Coronary heart disease Flashcards

1
Q

What is angina?

A

Angina is caused by coronary artery disease
=> atherosclerotic plaque in the coronary artery cause progressive narrowing of lumen
=> symptoms occur with reduced blood flow and increased oxygen demands
=> less commonly, angina is caused by valvular disease e.g. aortic stenosis

a) Stable angina = occurs with physical exertion or emotional stress. Lasts no more than 10 mins and relieved with rest ± GTN spray
b) Unstable angina = new onset angina or deterioration in previous stable angina. Symptoms occurring at rest

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2
Q

What are the risk factors of angina?

Non-modifiable and modifiable

Co-morbidity that increase risk of CVD

A

Non-modifiable:

  1. Age (mainly >50 years)
  2. Gender (men>women)
  3. Family hx of CVD
  4. Ethnic background e.g. south asian and african at an increased risk

Modifiable:

  1. Smoking
  2. Low blood levels of HDL cholesterol
  3. High levels of non HDL cholesterol
  4. Sedentary lifestyle / lack of physical activity
  5. Unhealthy diet
  6. Alcohol above recommended limits
  7. Overweight / obesity

Comorbidities:

  1. Hypertension
  2. Diabetes
  3. CKD
  4. Dyslipidaemia (drugs i.e. antipsychotics, immunosuppressants and steroids can cause dyslipidaemia)
  5. AF
  6. Anxiety
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3
Q

What are the complications of angina caused by coronary artery disease?

A
  1. MI
  2. Unstable angina
  3. Sudden cardiac death
  4. Stroke
  5. Anxiety & depression
  6. Reduced quality of life
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4
Q

Assessment of stable chest pain:

How do you classify typical and atypical angina?

What factors make angina more likely than others?

A
  1. Typical angina presents with all 3 features:
    => pain precipitated by physical exertion
    => constricting chest pain, in the neck, shoulders, jaws or arms
    => relieved by rest or GTN within about 5 mins
  2. Atypical angina presents with two of the above features and
    => GI discomfort ± breathlessness ± nausea
  3. Factors that make a diagnosis of angina likely:
    => Increasing age
    => Male sex
    => Presence of CVD
    => Hx of established coronary artery disease i.e. previous MI

Factors that make a diagnosis of angina unlikely:
=> Continuous or prolonged pain
=> Pain unrelated to activity
=> Pain on breathing
=> Pain assoc. with dizziness, palpitations, tingling and difficulty swallowing

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5
Q

How is stable angina investigated and diagnosed?

A

Clinical diagnosis

  1. ECG to exclude coronary syndrome, pathological Q waves, LVH, left bundle branch block
  2. Lab tests:
    => fasting blood glucose & HbA1c, fasting lipid profiles, U&E for CVD risk profile
    => FBC to check for anaemia - can exacerbate stable angina
    => Thyroid function test
  3. CXR - for atypical presentation, pulmonary disease, HF

If stable angina can’t be excluded by clinical assessment alone e.g. symptoms consistent with typical or atypical angina or ECG changes

1st line: CT coronary angiography

2nd line: non-invasive functional imaging (looking for reversible myocardial ischaemia)

3rd line: invasive coronary angiography

*can organise a 12-lead ECG if angina cannot be excluded clinically - an abnormal ECG makes CHD more likely but doesn’t confirm stable angina

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6
Q

Whilst awaiting diagnostic testing results, how do you manage a person with suspected stable angina?

A

GTN spray for symptoms relief whilst waiting specialist referral

Instruct patient that if they experience chest pain:
=> stop what they are doing and rest
=> use their GTN spray
=> take a second dose after 5 mins if pain has not eased
=> call 999 if the pain has not eased 5 mins after second dose or earlier if the pain is intensifying / person unwell

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7
Q

How do you manage a person with new diagnosis of angina?

A

Explain the diagnosis of stable angina to the person.
=> The explanation should include: factors which provoke angina i.e. exertion, emotional stress, exposure to cold, or eating a large meal.

The long-term progression and prognosis of angina.

Information on how angina is managed.

Encourage the person to ask questions about their angina and its management.

Explore and address any misconceptions the person might have about their angina. This includes:
Implications for daily activities.
Risk of myocardial infarction.
Life expectancy.

Advise the person to seek medical help if there is a sudden worsening in the frequency or severity of their angina.

Discuss the reasons for treatment, as well as the benefits and adverse effects (such as flushing, headache, and light-headedness).

Provide information on how to use a short-acting sublingual nitrate and when to administer it.

Assess the person’s need for lifestyle advice to manage their cardiovascular risk.

Explore and address issues according to the person’s needs, which may include:
=> Self-management skills such as pacing their activities and goal setting.
=> Concerns about the impact of stress, anxiety, or depression on angina.
=> Advice about physical exertion including sexual activity.
=> Advice about other activities such as driving, flying, and work.
=> Advise people that the aim of anti-anginal drug treatment is to prevent episodes of angina and the aim of secondary prevention treatment is to prevent CVD i.e heart attack and stroke

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8
Q

What drug treatment is prescribed for a person with stable angina?

A
  1. GTN spray for symptomatic relief and to use before performing activities known to cause symptoms of angina
  2. Prescribe a beta-blocker or a CCB as first line regular treatment to reduce symptoms of stable angina

=> If not controlled on CCB alone at optimum dose then add beta-blocker and vice-versa

=> Rate limiting CCB i.e. verapamil or diltiazem if used as monotherapy; if used in combination with beta blocker then use nifedipine.
*beta-blocker should not be prescribed concurrently with verapamil = risk of complete heart block

=> if neither tolerated, use long acting nitrate i.e. isosorbide mononitrate, nicorandil, ivabradine, ranolazine

=> Review response to treatment in 2-4 weeks

  1. Anti-platelet treatment (low dose aspirin 75mg) and statin in all patients with stable angina
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9
Q

How to manage CVD risk in person with angina?

a) Advice on work
b) Advice on driving
c) Advice on sex

A
  1. Optimize management of comorbidities
  2. Stop smoking
  3. Cardioprotective diet (fish, fruit & veg, fibre, less sugar, saturated fats, salt)
  4. Healthy weight - exercise at least 30 mins per day
  5. Limit alcohol consumption (14 units/week spread over 3 days or more)

Work: continue as before. If involves heavy manual work, may need to alter practice to adapt => discuss issue with occupational health department at work

Driving: 
Group 1 (cars) - cease driving if symptoms at rest, with emotions or whilst driving. Can resume when symptom controlled. Do not need to notify DVLA.

Group 2 (lorries/buses) - must not drive and notify DVLA when symptoms occur. Driving license may be revoked if symptoms continue. Re-licenced if free from angina for at least 6 weeks / no other disqualifying condition.

Sex: can continue as normal. If sex brings on angina, then take GTN immediately before sex to prevent attacks.
Sildenafil is contraindicated with GTN.

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10
Q

What is the next step in management if the patient still has symptomatic angina on two anti-anginas drugs?

A

Consider for revascularisation

PCI: single vessel disease ; multi-vessel <65 years ; suitable anatomy

CABG: Unsuitable anatomy ; multi-vessel disease >65 years ; diabetes

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11
Q

What is QRISK2?

Explain to patient.

A

QRISK2 is a tool to calculate the likelihood of you having a stroke or heart attack in the next 10 years.

The higher the score, the greater the risk and the more risk factors you have, the greater the risk.

Risk factors include:
=> Age, gender, ethnicity
=> High BP, cholesterol levels, BMI
=> Smoking and alcohol
=> Medical condition i.e. diabetes, CKD
=> Strong family hx of heart disease in relatives under 60 years

The risk of CVD naturally increases with age but all these other factors further increase it.

QRISK2 score tells you weather you are at a low, moderate or high risk of developing CVD in the next 10 years.

  1. Low risk = QRISK2 score of less than 10%
    => this means you have less than 1 in 10 chance of having a stroke or heart attack in the next 10 years
  2. Moderate risk - QRISK2 of 10-20%
    => This means that you have 1-2 in 10 chance of having a stroke or heart attack in the next 10 years
  3. High risk - QRISK2 score of >20%
    => This means you have at least a 2 in 10 chance of having a stroke or heart attack in the next 10 years.
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12
Q

How can you lower your QRISK?

A

NICE suggests QRISK of >10% = offered help to reduce their risk by making lifestyle changes.

=> Stop smoking – consider swapping to vaping initially which is considerably less risky.
=> Eat a healthy balanced diet - low in fat, sugar and salt. Eat 5 fruit / veg a day.
=> Reduce alcohol intake – aim for less than 14 units a week for men and women spread over 3 days
=> Keep an eye on your weight and take steps to lose weight if needed. Aim for BMI 20-25.
=> Exercise regularly 30 mins / day (walking is a great start).
=> Taking medication to reduce blood pressure if needed.

*can measure QRISK again in 6-12 months time to measure weight, height, BP and cholesterol levels to monitor progress.

If lifestyle changes ineffective, add statin (20mg atorvastatin), to be taken every night

QRISK Above 20% = STATIN
=> Statins can significantly reduce risk of heart attack and stroke by unto 25%.

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13
Q

Acute coronary syndrome comprises unstable angina, STEMI and NSTEMI.
What is the underlying pathophysiology of ACS?

A

Rupture of the fibrous cap of a coronary artery plaque.

This leads to platelet aggregation and adhesion, localised thrombosis, vasoconstriction & distal thrombus embolisation.

Presence of a rich lipid core and think fibrous cap = increased risk of rupture.

Thrombus formation and vasoconstriction produced by platelet release of serotonin and thromboxane-A2 => myocardial ischaemia due to reduction in coronary blood flow.

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14
Q

How do you differentiate between unstable angina and NSTEMI?

A

NSTEMI: occluding thrombus => myocardial necrosis and a rise in serum troponin I & T and creatinine kinase-MB.

Unstable angina: ruptured plaque with non-occlusive thrombus + no rise in troponin

No ST elevation in both

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15
Q

What are the risk factors in ACS?

A

Non-modifiable:
Age

Male
Family Hx of ischaemic heart disease (MI in 1st degree relative <55years)

Modifiable: 
Smoking 
Hypertension 
Diabetes 
Hyperlipidaemia 
Obesity 
Sedentary lifestyle 
Cocaine use 

Controversial risk factor:
Stress
Type A personality
Left ventricular hypertrophy

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16
Q

What are the symptoms of acute coronary syndrome (ACS)?

A

New onset acute central chest pain (at rest or deterioration of angina) lasting >20 mins

=> Assoc. w/ nausea, sweatiness, dyspnoea, palpitations

Atypical features = indigestion, pleuritic chest pain or dyspnoea

ACS w/o chest pain = silent (mostly seen in elderly & diabetic patients)
=> Silent MI’s present with syncope, pulmonary oedema, epigastric pain and vomiting

17
Q

Which investigations are carried out to confirm ACS?

A
  1. ECG
  2. Cardiac enzymes: Troponin I & T (most sensitive & specific markers of myocardial necrosis)

Others:
3. Chest X-ray

  1. Bloods: FBC, U&E, glucose, cholesterol/lipids, cardiac enzymes
  2. Echo
18
Q

Describe the changes seen in an ECG in STEMI and NSTEMI?

A

12-lead ECG : ST elevation & T-wave inversion highly suggestive of an ACS, esp assoc. with anginas chest pain.

ECG should be repeated when patient is in pain and monitor continuous ST segment.

STEMI : hyperacute, tall T waves, persistent ST elevation or new left bundle branch block occur within hours (due to complete occlusion of coronary vessel).
=> T-wave inversion and pathological Q waves follow over hours to days.

NSTEMI/unstable angina : ST depression, T wave inversion, non-specific changes or normal

*In 20% MI, ECG normal initially

19
Q

Which troponins are the most specific to the heart?

A

Troponin I & T => most specific and sensitive biochemical marker in ACS.

20
Q

Which two main scoring system is used to stratify ACS risk score?

A
  1. Thrombolysis in myocardial infarction (TIMI) score
  2. Global Registry of Acute Coronary Events (GRACE) score

The GRACE score is based on age, heart rate, systolic blood pressure, serum creatinine and the Killip score.

21
Q

What is the acute management for chest pain without ST elevation?

A

M - Morphine 5-10mg IV + metoclopramide 10mg IV

O - Oxygen if SaO2 <94% or breathless, low flow O2

N - Nitrates ; GTN spray or sublingual tablet

A - Aspirin 300mg loading dose then 75mg once daily

T - Tricagrelor or clopidogrel (2nd anti-platelet agent in confirmed ACS)

22
Q

What are the typical + atypical signs and symptoms of a STEMI?

A
  1. Severe chest pain lasting more than 20mins

Pain does not respond to sublingual GTN & opiate is required for analgesia

Pain may radiate to left arm, neck, jaw.

  1. In elderly/diabetic patients symptoms are atypical:
    Dyspnoea
    Fatigue
    Pre-syncope / syncope
  2. Autonomic symptoms are common:
    Pale & clammy
    Marked sweating
  3. Signs:
    Pulse thready with sig. hypotension, bradycardia or tachycardia.
23
Q

Which investigations are carried out in a STEMI?

A

ECG - if baseline ECG normal then continue monitoring every 15 mins if in continuous pain.

Continuous cardiac monitoring required in case of significant cardiac arrhythmias.

Blood tests: Cardiac troponin I & T ; FBC ; serum electrolyte ; glucose ; lipid profile ; U&E

Transthoracic echocardiography (TTE)

24
Q

Which ECG leads exhibit ST elevations anterior MI?

Which ECG leads exhibit changes in lateral MI?

Which ECG leads exhibit changes posterior MI?

A

Anterior MI = Leads V1-V4

Lateral MI = Leads I, AVL and V5/V6

Posterior MI = ST depression in V1-V3 with dominant R wave,
ST elevation in lead V5/V6

25
Q

Initial management for STEMI is the same as above using MONA to stabilise chest pain. STEMI patients are then referred to PCI centre be managed via reperfusion therapy.

Explain Primary percutaneous coronary intervention (PCI).

Which medications are required alongside PCI?

A

PCI is the preferred reperfusion therapy for STEMI + should be offered to all patients within 12h of symptom onset with a STEMI.
=> Radial access = preferred route as reduces complications.

Dual anti-platelet therapy: aspirin and ADP receptor blocker i.e. tricagrelor or prasugrel.

Anti-coagulant : Enoxaparin, anti-fractionated heparin

26
Q

Initial management for STEMI is the same as above using MONA to stabilise chest pain. If primary PCI centre not available within 120 mins then STEMI patients are first managed by thrombolysis.

Explain thrombolysis mechanism of action.

Which drug is used in thrombolysis therapy?

When should you thrombolyse?

When should you not thromboses?

Which medications are required alongside thrombolysis?

If fibrinolysis unsuccessful then transfer patient to primary PCI centre for rescue PCI or for angiography.

A

Thrombolytic agents enhance the break down of the thrombus occluding the vessel by activating plasmin from plasminogen.

Thrombolysis is appropriate if PCI not available within 120 mins of STEMI diagnosis.

Thrombolysis best achieved with tissue plasminogen activator (TPA) i.e tenecteplase as a single IV bolus

Do not thrombolyse ST depression alone, T-wave alone, or normal ECG.

Dual anti-platelet therapy: aspirin and ADP receptor blocker i.e. tricagrelor or prasugrel.

Anti-coagulant : Enoxaparin, anti-fractionated heparin

27
Q

What are the absolute and relative contraindications of thrombolysis?

A

Absolute:
1. Hemorrhagic stroke / stroke of unknown origin

  1. Ischaemic stroke <6months
  2. CVS damage
  3. Recent trauma/surgery/head injury
  4. GI bleeding within last month
  5. Bleeding disorder
  6. Aortic dissection

Relative:
1. Anticoagulant therapy

  1. Pregnancy or 1 week postpartum
  2. Refractory hypertension
  3. TIA <6months
  4. Infective endocarditis
  5. Active peptic ulcer
  6. Prolonged /traumatic resus
  7. Advanced liver disease
28
Q

What is coronary artery bypass surgery (CABG)?

A

CABG diverts blood from occluded coronary arteries to improve blood flow and oxygen supply to the heart.

CABG reserved for complications of MI i.e ventricular septal defect or mitral regurgitation.

29
Q

After acute management of chest pain using MONA in ACS without ST elevation, how do you manage a high risk patient whose troponin is rising, dynamic ST or T wave changes and the patient has either
=> diabetes,
=> CKD,
=> left ventricular ejection fraction <40,
=> early angina post MI,
=> recent PCI,
=> previous CABG or
=> intermediate to high risk GRACE score.

A
  1. Anti-thrombin drugs : Fondaparinux, enoxaparin (both = factor Xa inhibitor)
  2. 2nd anti-platelet agent (if not already added) : ticagrelor (or clopidogrel in lower risk patients)
  3. IV nitrate if pain continues, titrate to pain and maintain systolic BP >100mmHg
  4. Oral B-blocker : Bisoprolol 2.5mg OD
  5. ACE-inhibitor + monitor renal function
  6. Lipid management : Atorvastatin 80mg OD
  7. Cardiologist review for angiography urgent if:

Ongoing angina (<120min after presentation) and evolving ST changes, signs of cardiogenic shock or life threatening arrhythmias

Early (<24h) if GRACE score >140 and high risk patient

Within 72h if lower risk patient

30
Q

When may beta-blockers be contraindicated?

What alternative may be used?

A

Cardiogenic shock

Asthma/COPD

Heart block

Rate limiting calcium antagonist i.e. verapamil / diltiazem

31
Q

What is the prognosis for ACS without ST elevation (unstable angine and NSTEMI)?

Which risk factors increase the risk of death?

A

Risk of death 1-2% ; 15% for refractory angina

Risk stratification (GRACE score) to predict and manage better.

Risk factors:
Hx of unstable angina
ST depression or widespread T-wave inversion
Raised troponin
Age >70yrs
Comorbidity (previous MI, diabetes, poor left ventricle function)

32
Q

What other interventions may be needed for a high risk NSTEMI patient (GRACE score >140) with
persistent chest pain not responding to medical therapy,
clinical signs of heart failure,
haemodynamically unstable,
cardiogenic shock or
life-threatening arrhythmias (ventricular fib/tachycardia)?

A

Very high risk = Urgent angiography within 2h

High risk (GRACE score >140) = Coronary angiography ± PCI within 24h

Intermediate risk (GRACE score 109-140) = Angiography within 72h

Patients with multi-vessel disease = consider CABG not PCI

33
Q

How do you manage a low risk ACS patient without ST elevation after acute management of chest pain?

After acute management of chest pain using MONA in ACS without ST elevation, how do you manage a low risk patient who has 
No recurrent chest pain 
No signs of heart failure 
Normal ECG 
No rise in troponin
A

Conservative management
Medical therapy

Outpatient investigations e.g. stress test

34
Q

What are the complications of MI?

A
  1. Heart failure : post MI = poor prognosis
    * Killip classification assesses patients with heart failure post MI
  2. Myocardial rupture and aneurysm dilation
  3. Ventricular septal defect
  4. Mitral regurgitation
  5. Cardiac arrhythmias : Ventricular tachycardia and fibrillation / bradyarrhythmias
  6. Conduction disturbances
  7. Dressler syndrome (immune response after injury => pericarditis)
  8. Cardiac tamponade
35
Q

What are post ACS lifestyle modifications?

A

Cardiac rehab program: education and information on lifestyle

Exercise rehab part of program

Dietary control: calorie control of obesity, increase fruit & vegetables, reduce trans & saturated fat, reduce salt intake (patients with hypertension)

Alcohol within safe limits (<14 units per week), no binge drinking

Physically active (30 mins of moderate aerobic exercise 5x a week)

Stop smoking

BP reduced to systolic <140mmHg

Diabetes maintained 53mmol/mol

36
Q

What are post ACS drug therapy and assessment?

A
  1. Aspirin 75mg
  2. ADP receptor blocker ie tricagrelor, clopidogrel
  3. Oral beta-blocker to maintain heart rate <60bpm
  4. PPI (for patients high risk of bleeding while on dual anti-platelet therapy)
  5. ACE inhibitor or ARB (angiotensin receptor blocker) esp if LVEF <40%
  6. Statin (cholesterol <1.8mmol/L)