Acute Coronary Syndromes

Question 1

Acute coronary syndrome (ACS) is an umbrella term covering a number of acute presentations of ischaemic heart disease. What are these?

Answer 1

ST-elevation myocardial infarction (STEMI): ST-segment elevation + elevated biomarkers of myocardial damage
non ST-elevation myocardial infarction (NSTEMI): ECG changes but no ST-segment elevation + elevated biomarkers of myocardial damage
unstable angina

Question 2

Ischaemic heart disease is a term synonymous with coronary heart disease and coronary artery disease.

Answer 2

True

Question 3

Describe pathophysiology of Acute coronary syndrome?

Answer 3

1. Gradual narrowing, resulting in less blood and therefore oxygen reaching the myocardium at times of increased demand. This results in angina, i.e. chest pain due to insufficient oxygen reaching the myocardium during exertion
2. The risk of sudden plaque rupture. The fatty plaques which have built up in the endothelium may rupture leading to sudden occlusion of the artery. This can result in no blood/oxygen reaching the area of myocardium.

Question 4

What are Unmodifiable risk factors?

Answer 4

Increasing age
Male gender
Family history

Question 5

What are modifiable risk factors?

Answer 5

Smoking
Diabetes mellitus
Hypertension
Hypercholesterolaemia
Obesity

Question 6

Poor prognostic factors?

Answer 6

age
development (or history) of heart failure
peripheral vascular disease
reduced systolic blood pressure
Killip class*
initial serum creatinine concentration
elevated initial cardiac markers
cardiac arrest on admission
ST segment deviation

Question 7

What is Killip Class?

Answer 7

system used to stratify risk post myocardial infarction

Question 8

Describe Killip Classes

Answer 8

I No clinical signs heart failure, 6% 30 day mortality
II Lung crackles, S3 17% 30 day mortality
III Frank pulmonary oedema 38% 30 day mortality
IV Cardiogenic shock 81% 30 day mortality

Question 9

initial endothelial dysfunction in IHD is triggered by a number of factors such as

Answer 9

smoking, hypertension and hyperglycaemia

Question 10

initial endothelial dysfunction results in a number of changes such as?

Answer 10

pro-inflammatory, pro-oxidant, proliferative and reduced nitric oxide bioavailability

Question 11

What type of lipoproteins infiltrate the subendothelial space in IHD?

Answer 11

by low-density lipoprotein (LDL) particles

Question 12

How do foam cells form?

Answer 12

monocytes migrate from the blood and differentiate into macrophages. These macrophages then phagocytose oxidized LDL, slowly turning into large ‘foam cells’. As these macrophages die the result can further propagate the inflammatory process.
smooth muscle proliferation and migration from the tunica media into the intima results in formation of a fibrous capsule covering the fatty plaque.

Question 13

What are the complications of atherosclerosis?

Answer 13

the plaque forms a physical blockage in the lumen of the coronary artery. This may cause reduced blood flow and hence oxygen to the myocardium, particularly at times of increased demand, resulting clinically in angina
the plaque may rupture, potentially causing a complete occlusion of the coronary artery. This may result in a myocardial infarction

Question 14

What is the classic and most common feature of ACS?

Answer 14

chest pain.

Question 15

What are the symptoms of ACS?

Answer 15

typically central/left-sided
may radiate to the jaw or the left arm
often described as ‘heavy’ or constricting, ‘like an elephant on my chest’
it should be noted however in real clinical practice patients present with a wide variety of types of chest pain and patients/doctors may confuse ischaemic pain for other causes such as dyspepsia
certain patients e.g. diabetics/elderly may not experience any chest pain
dyspnoea
sweating
nausea and vomiting

Question 16

Patients presenting with ACS often have very few physical signs to ellicit

Answer 16

true
pulse, blood pressure, temperature and oxygen saturations are often normal or only mildly altered e.g. tachycardia
if complications of the ACS have developed e.g. cardiac failure then clearly there may a number of findings
the patient may appear pale and clammy

Question 17

What are the two most important investigations when assessing a patient with chest pain?

Answer 17

ECG

cardiac markers e.g. troponin

Question 18

Which cardiac marker is first to rise?

Answer 18

myoglobin is the first to rise

Question 19

Which marker is useful to look at for re-infarctation?

Answer 19

CK-MB is useful to look for reinfarction as it returns to normal after 2-3 days

Question 20

How long does troponin T remain elevated?

Answer 20

10 days

Question 21

What are the cardiac enzymes and protein markers?

Answer 21

Myoglobin
CK-MB
CK
Trop T
AST
LDH

Question 22

Interpretation of the various cardiac enzymes has now largely been superceded by the introduction of troponin T and I. Questions still however commonly appear in exams.

Answer 22

true

Question 23

Describe the orrelation between ECG changes and coronary territories

Answer 23

Anterior V1-V4 usually Left anterior descending artery

Inferior II, III, aVF usually Right coronary artery

Lateral I, V5-6 usually Left circumflex artery

Question 24

What are the aims of ACS treatment?

Answer 24

prevent worsening of presentation (i.e. further occlusion of coronary vessel)
revascularise (i.e. ‘unblock’) the vessel if occluded (patients presenting with a STEMI)
treat pain

Question 25

A commonly taught mnemonic for the intial treatment of ACS is MONA, what does it stand for?

Answer 25

morphine should only be given for patients with severe pain previously IV morphine was given routinely evidence, however, suggests that this may be associated with adverse outcomes oxygen should only be given if the patient has oxygen saturations < 94% nitrates can be given either sublingually or intravenously useful if the patient has ongoing chest or hypertension should be used in caution if patient hypotensive aspirin 300mg

Question 26

After pharmacological treatment (MONA) what is the next step?

Answer 26

determine whether they meet the ECG criteria for STEMI

Question 27

What is STEMI criteria?

Answer 27

clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with persistent (> 20 minutes) ECG features in ≥ 2 contiguous leads of: 2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years 1.5 mm ST elevation in V2-3 in women 1 mm ST elevation in other leads new LBBB (LBBB should be considered new unless there is evidence otherwise)

Question 28

In management of a STEMI all patients should be given?

Answer 28

aspirin a second antiplatelet drug should be given in addition to aspirin. P2Y12-receptor antagonist (ticagrelor is often favoured or prasugrel if the patient is going to have a PCI) unfractionated heparin is usually given for patients who're are going to have a PCI

Question 29

In STEMI management what should you do in terms of oxygen therapy?

Answer 29

do not routinely administer oxygen, but monitor oxygen saturation using pulse oximetry as soon as possible, ideally before hospital admission. Only offer supplemental oxygen to: people with oxygen saturation (SpO2) of less than 94% who are not at risk of hypercapnic respiratory failure, aiming for SpO2 of 94-98% people with chronic obstructive pulmonary disease who are at risk of hypercapnic respiratory failure, to achieve a target SpO2 of 88-92% until blood gas analysis is available.

Question 30

What is gold standard treatment for STEMI?

Answer 30

Primary percutaneous coronary intervention (PCI) In this procedure the blocked arteries are opened up using a balloon (angioplasty) following which a stent may be deployed to prevent the artery occluding again in the future. This is done via a catheter inserted into either the radial or femoral artery radial access is preferred to femoral access in PCI

Question 31

When should PCI be offered?

Answer 31

should be offered if the presentation is within 12 hours of onset of symptoms AND PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given (i.e. consider fibrinolysis if there is a significant delay in being able to provide PCI) if patients present after 12 hours and still have evidence of ongoing ischaemia then PCI should still be considered

Question 32

When should fibrinolysis be offered?

Answer 32

should be offered within 12 hours of onset of symptoms if primary PCI cannot be delivered within 120 minutes of the time when fibrinolysis could have been given

Question 33

Which drugs are used in fibrinolysis?

Answer 33

tissue plasminogen activator (tPA) has been shown to offer clear mortality benefits over streptokinase tenecteplase is easier to administer and has been shown to have non-inferior efficacy to alteplase with a similar adverse effect profile Patients undergoing fibrinolysis should also be given an antithrombin drug.

Question 34

What test should be performed after fibrinolysis?

Answer 34

An ECG should be performed 90 minutes following thrombolysis to assess whether there has been a greater than 50% resolution in the ST elevation if there has not been adequate resolution then rescue PCI is superior to repeat thrombolysis for patients successfully treated with thrombolysis PCI has been shown to be beneficial. The optimal timing of this is still under investigation

Question 35

What is the guidance on the management of hyperglycaemia in acute coronary syndromes for diabetic patients?

Answer 35

it recommends using a dose-adjusted insulin infusion with regular monitoring of blood glucose levels to glucose below 11.0 mmol/l intensive insulin therapy (an intravenous infusion of insulin and glucose with or without potassium, sometimes referred to as 'DIGAMI') regimes are not recommended routinely

Question 36

NICE produced guidelines on the management of patients following a myocardial infarction (MI) in 2013. Some key points are?

Answer 36

All patients should be offered the following drugs: dual antiplatelet therapy (aspirin plus a second antiplatelet agent) ACE inhibitor beta-blocker statin

Question 37

What are the lifestyle points post MI?

Answer 37

diet: advise a Mediterranean style diet, switch butter and cheese for plant oil based products. Do not recommend omega-3 supplements or eating oily fish exercise: advise 20-30 mins a day until patients are 'slightly breathless' sexual activity may resume 4 weeks after an uncomplicated MI. Reassure patients that sex does not increase their likelihood of a further MI. PDE5 inhibitors (e.g, sildenafil) may be used 6 months after a MI. They should however be avoided in patient prescribed either nitrates or nicorandil

Question 38

What are the widely used drugs for dual antiplatelet therapy (DAPT)?

Answer 38

ticagrelor and prasugrel (ADP-receptor inhibitors)

Question 39

What DAPT does NICE reccomend post acute coronary syndrome (medically managed)?

Answer 39

add ticagrelor to aspirin, stop ticagrelor after 12 months this 12 month period may be altered for people at a high-risk of bleeding or those who at high-risk of further ischaemic events

Question 40

What DAPT does NICE reccomend post percutaneous coronary intervention?

Answer 40

add prasugrel or ticagrelor to aspirin, stop the second antiplatelet after 12 months this 12 month period may be altered for people at a high-risk of bleeding or those who at high-risk of further ischaemic events

Question 41

When are Aldosterone antagonists indicated post acute MI?

Answer 41

who have symptoms and/or signs of heart failure and left ventricular systolic dysfunction aldosterone antagonist licensed for post-MI treatment (e.g. eplerenone) should be initiated within 3-14 days of the MI, preferably after ACE inhibitor therapy

Question 42

What complications can you get post-MI?

Answer 42

``` Cardiac arrest Cardiogenic shock Chronic heart failure Tachyarrhythmias Bradyarrhythmias Pericarditis Left ventricular aneurysm Left ventricular free wall rupture Ventricular septal defect Acute mitral regurgitation ```

Question 43

Cardiac arrest most commonly occurs due to patients developing ventricular fibrillation

Answer 43

true | is the most common cause of death following a MI. Patients are managed as per the ALS protocol with defibrillation

Question 44

How does cardiogenic shock occur post MI?

Answer 44

If a large part of the ventricular myocardium is damaged in the infarction the ejection fraction of the heart may decrease to the point that the patient develops cardiogenic shock. Other causes of cardiogenic shock include the 'mechanical' complications such as left ventricular free wall rupture Patients may require inotropic support and/or an intra-aortic balloon pump.

Question 45

How does Chronic heart failure occur post MI?

Answer 45

if the patient survives the acute phase their ventricular myocardium may be dysfunctional resulting in chronic heart failure

Question 46

Both ACE-inhibitors and beta-blockers have been shown to improve the long-term prognosis of patients with chronic heart failure.

Answer 46

true | Loop diuretics such as furosemide will decrease fluid overload

Question 47

Atrioventricular block is more common following what type of MI?

Answer 47

inferior myocardial infarctions.

Question 48

When does Pericarditis typically occur?

Answer 48

first 48 hours following a transmural MI is common (c. 10% of patients).

Question 49

How does Pericarditis typically occur?

Answer 49

pain is typical for pericarditis (worse on lying flat etc), a pericardial rub may be heard and a pericardial effusion may be demonstrated with an echocardiogram.

Question 50

When does Dressler's syndrome typically occur?

Answer 50

2-6 weeks following a MI

Question 51

What is the pathophysiology of Dressler's syndrome?

Answer 51

The underlying pathophysiology is thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers

Question 52

What are the characteristics of Dressler's syndrome?

Answer 52

combination of fever, pleuritic pain, pericardial effusion and a raised ESR. It is treated with NSAIDs.

Question 53

What is Left ventricular aneurysm typically associated with?

Answer 53

persistent ST elevation and left ventricular failure | ischaemic damage sustained may weaken the myocardium resulting in aneurysm formation

Question 54

What is a complciation of left ventricular aneurysm?

Answer 54

Thrombus may form within the aneurysm increasing the risk of stroke. Patients are therefore anticoagulated.

Question 55

When does Left ventricular free wall rupture typically occur?

Answer 55

1-2 weeks post MI afterwards

Question 56

Left ventricular free wall rupture is seen in 3% of MIs

Answer 56

true

Question 57

How does Left ventricular free wall rupture present?

Answer 57

acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds). Urgent pericardiocentesis and thoracotomy are required.

Question 58

When does Ventricular septal defect occur?

Answer 58

Rupture of the interventricular septum usually occurs in the first week and is seen in around 1-2% of patients.

Question 59

What are the features of Ventricular septal defect?

Answer 59

acute heart failure associated with a pan-systolic murmur. An echocardiogram is diagnostic Urgent surgical correction is needed.

Question 60

acute mitral regurgitation presents in a similar fashion to?

Answer 60

Ventricular septal defect | Excluded with echo

Question 61

acute mitral regurgitation is more common with?

Answer 61

infero-posterior infarction and may be due to ischaemia or rupture of the papillary muscle.

Question 62

How does Acute mitral regurgitation present?

Answer 62

Acute hypotension and pulmonary oedema may occur. An early-to-mid systolic murmur is typically heard. Patients are treated with vasodilator therapy but often require emergency surgical repair.

Question 63

What Further antiplatelet prior to PCI is required?

Answer 63

'dual antiplatelet therapy', i.e. aspirin + another drug if the patient is not taking an oral anticoagulant: prasugrel if taking an oral anticoagulant: clopidogrel

Question 64

What Drug therapy is required during PCI?

Answer 64

patients undergoing PCI with radial access: unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI) - this is the action of using a GPI during the procedure when it was not intended from the outset, e.g. because of worsening or persistent thrombus patients undergoing PCI with femoral access: bivalirudin with bailout GPI

Question 65

What other procedure may be considered during PCI?

Answer 65

thrombus aspiration, but not mechanical thrombus extraction, should be considered complete revascularisation should be considered for patients with multivessel coronary artery disease without cardiogenic shock

Question 66

The management of NSTEMI/unstable angina is complicated and depends on individual patient factors and a risk assessment.

Answer 66

true

Question 67

What is the first step after NSTEMI/Unstable angina is identified?

Answer 67

Aspirin 300mg | Fondaparinaux if no immediated PCI planned

Question 68

What is the 2nd step after NSTEMI/Unstable angina is identified?

Answer 68

Estimate 6 - month mortality such as using GRACE tool

Question 69

The Global Registry of Acute Coronary Events (GRACE) is the most widely used tool for risk assessment. It can be calculated using online tools and takes into account the following factors?

Answer 69

``` age heart rate, blood pressure cardiac (Killip class) and renal function (serum creatinine) cardiac arrest on presentation ECG findings troponin levels ```

Question 70

GRACE tool predicts 6 month mortality - what are the categories?

Answer 70

``` 1.5% or below Lowest > 1.5% to 3.0% Low > 3.0% to 6.0% Intermediate > 6.0% to 9.0% High over 9.0% Highest ```

Question 71

Which patients with NSTEMI/unstable angina should have a coronary angiography (with follow-on PCI if necessary)?

Answer 71

immediate: patient who are clinically unstable (e.g. hypotensive) within 72 hours: patients with a GRACE score > 3% i.e. those at immediate, high or highest risk coronary angiography should also be considered for patients is ischaemia is subsequently experienced after admission

Question 72

In Primary coronary intervention for patients with NSTEMI/unstable angina what is the drug therapy?

Answer 72

- Prasugrel or Ticagrelor - Unfractionated heparin - Drug-eluting stents Further drug therapy unfractionated heparin should be given regardless of whether the patient has had fondaparinux or not further antiplatelet ('dual antiplatelet therapy', i.e. aspirin + another drug) prior to PCI if the patient is not taking an oral anticoagulant: prasugrel or ticagrelor if taking an oral anticoagulant: clopidogrel

Question 73

What is Conservative management for patients with NSTEMI/unstable angina?

Answer 73

``` further antiplatelet ('dual antiplatelet therapy', i.e. aspirin + another drug) if the patient is not at a high risk of bleeding: ticagrelor if the patient is at a high risk of bleeding: clopidogrel ```

Question 74

What ECG changes would you see in Acute MI?

Answer 74

hyperacute T waves are often the first sign of MI but often only persists for a few minutes ST elevation may then develop the T waves typically become inverted within the first 24 hours. The inversion of the T waves can last for days to months pathological Q waves develop after several hours to days. This change usually persists indefinitely

Question 75

A posterior MI causes ST depression not elevation on a 12-lead ECG.

Answer 75

true