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3.1 Acute Coronary Syndromes (ACS)
Acute Coronary Syndromes (ACS)
Learning Outcomes
Describe the spectrum of ischaemic heart disease and compare and contrast chronic stable angina with the acute coronary syndromes
Explain the pathophysiology of the acute coronary syndromes
List the diagnostic criteria including ECG changes and troponins
Describe the initial management of acute chest pain (suspected ACS)
Define ST-segment Elevation Myocardial Infarction (STEMI) and describe the options for its initial (acute) treatment and long-term treatment
Define Non-ST-segment Elevation Acute Coronary Syndromes (NSTACS) and describe the options for the initial (acute) treatment and long-term treatment
Describe the pharmacology of the antiplatelet drugs used as part of the treatment protocols discussed.
Introduction to ACS
Ischaemic heart disease (IHD) is an umbrella term that includes a spectrum of disorders ranging from chronic stable angina through to unstable angina and myocardial infarctions (also known as heart attacks).
Patients with stable angina have chronic, stable symptoms. In contrast, the acute coronary syndromes are situations whereby there are new or worsening symptoms associated with a sudden obstruction of coronary blood flow.
The acute coronary syndromes comprise of the following:
It is also important to remember that the IHD spectrum can be progressive. For example, unstable angina can progress to a NSTEMI which can progress suddenly to a STEMI.
The ACS involve some degree of myocardial ischaemia. It is the extent and severity of the ischaemia that differs. As we progress to the right of the diagram, the ischaemia becomes more severe and lasts longer. When the ischaemia is severe and persistent enough to cause permanent damage to the myocardium, the result is a myocardial infarction of some type (NSTEMI or STEMI & we’ll discuss the differences later in this module). Such major cardiovascular events can result in cardiac arrest and death. If the person does survive, they may be left with impaired heart function, for example a diagnosis of heart failure and/or a dysrhythmia.
🎞️ Video 1: Watch the following video, “What is a heart attack?” ⏲️1:51 mins
🎞️ Video 2: Watch the following lecture video, “ACS Part 1″ ⏲️13:42 mins
Diagnostic Tests
When it comes to diagnosis, the clinical presentation will be important. There will often be key diagnostic factors like central crushing chest pain as well as other symptoms like dyspnoea or nausea/vomiting. But there will also be an assessment of the patient’s atherosclerotic risk factors, which were discussed last week. For example, the physician will consider if the patient has hypertension, dyslipidaemia, diabetes, if they are a smoker, if they have a family history of heart disease, and so on.
Once all of that has been considered, the key investigations that follow will be an electrocardiogram (ECG) and a blood test that includes an order for cardiac biomarkers (i.e., a high-sensitivity troponin assay).
Image adapted from: Australian National Heart Foundation ACS Treatment Algorithm 2011
The Electrocardiogram (ECG)
As soon as an acute coronary syndrome is suspected (even if there is only a tiny bit of suspicion that the patient might be having an acute coronary event), the patient will receive a 12-lead ECG. That will be reviewed by an experienced physician within 10 minutes of the patient’s presentation to an emergency department.
The ECG will be repeated every 10-15 minutes generally until the patient is pain-free and a cardiologist has approved cessation of the ECG monitoring. Telemetry may be an alternative to serial ECG monitoring. Telemetry is continuous monitoring of a patient’s heart rate and rhythm.
The most important ECG change that ED physician is looking for is ST segment elevation. This is so important because it plays a large role in dictating the treatment protocol the patient receives. For example, for patients with ST elevation, there is a proven benefit associated with using immediate reperfusion therapy (either by fibrinolytic medication or by percutaneous coronary intervention with stenting). In contrast, fibrinolytic medication is not used if there is no ST-segment elevation on the ECG. This will be discussed more later on.
Troponin is a protein that lives in myocardial cells. There are different types (TnC, TnI, and TnT), but TnI is most commonly used for diagnosing ACS. Raised levels of troponin in the blood signifies myocardial injury.
In October 2018, Queensland Health Hospitals introduced a new high-sensitivity cardiac troponin assay. This new assay can reliably detect circulating troponin at lower levels.
Historically, troponin levels were checked on presentation and then again 6 hours later (i.e., at 0 and 6 hours). Now, troponin levels are checked on presentation and then again 3 hours later (i.e., at 0 and 3 hours). If troponin levels return normal on both occasions, it is unlikely that the person has had a myocardial infarction.
If a patient has had a myocardial infarction, after approximately 3 hours have elapsed, you would expect troponin levels to be higher than they were at the initial presentation. This is because TnI leaks out of myocardial cells slowly. TnI also persists in the bloodstream for anywhere between 4 and 7 days, which makes it difficult for us to use TnI to diagnose a second myocardial infarction within 7 days of the first one!
It is also important to note that the turn-around time (the time it takes for the troponin result to be returned from the laboratory) can be variable (up to approximately 50 minutes). So…. if there is ST elevation on the ECG, troponin will be tested and it will be positive, but we don’t wait for the blood to be collected and for the troponin results to return from the lab before reacting to the ST elevation seen on the ECG trace. That is to say, cardiac biomarkers are not necessary to confirm the diagnosis of STEMI. Troponin levels are, however, necessary to differentiate the NSTEACS (i.e. NSTEMI vs. unstable angina). Raised troponin levels will confirm the diagnosis of NSTEMI.
Initial Management of ACS
Time is heart muscle (and mortality) !! First steps:
Seek medical help, call an ambulance!
Paramedics will:
Notify hospital emergency department of impending arrival
12 lead ECG
Monitor vital signs
E.g. blood pressure, heart rate, respiratory rate, oxygen saturation, temperature, etc.
Give aspirin 300mg orally (chewed or dissolved) unless contraindicated
Give sublingual GTN spray 400micrograms every 5 minutes if pain persists
Up to a total of 3 doses if tolerated
Give an intravenous opioid if necessary for persistent chest pain, e.g., morphine 2.5 – 5mg IV every 5 – 10 minutes if necessary (monitor sedation score and blood pressure)
Give oxygen (only if necessary, i.e., if the patient’s oxygen saturation is less than 94%).
🎞️ Video 3: Watch the following lecture video, “ACS Part 2″ ⏲️9:06 mins
📚 Read/Explore
Compare and contrast the following in a table:
NSTEACs
STEMI
Unstable Angina
NSTEMI
STEMI
Pathophysiology
Diagnosis
Management of STEMI
There are important differences when it comes to the management of a STEMI and the NSTEACS (unstable angina or NSTEMI). These are directly related to the aims of treatment.
For patients with a confirmed STEMI who have presented to the emergency department within 12 hours of symptom onset, emergency reperfusion therapy is indicated.
Note that ‘percutaneous coronary intervention’ is commonly abbreviated to ‘PCI’. This is synonymous with ‘percutaneous transluminal coronary angioplasty’ or ‘PTCA’ that was introduced in week 1 on the possible surgical management of stable angina.
🎞️ Video 4: Watch the video below for a reminder about what this is referring to. ⏲️1:08 mins
Fibrinolysis is the use of an intravenous medication (Tenecteplase, Reteplase, or Alteplase) that works to dissolve the clot that has formed in the coronary artery. The pharmacology of these thrombolytics will be discussed in the week 5 lecture on anticoagulation.
“For the purposes of reperfusion therapy, PCI is preferred over fibrinolysis if it can be performed within 90 minutes of the first medical contact. Otherwise, fibrinolytic therapy is preferred for those without contraindications.”Source: National Heart Foundation of Australia & Cardiac Society of Australia and New Zealand. Australian Clinical Guidelines for the Management of Acute Coronary Syndromes 2016.
Note the following contraindications to fibrinolytic therapy (not an exhaustive list, consult product information, and note that each patient requires individual assessment with regards to risk vs benefit of proceeding with thrombolysis).
Known hypersensitivity (allergy) to the active ingredient or to gentamicin (a trace residue from the manufacturing process)
Active bleeding (excluding menses) or significant bleeding disorder
Severe thrombocytopenia
Prior intracranial or subarachnoid haemorrhage
A structural cerebrovascular lesion (e.g., arterial aneurysm or arteriovenous malformation)
Malignant intracranial neoplasm (primary or metastatic)
Ischaemic stroke or transient ischaemic attack (TIA) within the previous 6 months
Severe uncontrolled hypertension (i.e., BP >180/110mmHg)
Trauma or major surgery (especially involving the head and/or face) within the previous 3 months
Non-compressible vascular punctures in the past24 hours (e.g., lumbar puncture)
Suspected aortic dissection
Severe hepatic dysfunction, including hepatic failure, cirrhosis, portal hypertension, and active hepatitis
Active peptic ulcer within the previous 3 months
Prolonged or traumatic CPR (> 2 minutes) within the previous 10 days
Current therapeutic anticoagulation for another indication
Early management of a STEMI also includes adjuvants to reperfusion therapy.
You may find the following algorithm from the eTG useful in following the management of STEMI. Note that the timeframe primarily used to determine whether PCI or fibrinolysis is used in 120 minutes but in the NHF ACS guidelines the time referenced is 90 minutes. You will also note that even after fibrinolysis is performed, arrangements should be made to immediately transfer the patient to a PCI-capable hospital for further management.
🎞️ Video 5: Watch the following lecture video, “ACS Part 3” ⏲️20:31 mins
Management of NSTEACS
Management of the NSTEACS is a little bit more complicated than management of STEMIs. It can help to remember the aims of treatment.
Unstable angina and the NSTEMI are considered a continuum and both are treated under the overarching term that is NSTEACS. The chosen treatment regimen depends on an initial risk assessment. Patients with confirmed NSTEACS are classified as having either a very high, high, or intermediate or low acute risk of a recurrent cardiovascular event and mortality. NHF ACS Guidelines or eTG guidelines can be followed to guide management of NSTEACs. See below for the algorithms to stratify NSTEACs as very high-, high-, intermediate-risk or low risk.
Specifically, this risk assessment determines when a patient with confirmed NSTEACS should undergo invasive management with PCI or CABG. Remember that fibrinolytic therapy is NEVER used to treat NSTEACS.
Very high risk = PCI or CABG recommended within 2 hours of presentation
High risk = PCI or CABG recommended within 24 hours of presentation
Intermediate risk = PCI or CABG recommended within 72 hours of presentation, but angiography may be delayed and completed post-discharge if this is deemed clinically and logistically appropriate by the cardiologist in consultation with the patient and their family
Low risk = Further monitoring and investigations are required. Consider later outpatient cardiac assessment.
A summary of NSTEACS management is outlined in the table below:
Secondary Prevention of all ACS
Non-adherence with medications prescribed for secondary prevention of ACS can be a real issue for a number of reasons. When a patient is ready to be discharged from hospital, they are given a massive amount of information all at once – follow up GP and specialist appointments, information about their cardiac diagnosis, non-pharmacological advice (including exercises from the physiotherapist and dietary advice from the dietitian) AND very often a BIG bag of NEW medications associated with extensive verbal counselling from the pharmacist and printed CMIs. Sometimes, certain medications are not available at the patient’s community pharmacy and must instead be sourced only through the hospital pharmacy. This can be a significant barrier to adherence, especially for patients who live in rural towns. Think about the role pharmacists can play in encouraging and facilitating adherence to long-term medications.
🎞️ Video 6: Watch the following lecture, “ACS Part 4″⏲️15:29 mins
Create a new NPS MedicineWise account if you don’t have one already.
Note that the case used in this module reports a troponin level that is raised initially, but you are later informed that the repeat level returns to normal, hence the diagnosis of unstable angina as opposed to NSTEMI.
The pharmacological treatment regimen suggested in the module is appropriate for a high-risk NSTEACS diagnosis.
Pharmacology of Antiplatelet Drugs
We introduced antiplatelet drugs in week 1 when we discussed secondary prevention of stable angina. We will revise antiplatelets as part of secondary prevetion of ACS.
🎞️ Video 7: Watch the following lecture, “ACS Part 5” ⏲️30:26 mins
Once you have revised this material, you should be able to:
Understand the normal haemostatic response to vascular injury.
Understand the mechanism of action of the 3 main antiplatelet drug classes (aspirin, P2Y12 antagonists, and glycoprotein IIb/IIIa inhibitors).
Understand why glycoprotein IIb/IIIa inhibitors are the most potent of the available antiplatelets.
Explain why non-steroidal anti-inflammatory drugs (NSAIDs) should not be taken by patients with cardiovascular disease.
List the common side effects associated with any given antiplatelet drug.
Download the lecture notes here:
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