Acute Coronary Syndromes Flashcards
What do acute coronary syndromes (ACSs) include?
STEMI
NSTEMI
Unstable Angina
Simplified diagnosis of ACSs.
Clinical history
12 lead ECG
Biochemical markers
What biochemical markers are used to investigate ACSs?
Troponin T
Troponin I
Creatine kinase-MB (CK-MB)
Five types of MI.
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
Pathophysiology common to all ACSs.
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.
Clinical features of ACS.
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
What is a silent MI?
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”.
Investigations done in ACSs.
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.
If the initial troponin assay is negative, what should be done?
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
What does troponin levels tell us about the ACSs?
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.
Explain the relationship between troponin I and risk of death in ACS.
Explain the regimen of carrying out troponin assays.
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.
How does rising and/or falling cardiac troponin levels differentiate acute from chronic cardiomyocyte damage?
The more pronounced the change, the higher the likelihood of acute MI.
In males, what levels of hs-TnI suggests a high likelihood of myocardial necrosis?
> 34 ng/L
In females, what levels of hs-TnI suggests a high likelihood of myocardial necrosis?
> 16 ng/L
What else might increase your troponin levels?
Advanced renal failure
Large PE
Severe congestive cardiac failure
Myocarditis
Aortic dissection
Aortic stenosis
Hypertrophic cardiomyopathy
Takotsubo cardiomyopathy
Malignancy
Stroke
Sepsis
How is risk stratification done in NSTEMI and unstable angina?
TIMI score and GRACE score
Explain TIMI score for NSTEMI and UA
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.
Explain the GRACE score.
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.
Diagnosis of STEMI.
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
When might transient ST elevation be seen?
Coronary vasospasms
Prinzmetal’s angina
Diagnosis of NSTEMI.
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
Diagnosis of unstable angina.
Cardiac-sounding chest pain
ST segment depression, T wave inversion or may be normal.
hs-TnI will be within the normal reference range.
What is required in very high risk patients of ACS?
Urgent coronary angiography within 2 hours
What patients are included in very high risk patients?
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)
What is required in high-risk patients?
Coronary angiography within 24h.
What is required in intermediate risk patients?
Coronary angiography within 72h.
What is required in low-risk patients?
Managed initially with medical therapy but an invasive strategy with cardiac catheterisation is preferred in most patients.
What is a CABG and IMA?
What might ST depression in leads V1 to V4 suggest?
It can be a true posterior myocardial infarction and show be treated in the same manner as STEMI.
In addition to the 12 ECG leads what should all patients routinely have?
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.
Pathophysiology of STEMI.
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.
Clinical features of STEMI.
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.
Sites of MI
Conditions that can mimic STEMI on ECG.
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
Treatment algorithm in ACS without ST-elevation.
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.
Treatment algorithm in ACS without ST elevation if they are high-risk patient as per GRACE score.
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.
Mnemonic for management of NSTEMI.
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
Treatment algorithm for acute STEMI.
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.
When an ACS has settled and is no longer acute.
What are further measures to be done?
Check for complications
Symptom control
Modify risk factors
Cardioprotective medications
Modification of risk factors post-ACS.
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.
Cardioprotective medications given post-ACS.
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.
What is triple therapy post ACS?
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.
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.
Acute inferior wall STEMI.
ST elevation and Q waves in inferior leads II, III and AVF.
What is the primary choice of ADP in STEMI?
Prasugrel
When should prasugrel be used in STEMI?
Undergoing PCI for STEMI
Under age of 75
Weigh more than 60 kg
No prior TIA or stroke.
If the prasugrel criteria are not filled what can be given?
Clopidogrel.
Ticagrelor can also be used.
ECG changes in STEMI.
Complications of MI.
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
Explain Dressler’s syndrome post-MI.
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
Clinical features of Dressler’s syndrome
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).
Treatment of Dressler’s syndrome
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.
