Stable Ischaemic Heart Disease and Angina Therapy Flashcards by Chloe Mackle

What are the risk factors for stable IHD and angina?

Hypertension
Smoking 
Hyperlipidaemia
Hyperglycaemia
Male
Post-menopausal

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What is hyperlipidaemia a disease of?

Muscular arteries - cerebral or coronary, not veins

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From what age do fatty streaks appear?

Around 20

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How does hyperlipidaemia affect the arteries?

Lesions start as fatty streaks
There is subendothelial accumulation of large foam cells derived from the macrophages and smooth muscles cells filled with lipids

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How do fibrous plaques affect the arteries?

Develop from fatty streaks and project into the arterial lumen, reducing blood flow

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Where do most of the changes to the artery in IHD occur?

In the intimal layer

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What changes occur in the intimal layer in IHD?

Accumulation of monocytes, lymphocytes, foam cells and connective tissue

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What are the usual features of foam cells?

Most are of smooth muscle origin

Necrotic core and fibrous cap

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What does stable ischaemic heart disease result from?

Mismatch between myocardial blood and oxygen supply and demand

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What are episodes of angina precipitated by?

Any activity which causes cardiovascular stress

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How can drugs help to correct the imbalance in stable IHD?

Decrease myocardial oxygen demand by reducing cardiac workload
Increase supply of oxygen to ischaemic myocardium

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What are the purposes of drug treatment of stable IHD?

Relieve symptoms
Halt disease process
Regress disease process
Prevent MI 
Prevent death

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What drugs can be used in the treatment of stable IHD?

Beta blockers 
Ivabradine 
CCBs - rate limiting and vasodilation 
Nitrates
Potassium channel openers
Aspirin 
Clopidogrel
Tigagrelor
Cholesterol lowering agents e.g. HMG CoA reductase inhibitors

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Give an example of a beta blocker used in the treatment of stable IHD

Atenolol

Bisoprolol

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How do beta blockers work to treat stable IHD?

Reversible antagonists of beta-1 and beta-2 receptors (newer drugs are cardioselective and act primarily on beta-1 receptors)
Block the physiological responses to adrenaline and noradrenaline and so decrease 3 major determinants of myocardial oxygen demand - HR, contractility and systolic wall tension
Also allow improved perfusion of subendocardium by increasing diastolic perfusion time

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What effect do beta blockers have on HR, force of myocardial contraction, CO, velocity of contraction and BP?

Decrease all of these

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What do beta blockers protect the caardiomyocytes from?

Oxygen free radicals formed during ischaemic episodes

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By reducing HR, force of contraction and BP, beta blockers increase what?

Exercise threshold at which angina occurs and so move the balance point at which demand for oxygen outweighs the supply of oxygenated blood

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What is rebound phenomena?

When sudden cessation of beta-blocker therapy may precipitate MI, those at risk include patients with angina and males over 50 years old who are receiving beta blockers for other reasons

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What are the contraindications to beta blocker use?

Asthma
Peripheral vascular disease (relative contraindication) 
Reynaud's 
Heart failure 
Bradycardia
Heart block

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What are the potential adverse drug reactions from beta blocker use?

Tiredness/fatigue 
Lethargy 
Impotence
Bradycardia 
Bronchospasm

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What are the possible drug-drug interactions with beta blockers?

Hypotension when used with other hypotensive agents
Bradycardia when used with other rate limiting drugs
Cardiac failure when used with negatively inotropic agents
NSAIDs antagonise antihypertensive actions
Exaggeration and masking of hypoglycaemic actions of insulin or oral hypoglycaemics

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Give an example of a calcium channel blocker used in treatment of stable IHD

Diltiazem
Verapamil
Amlodipine

How do CCBs work?

Prevent calcium influx into the myocytes and smooth muscle lining the arteries and arterioles by blocking L type calcium channels

How do rate-limiting CCBs treat stable IHD?

Reduce HR and force of contraction which reduces myocardial oxygen requirements

How do vasodilation CCBs treat stable IHD?

Reduce vascular tone and so produce vasodilatation and reduce afterload, reducing myocardial workload

What are the contraindications for CCBs use?

Evidence that use of rapid acting vasodilatory CCB may precipitate acute MI or stroke Post-MI patients Unstable angina

What are the possible adverse drug reactions from CCB use?

Ankle oedema Headache Flushing Palpitations

What percentage of patients on CCBs will experience ankle oedema?

15-20%

Give an example of a nitrovasodilator used in treatment of stable IHD

Glyceryl trinitrate Isosorbide mononitrate Isosorbide dinitrate

What routes can GTN be given via?

Sublingual Buccal Transdermal

What routes can isosorbide mono and dinitrate be given via?

Sustained release formula | Oral tablets

How do nitrovasodilators work?

Relax almost all smooth muscle by releasing NO which then stimulates the release of cGMP which produces smooth muscle relaxation

How do nitrovasodilators treat IHD?

Reduce preload and afterload so reduce myocardial oxygen consumption

How do nitrates relieve angina?

Arteriolar dilatation - reducing cardiac afterload and myocardial work and oxygen demand Peripheral venodilatation - reducing venous return, cardiac preload and myocardial workload Relieve coronary vasospasm Redistribute myocardial blood flow to ischaemic areas of the myocardium

What are the benefits of GTN use?

Rapid treatment of angina pain Avoid first pass metabolism - given via sublingual route May be used frequently and prophylactically

How are oral nitrates used?

As once-a-day sustained release formulation | Used for prophylaxis

How are IV nitrates used?

Mainstay of treatment of unstable angina, used in combination with heparin

What is the problem associated with nitrate therapy? How can this be overcome?

Tolerance to effects of nitrate therapy can develop rapidly Can be overcome by giving an asymmetric dose of nitrate at 8am and 2pm and by using a sustained release preparation which incorporates a nitrate-free period

What are the potential adverse drug reactions from nitrate use?

Headache | Hypotension

Give an example of a potassium channel opener used in stable IHD treatment

Nicorandil

How do potassium channel openers work?

Activate silent potassium channels, allows entry of potassium into the cardiac myocyctes which inhibits the calcium influx so has a negative inotropic action

Why are potassium channel openers third line therapy?

Due to risk of bowel ulceration

How does Ivabradine work?

Selective sinus node If channel inhibitor Slows the diastolic depolarisation slope of the sinoatrial node Results in reduction in HR which reduces myocardial oxygen demand

What is the standard dose of aspirin used for treatment of stable IHD?

Low dose 75-100mg

How does aspirin treat stable IHD?

Formation of platelet aggregates are important in the pathogenesis of angina, unstable angina and acute MI Thromboxane stimulates platelet aggregation and vasoconstriction Aspirin is a potent inhibitor of platelet thromboxane production

When is aspirin useful as a treatment of IHD?

For the symptomatic treatment of chronic stable angina in adults with normal sinus rhythm and heart rate of 70bpm or greater Only effective to reduce incidence of coronary artery disease outcomes in patients with heart rate of 70bpm or greater

What are the indications for aspirin use?

Adults unable to tolerate or who have contraindications to beta blockers Use in combination with beta blockers in patients with inadequately controlled stable angina at an optimal beta blocker dose

What is the effect of aspirin on mortality of acute MI in stable angina patients?

Regular daily use of aspirin can reduce mortality of acute MI by 23% In combination with streptokinase it can reduce mortality by 42% and re-infarction by 52%

What is the effect of aspirin on mortality of acute MI in unstable angina patients?

Can reduce MI and death by 50% | In secondary prevention is can reduce re-infarction by 32% and combined vascular events by 25%

Low dose aspirin is the most common cause of what hospital admission?

Admission due to GI bleed

How does clopidogrel work?

Inhibits ADP receptor activated platelet aggregation | Prevention of atherosclerotic events in PVD

Give an example of a cholesterol lowering agent used in treatment of IHD

Simvastatin Pravastatin Atorvastatin

What cholesterol lowering agents are the most effective?

HMG CoA reductase inhibitors e.g. simvastatin

What effect does cholesterol lowering have on cardiovascular mortality and total mortality in post-MI patients?

Can reduce cardiovascular mortality by 42% and total mortality by 30%

What is the typical progression of a treatment regime of stable IHD?

``` Beta blocker Aspirin Statin CCB Nitrate Nicorandil Refer for cardiology work up for possible stenting ```