ACS

Question 1

What is the main cause of cardiovascular disease (CVD)?

Answer 1

Cardiovascular disease (CVD) is generally due to reduced blood flow to the heart, brain or body caused by atheroma or thrombosis.
It is increasingly common after the age of 60, but rare below the age of 30.
Plaques (plates) of fatty atheroma build up in different arteries during adult life. These can eventually cause narrowing of the arteries, or trigger a local thrombosis (blood clot) which completely blocks the blood flow

Question 2

What are the main types of CVD?

Answer 2

The main types of CVD are: coronary heart disease (CHD), stroke and peripheral arterial disease (PVD).

Question 3

Risk factors for CVD

Answer 3

In more than 90% of cases, the risk of a first heart attack is related to nine potentially modifiable risk factors:

• smoking/tobacco use
• poor diet
• high blood cholesterol
• high blood pressure
• insufficient physical activity
• overweight/obesity
• diabetes
• psychosocial stress (linked to people’s ability to influence the potentially stressful environments in which they live)
• excess alcohol consumption.

Question 4

Who is a typical patient with ACS?

Answer 4

Middle-aged (man) or elderly (either sex) patient, often with FH of CHD and one or more of the major reversible risk factors.
In many patients, there is no preceding history of angina.

Question 5

What are the signs and symptoms of ACS?

Answer 5

Central chest pain often describes as heaviness or tightness with radiation to neck, jaw or arms.
Dyspnoea
Autonomic disturbances- nausea, sweating (diaphoresis) and vomiting
Tachycardia (anterior MI), bradycardia (inferior MI).
Pulmonary oedema with large infarcts.
Atypical presentations are common over 75
years of age.

Question 6

What are the sub-types of ACS?

Answer 6

There are 3 sub-types of ACS.
ST-elevation MI (STEMI)
Non-STEMI (NSTEMI)
Unstable angina

Question 7

What is STEMI?

Answer 7

ECG shows persistent ST-segment elevation in 2 or more anatomically contiguous leads.
Atherosclerosis with plaque rupture and thrombus formation is the underlying aetiology for STEMI.
Probable proximal occlusion of a major coronary artery.
STEMI is usually associated with a relatively large amount of damage to the myocardium (heart muscle) caused by a major blockage in the coronary artery

Question 8

What is unstable angina?

Answer 8

Defined by the absence of myocardial necrosis.
Prolonged (>20 minutes) angina at rest.
ECG typically shows ST-segment depression and T-wave inversion but may be normal.

Question 9

What is the initial treatment of presumed MI?

Answer 9

Oxygen (if needed) should be >90%
Aspirin in addition with ticagrelor or clopidogrel.
Beta-blocker

Question 10

What is NSTEMI?

Answer 10

An acute ischaemic event causing myocyte necrosis.
ECG may show ST-segment depression or T wave inversion.
The distinction from unstable angina is based on cardiac biomarkers.
History and cardiac markers are the most useful diagnostic tools in NSTEMI.
NSTEMI is often associated with relatively less damage to the myocardium, caused by either partial blockage of the coronary artery or blockage of a smaller artery.

Question 11

ECG changes in MI

Answer 11

1) Pathological Q waves usually indicate current or prior myocardial infarction. Q waves are considered pathological if:
> 40 ms (1 mm) wide
> 2 mm deep
> 25% of the depth of QRS complex
Seen in leads V1-3
2) Left bundle branch block (LBBB). ECG characteristics of LBBB are:
Broad QRS (>3small square/0.12sec) and
Deep S wave in V1 and
No Q wave in V5/V6
3) ST-segment (STEMI) and T wave abnormalities (e.g. ST-segment depression or T wave flattening or inversion-inversion due to changes in ventricular depolarisation (NSTEMI or Unstable angina)

Question 12

Does a normal ECG exclude MI?

Answer 12

NICE guidance is clear that a normal ECG does not exclude ACS.
ECG may be difficult to interpret if there is a bundle branch block or previous MI.

Question 13

Diagnosis of MI

Answer 13

ECG.
Cardiac biomarkers- troponins and creatine kinase

FBC- may indicate anaemia or thrombocytopenia
Electrolytes- may be deranged
Blood sugar and lipids to rule out diabetes and high cholesterol

Question 14

Which tool is used to predict the likelihood of future CHD events?

Answer 14

Using the GRACE risk score, eight factors independently predict the risk of heart attack and/or death:
age
heart rate
systolic blood pressure
renal function
congestive heart failure
ST-segment deviation
cardiac arrest
elevated biomarkers

Question 15

Based on the risk stratification of ACS, what should be done?

Answer 15

High risk-
 Echocardiogram (could be stress)
Coronary angiography
Low risk- 
Perfusion imaging using adenosine, dipyridamole or dobutamine

Question 16

How do you assess troponin in an ACS setting?

Answer 16

Cardiac troponin I and cardiac troponin T are biological markers of cardiomyocyte necrosis.
They are released into the circulation when damage to cardiac muscle has occurred.
Troponins (>99%) are raised in STEMI and NSTEMI but not in unstable angina.
The higher the levels of troponin, the higher the mortality.
Levels of troponin increase within 3-6 hours, peak at 36 hours and is elevated for 2 weeks.
Conditions other than acute MI that may cause troponin levels to be raised include myocarditis, congestive heart failure, severe infections, musculoskeletal conditions and renal disease.

Question 17

Why are troponins preferred to creatine kinase?

Answer 17

Raised troponins are more specific than creatine kinase.

Creatine kinase can be released from any damaged muscle in the body.

Question 18

When is myocardial necrosis irreversible?

Answer 18

After 30 minutes.

Question 19

What is the coronary sinus?

Answer 19

The venous drainage from the heart is via the coronary sinus.
The coronary sinus is a collection of veins joined together to form a large vessel that collects blood from the myocardium.
It delivers deoxygenated blood to the right atrium.
The coronary sinus may be readily cannulated by the cardiologist.

Question 20

What are the key branches of the right and left coronary artery?

Answer 20

The key branches of the right (Right marginal and posterior descending) and left (Left anterior descending, left marginal and left circumflex) main coronary vessels.
The coronary arteries originate from the aortic sinuses.

Question 21

What does tachycardia do to the heart?

Answer 21

Tachycardia increases myocardial oxygen demand (as the heart has to beat faster and hence do more work) and decreases coronary blood flow (as the duration of diastole is shortened considerably).

Question 22

How do you monitor patients with acute chest pain?

Answer 22

Monitor people with acute chest pain, using clinical judgement to decide how often this should be done, until a firm diagnosis is made. This should include:
• exacerbations of pain and/or other symptoms
• pulse and blood pressure
• heart rhythm
• oxygen saturation by pulse oximetry
• repeated resting 12-lead ECGs
• checking pain relief is effective.

Question 23

How could the ECG be normal in ACS?

Answer 23

Ischaemia in circumflex territory
• Isolated RV ischaemia
• (these are detected using V7-V9 and V3R and V4R leads)
• transient episodes of bundle branch block
(either RBBB or LBBB)

Question 24

Management of NSTEMI?

Answer 24

NSTEMI is more common than STEMI.
GTN is initial treatment. (N)
Analgesia and IV opioid used for pain that doesn’t settle with nitrate. (M)
Oxygen if sats is below 94% (normal) or 88% (COPD)- oxygen avoided if there is no hypoxaemia. (O)
Loading dose of aspirin (300 mg OD) and clopidogrel (300mg OD) for a year then clopidogrel stopped after a year. (A)
MONA
Beta-blocker is the first choice of anti-anginal treatment and can reduce subsequent ischaemic events. Calcium-channel blocker used if beta-blocker is CI.
THEN assess needs for an invasive or conservative approach.
People with NSTEMI and Unstable angina should be investigated with coronary angiography (with PCI if indicated) within 72 hours of admission unless the patient has serious comorbidities including cancer or end-stage liver disease.

Question 25

Imaging to confirm the diagnosis of MI

Answer 25

Imaging for confirmation of diagnosis
o ECG
o Transthoracic echocardiography
o Stress echocardiography
o Cardiac MRI
o Nuclear myocardial perfusion imaging
o CT coronary angiography

Question 26

When is an invasive approach recommended in NSTEMI?

Answer 26

Recurrent angina or ischaemia at rest or low-level activities. 
Elevated cardiac biomarkers. 
Signs or symptoms of heart failure. 
New or worsening mitral regurgitation. 
High-risk score (TIMI or GRACE)
Prior CABG
Reduced left ventricular function (<40%)

Question 27

Long-term management of ACS

Answer 27

Aspirin for life, dual antiplatelet therapy for 12 months
• Statins for all early, aiming for LDL<1.8mmol/l
• Beta blockade to all with left ventricular impairment (LVEF<40%)
• Angiotensin Converting Enzyme Inhibitors (ACEI) to all, especially those with LVEF<40%
• Angiotensin Receptor Blockers (ARB) to those patients intolerant of ACEI
• Aldosterone antagonists to patients already taking beta blockers and ACE
inhibitors with a left ventricular ejection fraction <35%
• Enrolment in secondary prevention programme (diet, exercise, lifestyle)

Question 28

What is PCI?

Answer 28

Angioplasty is coupled with the placement of stents.
Complications include coronary perforation, dissection, or rupture, cardiac tamponade, malignant arrhythmias, cholesterol emboli and bleeding from the access site.

Question 29

What is fibrinolysis?

Answer 29

Breaking down thrombus in the arteries.
Anticoagulation with heparin (60 units per kg bolus initially, followed by 12 units/kg/hour infusion), or enoxaparin (LMWH) (30mg IV bolus initially followed by 1mg/kg subcutaneously every 12 hours) or dalteparin OR fondaparinux AND heparin
ANSWER IS VERY QUESTIONABLE, CHECK WHEN FREE

Question 30

Management of STEMI?

Answer 30

MONA initially.
Haemodynamically unstable- PCI or CABG if PCI fails
Anticoagulation- heparin, bivalirudin OR enoxaparin. Heparin preferred.
Aspirin (300mg then 75mg OD) + P2Y12 inhibitor such as ticagrelor (180mg as a loading dose then 90 mg TDS)
Glucose control if needed
Haemodynamically stable:
Electrically unstable post-cardiac arrest-
-Emergency revascularisation: PCI or CABG
-Hypothermia
-Anticoagulation
-Aspirin + P2Y12 inhibitor
-Beta-blocker
-Statin

Question 31

Secondary prevention of MI

Answer 31

Long-term prevention of cardiovascular events
(STEMI and NSTEMI)
o Pharmacotherapy
 Aspirin for life, dual antiplatelet therapy for 12 months
(aspirin and another antiplatelet)
 Statins, aiming for LDL <1.8mmol/L, primary prevention if QRISK2 >10%: atorvastatin 20mg, secondary prevention after an MI: atorvastatin 80mg
 Beta-blockers for L ventricular impairment
(LVEF <40%)
 ACE-I for all e.g.Ramipril, lisinopril
(ARB as an alternative, candesartan, losartan)
 Aldosterone antagonists(spironolactone, eplerenone)
if the patient does not respond to ACE-I or ARB, or symptoms of heart failure & L ventricular systolic function
o Lifestyle changes
 Smoking cessation, safe alcohol consumption
 Keep weekly alcohol consumption≤14 units for men and women, avoid binge drinking (>3 drinks in 1-2 hours)
 Diet- Shift towards a diet with more bread, fruit, vegetables, and fish; less red meat, and replacing dairy products with plant oil products.
 Do NOT offer omega-3 fatty acid supplementation, beta-carotene, antioxidant supplements or folic acid.
Weight management
–offer all patients who are overweight or obese (BMI >25)
the advice in line with NICE guidelines on weight loss, including diet changes, physical activity and behavioural changes; only resorting to the drug (orlistat) or bariatric surgery after these have been tried.
 Exercise
–advise people to undertake regular physic
al activity, for 20-30 minutes a day, increasing in a step-wise program
Cardiac rehabilitation programme
oAll patients, regardless of age, should be given advice about and offered a cardiac
rehabilitation programme with an exercise component
o Offer stress management in the context of comprehensive rehabilitation
o Do NOT routinely offer complex psychological interventions such as CBT.
o Involve partners or carers in the cardiac rehabilitation programme if the patient wishes.

Question 32

Which areas of life are affected after MI?

Answer 32

 Affected areas of life
o Driving
 Cars:
Don’t need to tell DVLA, but recommended to stop driving for 1 week after a successful angioplasty, or 4 weeks for unsuccessful angioplasty/no angioplasty.
Check with the doctor to find out when it’s safe to drive again.
 Bus, coaches, and lorries:
MUST tell the DVLA AND stop driving for 6 weeks
.Must take an assessment with a doctor after 6 weeks to see if they are fit to drive
again.
o Flying
 After an MI without complications, people who wish to travel by air should seek advice from the Civil Aviation Authority; complicated MIs need expert individual
advice.
The UK CAA recommends flying 7-10 days after an uncomplicated MI

Question 33

What are the causes of MI?

Answer 33

Atherosclerosis> Rupture> Thrombus

Aortic stenosis- A severe stenosis in the aortic valve causes poor blood flow out of the heart which can result in the poor filling of the coronary arteries (which arise after the aortic valve from the aorta) and myocardial ischaemia.

Hypertrophic cardiomyopathy- HOCM is a disorder which causes the cardiac muscle to hypertrophy (overgrow). Hypertrophy of the interventricular septum can obstruct blood flow and cause poor filling of the coronary arteries and myocardial ischaemia.

Tachyarrhythmias

Cocaine use- Cocaine is a powerful vasoconstrictor and can cause severe coronary artery spasm resulting in myocardial ischaemia and necrosis.

Anaemia- Severe anaemia can cause poor oxygenation of cardiac muscle resulting in ischaemia.
Thyrotoxicosis

Question 34

Complications after MI

Answer 34

Arrhythmias usually sinus bradycardia.
Left ventricular failure with hypotension
Pulmonary congestion which can progress to pulmonary oedema and respiratory impairments.
Cardiac tamponade
Pericarditis
Infarct expansion
Mural thrombus, papillary muscle dysfunction and progressive late heart failure.
Recurrent chest pain.

Question 35

Differentials of MI

Answer 35

Unstable angina 
NSTEMI 
PE
Pneumothorax
Pneumonia 
Pericarditis 
Myocarditis 
GORD
Oesophageal spasm 
Anxiety 
Costochondritis