SIHD and Angina - Presentation and Investigation Flashcards

1
Q

Describe the pathophysiology of stable angina

A

Mismatch between supply of O2 and metabolites to myocardium and the myocardial demand for them.

By far most commonly due to: a reduction in coronary artery blood flow to the myocardium, caused by:
- Obstructive coronary atheroma (Very common)
- Spasm of a portion of coronary artery (Uncommon)
- Abnormal coronary flow (Uncommon).

Uncommonly due to reduced O2 transport:
Anaemia of any cause.
Uncommonly due to pathologically increased myocardial O2 demand:
- Left ventricular hypertrophy caused by years of persistent hypertension, significant aortic stenosis or hypertrophic cardiomyopathy.
- Thyrotoxicosis.
Most common cause of angina is coronary atheroma.
When there is increased myocardial oxygen demand the increase of coronary blood flow is obstructed and this leads to myocardial ischaemia and then angina symptoms.
Myocardial oxygen demand increases in situations where HR and BP rise for example: exercise, anxiety/emotional stress and after a large meal.

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2
Q

What is the epidemiology of stable angina?

A
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3
Q

What are the risk factors of stable angina?

A

NON-MODIFIABLE
- Age, gender, creed, family history & genetic factors.

MODIFIABLE
- Smoking
- Lifestyle- exercise & diet
- Diabetes mellitus (glycaemic control reduces CV risk)
- Hypertension (BP control reduces CV risk)
Hyperlipidaemia (lowering reduces CV risk)

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4
Q

What are the clinical presentation of stable angina?

A
  • Chest pain on left side
  • Radiating pain down left shoulder and arm
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5
Q

Discuss relevant investigations of stable angina (list 7)

A

BLOODS
Full blood count, lipid profile and fasting glucose; Electrolytes, liver & thyroid tests would be routine.

CXR
Often helps show other causes of chest pain and can help show pulmonary oedema.

ELECTROCARDIOGRAM
- Normal in over 50% of cases.
- May be evidence of prior myocardial infarction i.e. pathological Q-waves.
- May be evidence of left ventricular hypertrophy i.e. high voltages, lateral ST-segment depression or “strain pattern”.

EXERCISE TOLERANCE TEST/ETT
- Often can confirm diagnosis of angina.
- Relies on ability to walk for long enough to produced sufficient CV stress.
- Typical symptoms and ST-segment depression for positive test.
- -ve ETT doesn’t exclude significant coronary atheroma but if negative at high workload overall prognosis is good

MYOCARDIAL PERFUSION IMAGING
- Superior to ETT in detection of CAD, localisation of ischaemia and assessing size of area affected.
- Expensive, involves radioactivity; depending on availability used where ETT not possible/equivocal.
- Either exercise or pharmacological stress: adenosine, dipyridamole or dobutamine.

CT (coronary angiography)

INVASIVE ANGIOGRAPHY IF:
- Early or strongly positive ETT (suggests 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 etc.

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6
Q

Explain the importance of diagnosis and treatment of stable angina

A

GENERAL MEASURES
- Address ASCVD risk factors: BP, DM, Cholesterol, Lifestyle: physical activity & smoking.

MEDICAL TREATMENT
- Drugs to reduce disease progression & symptoms

REVASCULARISATION (if symptoms not controlled).
- Percutaneous coronary intervention (PCI) & coronary artery bypass grafting (CABG)

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7
Q

Define angina

A

“ a discomfort in the chest and/or adjacent areas associated with myocardial ischaemia but without myocardial necrosis”

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8
Q

Making the diagnosis of angina: history

A

Essential to establish the characteristics of patients pain to differentiate from other causes of chest pain:
- Site of pain (watch for patient gestures): retrosternal
- Character of pain: often tight band/pressure/heaviness.
- Radiation sites: neck and/or into jaw, down arms.
- Aggravating e.g. with exertion, emotional stress & relieving factors e.g. rapid improvement with GTN or physical rest.

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9
Q

Making the diagnosis: examination

A
  • Tar stains on fingers.
  • Obesity (centripedal).
  • Xanthalasma and corneal arcus (hypercholesterolaemia).
  • Hypertension.
  • Abdominal aortic aneurysm arterial bruits, absent or reduced peripheral pulses.
  • Diabetic retinopathy, hypertensive retinopathy on fundoscopy.
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10
Q

Medical treatment of stable angina FOR INFLUENCING DISEASE PROGRESSION

A

STATINS: consider if total cholesterol >3.5 mmol/l.
- Reduce LDL-cholesterol deposition in atheroma and also stabilise atheroma reducing plaque rupture and ACS.

ACE INHIBITORS: if increased CV risk and atheroma
- Stabilise endothelium and also reduce plaque rupture.

ASPIRIN: 75mg or Clopidogrel if intolerant of aspirin.
- May not directly affect plaque but does protect endothelium and reduces of platelet activation/aggregation.

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11
Q

Medical treatment of stable angina FOR RELIEF OF SYMPTOMS

A

ß-BLOCKERS; achieve resting hr <60 bpm.
- Reduced myocardial work and have anti-arrhythmic effects

Ca2+ CHANNEL BLOCKERS; achieve resting hr <60 bpm.
- Central acting eg diltiazem/verapamil if ß-blockers C-I.
- Peripherally acting dihydropyridines e.g. amlodipine, felodipine

Ik CHANNEL BLOCKERS; achieve resting hr <60 bpm.
- Ivabridine is a newer medication which reduces sinus node rate

NITRATES; produce vasodilatation
- Used as short or prolonged acting tablets, patches or as rapidly acting sublingual GTN spray for immediate use.

K+ CHANNEL BLOCKERS; nicorandil
- Nitrate molecule and K+ channel helpful in ‘pre-conditioning’.

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