs slow the heart?

Describe their mechanism of action.

A
  • β-blockers
  • Ivabradine
  • These slow down the heart.
  • They work by decreasing the metabolic demand of the muscle.
23
Q

Define preload.

A

Venous pressure and venous return to the heart (end diastolic pressure / volume) (EDP/EDV).

24
Q

Define afterload.

A

Aortic / pulmonary artery pressure.

25
Q

Describe the action of β-blockers in the treatment of angina.

Give examples.

A
  • Important (first line) treatment in the prophylaxis and treatment of stable and unstable angina.
  • Decreases cardiac oxygen consumption by slowing the heart.
  • Also have an antidysrhythmic action.
    • Reduces death after MI.
  • Bisoprolol
  • Atenolol
26
Q

Describe the action of calcium antagonists in the treatment of angina.

Give examples.

A
  • Preventing opening of voltage-gated L-type Ca2+ channels
    • Therefore block the entry of Ca2+ entry.
    • Mainly affect the heart and smooth muscle to inhibit calcium entry upon muscle cell depolarisation.
  • Two main types:
    • Dihydropyridine derivatives
      • Amlodipine
      • Lercanidipine
    • Rate-limiting
      • Verapamil
      • Diltiazem
  • Vasodilator effect mainly on resistance vessels
    • Therefore reduces afterload
    • Also dilates coronary vessels (important in variant angina)
  • Verapamil and diltiazem can reduce and impair AV conduction and myocardial contractility.
27
Q

Describe the depolarisation of the SA node.

A
  • Phase 1
    • ​Gradual drift upwards in resting membrane potential due to increased gNa+ as ‘funny’ F-type Na+ channels open and decreased gK+ as K+ channels slowly close.
    • Transient (T) Ca2+ channels help with the final push.
  • Phase 2
    • ​Moderately rapid depolarisation due to Ca2+ entry via slow (L) channels.
  • Phase 3
    • ​Rapid repolarisation as elevated internal Ca2+ stimulates opening of K+ channels and an increase in gK+.
28
Q

What are the clinical uses of calcium antagonists in angina?

A
  • Choice depends on comorbidity and drug interactions.
    • Amlodipine or lercanidipine safe in patients with heart failure; used instead of a β-blocker in Prinzmetal angina or alongside β-blockers in most angina.
    • Diltiazem or verapamil used but contraindicated in heart failure, bradycardia, AV block or in presence of β-blocker.
  • Side effects include:
    • Headache
    • Constipation
    • Ankle oedema
29
Q

What are the other clinical uses of calcium antagonists?

A
  • Antidysrhythmics
    • Mainly verapamil
      • Slows ventricular rate in rapid atrial fibrillation.
      • Prevents recurrence of supraventricular tachycardia (SVT).
      • No effect on ventricular arrhythmias.
  • Hypertension
    • Mainly amlodipine or lercanidipine.
30
Q

Describe the action of organic nitrates in the treatment of angina.

A
  • Glyceryl trinitrate and isosorbide mononitrate
    • ​Powerful vasodilators
    • Work by being metabolised to nitric oxide (NO) and relax smooth muscle (particularly vascular smooth muscle).
    • Act on veins to decrease cardiac preload.
      • Higher concentrations can affect arteries, therefore decrease afterload.
    • Decreased cardiac workload is helped by dilation of collateral coronary vessels.
      • This therefore improves distribution of coronary blood flow towards ischaemic areas.
      • Dilation of constricted coronary vessels is particularly beneficial in variant angina.
31
Q

Describe the role of the endothelial cells in regulating vascular tone.

A
32
Q

What are the clinical uses of organic nitrates in angina?

A
  • Stable angina:
    • Prevention by sublingual glyceryl trinitrate shortly before exertion or isosorbide mononitrate long before.
  • Unstable angina:
    • Intravenous glycerly trinitrate (GTN)
  • Unwanted effects are common; headache and postural hypotension may occur.
33
Q

What are the other clinical uses of organic nitrates?

A
  • Acute heart failure (in specific circumstances)
    • Intravenous GTN
  • Chronic heart failure (CHF)
    • Isosorbide mononitrate with hydralazine in patients of African American origin especially, (or patient cannot tolerate more commonly used CHF drugs).
34
Q

Describe the action of potassium channel activators in the treatment of angina.

Give an example.

A
  • Nicorandil
    • ​Combines activation of potassium K+ATP channels with nitrovasodilator actions (has a NO donation effect).
      • Causes hyperpolarisation of vascular smooth muscle.
    • Both an arterial and venous dilator.
    • Causes headaches, flushing and dizziness.
    • Used for patients who remain symptomatic despite optimal management with other drugs.
35
Q

Give examples of other anti-anginals and state their mechanism of action.

A
  • Ivabradine
    • ​Inhibits F-type channels in the heart.
    • Reduces cardiac pacemaker activity.
      • Therefore inhibits heart rate.
  • Ranolazine
    • ​Unique anti-anginal used as a last resort.
36
Q

What is the first-line therapy in pharmacological management of angina?

A
  • β-blockers should be used as first-line therapy for the relief of symptoms of stable angina.
  • Patients who are intolerant of β-blockers should be treated with either rate limiting calcium channel blockers, long-acting nitrates or nicorandil.
37
Q

Describe drug interventions to prevent new vascular events.

A
  • All patients with stable angina due to atherosclerotic disease should receive long-term standard aspirin and statin therapy.
  • All patients with stable angina should be considered for treatment with angiotensin-converting enzyme inhibitors.
38
Q

Describe combination therapy in pharmacological management of angina.

A
  • When adequate control of anginal symptoms is not achieved with β-blockade, a calcium channel blocker should be added.
  • Rate-limiting calcium channel blockers should be used with caution when combined with β-blockers.
  • Patients whose symptoms are not controlled on maximum therapeutic doses of 2 drugs should be considered for referral to a cardiologist.

Cardiovascular (12 decks)

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