Stable Angina - Diagnosis, Investigations and Management Flashcards

1
Q

Define angina.

A

Angina = pain, but it has been adopted to mean cardiac chest pain (angina pectoris).

It is a discomfort in the chest and/or adjacent areas associated with myocardial ischaemia but without myocardial necrosis.

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2
Q

Why does angina result from myocardial ischaemia?

A

Mismatch of oxygen supply and metabolites to myocardium and myocardial demand for them.

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3
Q

How might blood flow to the myocardium be restricted?

A

Obstructive coronary atheroma (v. common)
Coronary artery spasm (uncommon)
Coronary inflammation/arteritis (v. rare)

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4
Q

What might cause mismatch of delivery of oxygen and nutrients to the myocardium and the demand for them?

A

Reduced blood flow to the myocardium (most commonly)
Uncommonly due to reduced oxygen transport, e.g. anaemia
Uncommonly due to pathologically increased myocardial oxygen demand.

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5
Q

Give pathological situations where there would be an increased oxygen demand in the myocardial tissue?

A

Left ventricular hypertrophy (LVH) - seen in persistent hypertension, significant aortic stenosis and hypertrophic cardiomyopathy.
Thyrotoxicosis

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6
Q

What is the most common cause of angina?

A

Coronary atheroma.

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7
Q

Why does the patient only feel symptoms during excretion with stable angina?

A

On activity the increased myocardial oxygen demand obstructed by coronary blood flow leads to myocardial ischaemia and symptoms of angina, which result with rest as oxygen demand returns to normal.

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8
Q

In which situations does myocardial oxygen demand increase?

A

Any situation where HR and BP increase, e.g. exercise, anxiety/emotional stress and even after a large meal, cold weather.

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9
Q

How will patients typically show where the pain is? And how do they describe the pain?

A

Use hand to clutch over retrosternal area.

A tight band, or like a weight pushing on their chest. ON exertion.

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10
Q

How much occlusion of the coronary arteries is necessary to experience angina?

A

> 70% lumen occlusion by obstructive plaque.

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11
Q

How does the appearance of the coronary arteries differ in stable angina in comparison with acute coronary syndromes?

A

In stable angina, a fatty streak has developed into an atherosclerotic plaque. In ACSs there is spontaneous place rupture than leads to thrombosis formation leading to different degrees of occlusion.

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12
Q

What important things should you establish about the angina to make sure it is not a different cause of chest pain? i.e. what are the features making stable angina likely?

A

Site of pain - retrosternal
Character of pain - often tight band, pressure, heaviness
Radiation sites - neck and onto jaw and down arms
Aggregating factors - exerction, stress and relieving factors - improve with GTN rapidly or physical rest.

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13
Q

What features would make the diagnosis of stable angina less likely?

A

Sharp/stabbing pain, pleuritic or pericardial
Associated with body movements or positions
Very localised, pinpoint site
Superficial w/ or w/o tenderness.
No pattern to pain, particularly if occurring at rest
Begins some time after exercise
Lasts for hours

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14
Q

What are other possible differentials for chest pain?

A

Cardiovascular causes - aortic dissection (tearing, causes unremitting pain at rest), pericarditis (better when lying back , sharp stabbing pain)

Respiratory causes - pneumonia, pleurisy, peripheral pulmonary emboli (pleuritic)

Musculoskeletal causes - cervical disease, costochrondritis, muscle spasm or strain

GI causes - gastro-oesphageal reflux, oesophageal spasm, peptic ulceration, biliary colic, cholecystitis, pancreatitis

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15
Q

Very occasionally myocardial ischaemia present with no chest pain, what other symptoms might a patient present with that could point towards myocardial ischaemia? What kind of patients are most likely to present like this?

A

SoB on exertion
Excessive fatigue on exertion
Near syncope on exertion

Elderly or patients with diabetes mellitus probably due to reduced pain sensation.

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16
Q

How is the severity of stable angina assessed?

A

Canadian classification of angina severity.

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17
Q

What are the four stages of severity of stable angina?

A

I - ordinary physical activity does not cause angina, symptoms only on significant exertion.

II - slight limitation of ordinary activity, symptoms on walking 2 blocks or up more than one flight of stairs.

III - marked limitation, symptoms on walking only 1-2 blocks or 1 flight of stairs.

III - symptoms on any activity, getting washed/dressed etc.

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18
Q

What are some non-modifiable risk factors for coronary artery disease?

A

Age, gender (make more susceptible), creed, family history and genetic factors.

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19
Q

What are some modifiable risk factors for coronary artery disease?

A

Smoking, diet and exercise, diabetes mellitus (glycaemic control reduces CV risk), hypertension (BP control reduces risk), hyperlipidaemia (lowering reduces risk).

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20
Q

What are some things you might notice on examination of a stable angina patient?

A

Tar stains on fingers (smoking), obesity (centripetal), xanthalasma and corneal arcus (hypercholesterolaemia), hypertension, abdominal aortic aneurysm arterial bruits, absent or reduced peripheral pulses. Diabetic retinopathy, hypertensive retinopathy on fundoscopy.

21
Q

In patients with suspected stable angina, what signs might you notice of exacerbating or associated conditions?

A

Pallor of anaemia
Tachycardia, tremor, hyper-reflexia of hyperthyroidism
Ejection systolic murmur, plateau pulse of aortic stenosis
Pansystolic murmur of mitral regurgitation
Signs of heart failure such as basal crackles, elevated JVP, peripheral oedema.

22
Q

What investigations would you want to carry out if you suspect stable angina?

A

Bloods (full blood count, lipid profile, fasting glucose, electrolytes, liver and thyroid tests.

CXR to rule out other causes.

ECG

Exercise tolerance test

23
Q

What would be seen in the ECG of SA patients?

A

Normal in over 50% cases.
May be evidence of prior MI, e.g. pathological Q waves.
May be evidence of LVH, e.g. high voltages, lateral ST segment depression or strain pattern.

24
Q

What is the exercise tolerance test and why is it used?

A

Often confirms diagnosis of SA
Allows us to see what ECG looks like at point where patient is getting symptoms.

Exercise patient and measure ECG..

25
Q

What are the pros and cons of the ETT?

A

Advs - good to use when nothing shows up on the ECG at rest.

Disadvs - relies on patients ability to exercise and puts patients through discomfort of their symptoms.

26
Q

What can be concluded from a negative ETT?

A

-ve ETT doesn’t exclude significant coronary atheroma but if netgative at high work load overall prognosis is good.

27
Q

What would a positive ETT show?

A

ST segment depression AND typically symptoms.

28
Q

What imaging techniques can be used for investigation?

A

Myocardial perfusion imagng

CT coronary angiography

29
Q

In what ways is the myocardial perfusion imaging better than the ETT?

A

Superior in detection of CAD, localisation of ischaemia and assessing size of area affected.

30
Q

In what ways is the myocardial perfusion imaging disadvantageous compared with the ETT?

A

Expensive and involves radioactivity.

31
Q

What is the MPI?

A

Either exercise or pharmacological stress, radionuclide tracer injected (iv) at peak stress and images obtained, compared with at rest. Normal myocardium takes up tracer.

32
Q

How does the uptake of the tracer in MPI help us move towards a diagnosis?

A

Tracer seen at rest but not after stress = ischaemia.

Tracer not seen at rest or after stress = infarction.

33
Q

What drugs can be used to induce pharmacological stress for MPIs and how do they work?

A

Adenosine increases HR and BP (same as exercise)
Dipyridamole and dobutamine cause vasodilation but the obstructed ones will not dilate as much so less flow will be seen here (steal).

34
Q

What will a CT coronary angiogram allow?

A

To see if you have coronary disease, or might suggest coronary obstructive artery disease. Can visualise where problem is and rule out other diseases.

35
Q

In what situations would you do an invasive angiography?

A

Early or strong positive ETT (suggest multi-vessel ds)
Angina refractory to medical therapy
Diagnosis not clear after non-invasive tests
Young cardiac patients due to work/life effects
Occupation or lifestyle with risk, e.g. drivers

36
Q

What would a coronary angiography allow us to determine?

A

Where disease is, distribution, nature od atheromatous disease to allow best treatment.

Can determine whether medication alone or percutaneous coronary intervention (PCI) - e.g angioplasty and stenting or CABG surgery needed.

37
Q

How is a cardiac catheterisation/coronary angiography done?

A

Almost always done under local anaesthetic.
Arterial cannula inserted into femoral or radial artery.
Coronary catheters passed to aortic root and introduced into the osmium of coronary arteries.
Radio-opaque contrast injected down coronary arteries an visualised on Xray.

38
Q

Describe the picture produced from the coronary angiography.

A

2D lumenogram as iodinated contrast or dye is passed through arteries.
Looks different in areas disease and can see where reduced blood flow is.

39
Q

Why is it important to view the angiogram in different planes?

A

Atheroma are often eccentric in nature.

40
Q

What are some general measures that should be taken on diagnosis of SA?

A

Address risk factors, BP, DM, cholesterol, lifestyle.

41
Q

What is the aim of medical/drug treatment?

A

Reduce disease progression and symptoms.

42
Q

What can be done to treat SA in terms of revascularisation if symptoms aren’t controlled?

A

Percuntaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG).

43
Q

What drugs can be used to reduce disease progression?

A

Statins (if total cholesterol >3.5mmol/l) - reduce LDL-cholesterol deposition in atheroma and stabilise atheroma plaque rupture and ACS.

ACE inhibitors - if increased CV risk and atheroma (stabilise endothelium and reduce plaque rupture).

Aspirin - 75mg or clopidogrel if intolerant - may not directly affected plaque but does protect endothelium and reduces platelet activation/aggregation.

44
Q

What drugs can be used for relief of symptoms?

A

beta-blockers - achieve HR <60bmp.
Reduced myocardial work and have anti-arrhythmic effect.

Ca2+ channel blockers - achieve HR <60bmp. Central acting e.g. diltiazem/verapamil if beta-blockers C-I.

Ik channel blockers - achieve HR <60bmp - Ivabridine is a new medication which reduces sinus node rate.

45
Q

All angina patients should recieve what two drugs?

A

Aspirin

Statin

46
Q

What drug is used to abort angina attacks?

A

Sublingual GTN

47
Q

What drugs do NICE recommend in angina (based on comorbs, contraindications and patient preference?

A

Beta blocker or CCB

If CCB used as monotherapy - use rate limiting one (verapamil/diltiazem)
If in combo with BBlocker - use long-acting dihydropyridine CCB, e.g. MR nifedipine

If poor response - inc. to max dose/add in other drug

If both don’t work at max tolerated doses, consider adding one of: long-acting nitrate, ivabradine, nicrorandil or ranolazine + refer for PCI/CABG

48
Q

What is a major issue with nitrates?

A

Nitrate tolerance

49
Q

What do the BNF recommend for those who develop nitrate tolerance?

A

Take 2nd dose of isosorbide mononitrate after 8h as opposed to 12