Acute Coronary Syndromes

Question 1

What do acute coronary syndromes (ACSs) include?

Answer 1

STEMI

NSTEMI

Unstable Angina

Question 2

Simplified diagnosis of ACSs.

Answer 2

Clinical history

12 lead ECG

Biochemical markers

Question 3

What biochemical markers are used to investigate ACSs?

Answer 3

Troponin T

Troponin I

Creatine kinase-MB (CK-MB)

Question 4

Five types of MI.

Answer 4

Type 1 - Spontaenous MI with Ischaemia

Type 2 - MI secondary to ischaemia

Type 3 - Diagnosis of MI in sudden cardiac death

Type 4a - MI related to PCI

Type 4b - MI related to stent thrombosis

Type 5 - MI related to CABG

Question 5

Pathophysiology common to all ACSs.

Answer 5

Rupture or erosion of the fibrous cap of a coronary artery plaque.

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

A rich lipid pool with the plaque and a thin fibrous cap increases the risk of rupture.

This all leads to myocardial ischaemia due to reduction of coronary blood flow.

Acute Coronary Syndrome is usually the result of a thrombus from an atherosclerotic plaque blocking a coronary artery. When a thrombus forms in a fast flowing artery it is made up mostly of platelets. This is why anti-platelet medications such as aspirin, clopidogrel and ticagrelor are the mainstay of treatment.

Question 6

Clinical features of ACS.

Answer 6

New onset of chest pain. It is usually cardiac and at rest. It can also be deterioriation of pre-existing angina.

Atypical features might inlcude indigestion, pleuritic chest pain or dyspnoea.

Hypotension, basal crackles, fourth heart sounds and cardiac murmurs might be present.

Nausea and vomiting

Sweating and clamminess

Feeling of impending doom

Shortness of breath

Palpitations

Pain radiating to jaw or arms

Question 7

What is a silent MI?

Answer 7

Symptoms should continue at rest for more than 20 minutes. If they settle with rest consider angina. Diabetic patients may not experience typical chest pain during an acute coronary syndrome. This is often referred to as a “silent MI”.

Question 8

Investigations done in ACSs.

Answer 8

ECG 12-leads

Biochemical markers such as troponin I, T and C. Usually hs-TnI is used.

Creatine kinase levels are also done.

FBC, U&E, glucose and lipid profile should also be done.

CXR if it will not delay treatment.

Question 9

If the initial troponin assay is negative, what should be done?

Answer 9

According to Zero to Finals you should measure troponin at baseline, 6 hours and then 12 hours in.

Some say repeat 30 min - 3 hours after as well

Question 10

What does troponin levels tell us about the ACSs?

Answer 10

They begin to rise 3 to 4 hours after myocardial damage.
They can also stay elevated up to 2 weeks.

Five-fold increase of upper limit is very suggestive of type 1 MI (>90%). Elevations up to 3 times only suggest MI (50-60% of the time)

Rising and/or falling cardiac troponin levels differentiate between acute and chronic cardiomyocyte damage.

There is also a relationship between troponin I and risk of death in ACS.

Question 11

Explain the relationship between troponin I and risk of death in ACS.

Answer 11

Question 12

Explain the regimen of carrying out troponin assays.

Answer 12

hs-TnI should be taken on admission and again at 1 hour.

Only one assay is required if the onset of symptoms was 3 or more hours previously.

If there is still uncertainty a further sample can be taken 2 hours later (3 in total after first).

The second hs-TnI can be useful to assess whether the elevation is statit, rising or falling.

Question 13

How does rising and/or falling cardiac troponin levels differentiate acute from chronic cardiomyocyte damage?

Answer 13

The more pronounced the change, the higher the likelihood of acute MI.

Question 14

In males, what levels of hs-TnI suggests a high likelihood of myocardial necrosis?

Answer 14

> 34 ng/L

Question 15

In females, what levels of hs-TnI suggests a high likelihood of myocardial necrosis?

Answer 15

> 16 ng/L

Question 16

What else might increase your troponin levels?

Answer 16

Advanced renal failure

Large PE

Severe congestive cardiac failure

Myocarditis

Aortic dissection

Aortic stenosis

Hypertrophic cardiomyopathy

Takotsubo cardiomyopathy

Malignancy

Stroke

Sepsis

Question 17

How is risk stratification done in NSTEMI and unstable angina?

Answer 17

TIMI score and GRACE score

Question 18

Explain TIMI score for NSTEMI and UA

Answer 18

Provides a prognosis.

Based on Age, risk factors, known CAD, aspirin use in last 7 days, severe angina, ST deviation on EC, elevated cardiac markers.

Question 19

Explain the GRACE score.

Answer 19

First it gives a score based on age, resting heart rate, initial serum creatinine, history of CCF, systolic BP, elevated cardiac enzymes, ST depression on ECG and no PCI done.

It is then put into a scoring system that shows the mortality and likelihood of having a repeat MI after an NSTEMI.

>3% is considered high risk and angiography should be offered within 72 hours or immediately if haemodynamically unstable.
PCI might be indicated as well.

Question 20

Diagnosis of STEMI.

Answer 20

Patient presenting with cardiac sounding chest pain

Persistent ST elevation or new LBBB. (If this shows up there is no need to do troponins)

ST elevation should be > 1 mm in limb leads and > 2 mm in chest leads.

hs-TnI should be > 100 ng/L and CK usually > 400

Question 21

When might transient ST elevation be seen?

Answer 21

Coronary vasospasms

Prinzmetal’s angina

Question 22

Diagnosis of NSTEMI.

Answer 22

Cardiac sounding chest pain and then do ECG

ST segment depression, T wave inversion or may be normal.

Do troponins hs-TnI frequently > 100 ng/L

Previously established ECG changes such as old MI, LV hypertrophy or A-fib may be present.

Diagnose if clinical + troponin is elevated and/or ECG changes with ST depression/T wave inversion

Question 23

Diagnosis of unstable angina.

Answer 23

Cardiac-sounding chest pain

ST segment depression, T wave inversion or may be normal.

hs-TnI will be within the normal reference range.

Question 24

What is required in very high risk patients of ACS?

Answer 24

Urgent coronary angiography within 2 hours

Question 25

What patients are included in very high risk patients?

Answer 25

Persistent or recurrent chest pain not responding to medical therapy. Clinical signs of heart failure or haemodynamic instability or cardiogenic shock. Life-threatening arrhythmias. (V-fib, VT)

Question 26

What is required in high-risk patients?

Answer 26

Coronary angiography within 24h.

Question 27

What is required in intermediate risk patients?

Answer 27

Coronary angiography within 72h.

Question 28

What is required in low-risk patients?

Answer 28

Managed initially with medical therapy but an invasive strategy with cardiac catheterisation is preferred in most patients.

Question 29

What is a CABG and IMA?

Answer 29

Question 30

What might ST depression in leads V1 to V4 suggest?

Answer 30

It can be a true posterior myocardial infarction and show be treated in the same manner as STEMI.

Question 31

In addition to the 12 ECG leads what should all patients routinely have?

Answer 31

Posterior (V7-V9) and right ventricular leads on or soon after admission. This is especially important in inferior STEMI as diagnostic changes may be transient.

Question 32

Pathophysiology of STEMI.

Answer 32

**Subendocardial** myocardial damage due to ischaemia. With continued ischaemia the infarct zone extends throug hto the **subepicardial** myocardium leading to a **transmural Q wave MI**.

Question 33

Clinical features of STEMI.

Answer 33

Severe chest pain lasting more than 20 minutes. Pain usually does not respond to sublingual GTN. Opiate analgesia usually req. Pain radiating to left arm, neck or jaw. Atypical symptoms such as dyspnoea, pre-syncope or syncope. Autonomic symptoms such as pale, clammy, marked sweating. Pulse may be thready or significant hypotension, bradycardia or tachycardia.

Question 34

Answer 34

Question 35

Sites of MI

Answer 35

Question 36

Conditions that can mimic STEMI on ECG.

Answer 36

Early repolarisation causes up-sloping ST elevation. Especially in V1 and V2. This is seen in younger and especially athletic patients. Concave ST elevation in pericarditis Brugada syndrome can look like an anterior STEMI Takotsubo cardiomyopathy

Question 37

Treatment algorithm in ACS without ST-elevation.

Answer 37

Monitor closely and record ECG while in pain. If SaO2 is less than 90% or dyspnoeic give low flow O2 with aim at \> 94%. Analgesia like morphine 5-10 mg IV + metoclopramide 10mg IV. GTN spray or sublingual tablets as required. Aspirin 300 mg loading then 75 mg OD. Measure troponin and risk assess via GRACE. IF low risk treat conservatively (no recurrence of chest pain, no signs of HF, normal ECG, -ve baseline troponin) May be discharged and arrange further outpatient investigations.

Question 38

Treatment algorithm in ACS without ST elevation if they are high-risk patient as per GRACE score.

Answer 38

High risk if: Rise in troponin or Dynamic ST or T-wave changes. And also have either diabetes, CKD, LVEF \< 40%, earling angina post MI, recent PCI, prior CABG. Give 2.5mg OD **fondaparinux** or subcut **LMWH** Second antiplatelet agents like **ticagrelor, clopidogrel** or prasugrel. **IV nitrate** if pain continues. **Oral betablocker** like bisoprolol 2.5 mg OD Follow prompt cardiologist review for angiography as per risk assessment if further deterioration.

Question 39

Mnemonic for management of NSTEMI.

Answer 39

B – **Beta blockers** unless contraindicated A – **Aspirin** 300mg stat dose T – **Ticagrelor** 180mg stat dose (clopidogrel 300mg is an alternative) M – **Morphine** titrated to control pain A – **Anticoagulant**: Low Molecular Weight Heparin (LMWH) at treatment dose (e.g. enoxaparin 1mg/kg twice daily for 2-8 days) N – **Nitrates** (e.g. GTN) to relieve coronary artery spasm

Question 40

Treatment algorithm for acute STEMI.

Answer 40

ECG monitoring and 12-lead ECG. IV access and take bloods (FBC, U&E, glucose, lipids, troponin, CK, HbA1c) + pain relief. O2 if required. Brief assessment of patient by history of CV disease. Examinations such as pulse, BP in both arms, JVP, murmurs, signs of CCF, upper limb pulsess, scars from previous cardiac surgery, CXR if it won't delay. Check if there are contraindications for PCI or fibrinolysis. Aspirin 300mg loading + prasugrel 60mg (or clopidogrel 300mg) loading. **If STEMI is on ECG and symptoms presented within 12h primary PCI can be administered within 120 minutes of the time of giving fibrinolysis - then do primary PCI.** If it is not possible then do fibrinolysis. Then transfer to primary PCI centre for either rescue PCI if fibrinolysis is unsuccessful or for angiography.

Question 41

When an ACS has settled and is no longer acute. What are further measures to be done?

Answer 41

Check for complications Symptom control Modify risk factors Cardioprotective medications

Question 42

Modification of risk factors post-ACS.

Answer 42

Stop smoking Identify and treat diabetes (T1DM aim for \< 7% HbA1c, TD2m aim for \< 6.5 - 7.5%). Identify and treat hypertension ( \< 140 mmHg) Identify and treat hyperlipidaemia ( LDL-C \< 1.8 mmol/L, 40% reduction in non-HDL C, total cholesterol \< 4.0 mmol/l) Dietary recommendations (oily fish, fruits, veggies and fibres) Encourage daily exercise Healthy weight Safe limits alcohol \< 14 units per week.

Question 43

Cardioprotective medications given post-ACS.

Answer 43

**5+1 As** **Aspirin** 75 mg OD and a **ADP-receptor blocker** (ticagrelor or clopidogrel) for at least 12 months. (Consider adding a PPI) **Atenolol** to maintain heart rate \< 60 bpm (1.25 mg OD) **ACE inhibitor** like ramipril (2.5 mg OD) or ARB (losartan 25mg OD) to prevent muscle overdamage. Renal function needs to be evaluated and dose is then uptitrated to maximally tolerated. **Atorvastatin** such as atorvastatin 80 mg OD to achieve \< 1.8 mmol/L LDL-C, 40% reduction in non-HDL C and total cholesterol \< 4.0 mmol/L Aldosterone antagonist in those with clinical heart failure.

Question 44

What is triple therapy post ACS?

Answer 44

Some patients with atrial fibrillation may be taking anticoagulation as well. Bleeding risk needs to be assessed by HAS-BLED. If 0-2 points then patient can receive triple thearpy for 6 months (aspirin, clopidogrel and warfarin) and then dual therapy of an antiplatelet and anticoag. If score is \> 2 they can receive triple therapy for 4 weeks and then dual therapy for a further 11 months.

Question 45

Answer 45

Acute anteroseptal STEMI. ST elevation and path Q waves in V1-V3 Ischaemic changes with ST segment depression are also seen in inferior leads II, III and AVF.

Question 46

Answer 46

Acute inferior wall STEMI. ST elevation and Q waves in inferior leads II, III and AVF.

Question 47

What is the primary choice of ADP in STEMI?

Answer 47

Prasugrel

Question 48

When should prasugrel be used in STEMI?

Answer 48

Undergoing PCI for STEMI Under age of 75 Weigh more than 60 kg No prior TIA or stroke.

Question 49

If the prasugrel criteria are not filled what can be given?

Answer 49

Clopidogrel. Ticagrelor can also be used.

Question 50

ECG changes in STEMI.

Answer 50

Question 51

Complications of MI.

Answer 51

Heart failure (Heart failure DREAD) D – Death R – Rupture of the heart septum or papillary muscles E – “Edema” (Heart Failure) A – Arrhythmia and Aneurysm D – Dressler’s Syndrome Ventricular septal defect Conduction disturbances

Question 52

Explain Dressler's syndrome post-MI.

Answer 52

A type of pericarditis due to an autoimmune reaction triggered by myocardial or pericardial damage. It usually occurs around 2-3 weeks after an MI

Question 53

Clinical features of Dressler's syndrome

Answer 53

Pleuritic chest pain Low grade fever Pericardial rub on auscultation. It can cause a pericardial effusion and rarely a pericardial tamponade (where the fluid constricts the heart and prevents function). A diagnosis can be made with an ECG (global ST elevation and T wave inversion), echocardiogram (pericardial effusion) and raised inflammatory markers (CRP and ESR).

Question 54

Treatment of Dressler's syndrome

Answer 54

**High dose aspirin first line** Management is with NSAIDs (aspirin / ibuprofen) and in more severe cases steroids (prednisolone). Colchicine can also be tried They may need pericardiocentesis to remove fluid from around the heart.