Case 3: ACS - STEMI Flashcards
Role of atherosclerotic plaque in ACS
Atherosclerotic plaque – fatty plaques (atheroma) can start building up on the inside walls of the coronary arteries. This is due to damage to the vessel wall, often caused by smoking or hypertension, which leads to infiltration of cholesterol into the vessel wall, causing inflammation and subsequent infiltration of WBCs. Over the years, the build up of these plaques increases, and they become larger. As a result, the arteries gradually become narrower and less elastic, resulting in less room for blood to flow through. At this stage, chest pain (angina) may be experienced.
Role of platelets + coagulation system in ACS
– if the atherosclerotic plaque is ruptured, this can trigger the coagulation system to activate and aggregate platelets. When platelets are activated, thrombin-induced conversion of fibrinogen to fibrin occurs and the formation of a fibrin mesh that traps platelets, which results in a thrombus or blood clot on the plaques.
This can block the artery, which cuts off the blood flow through that artery to that part of the heart, resulting in a heart attack occurring.
Likely risk factors for Coronary artery disease
Non-modifiable:
- family history
- older age
- male sex (greater risk than females)
Modifiable
- Smoker (2-4 times more likely to get heart attack)
- High BMI
- High cholesterol
- High BP
- Sedentary lifestyle
Symptoms suggestive of ACS
- Chest pain and/or pain in areas such as the upper arms, back or jaw, that lasts longer than 15 minutes
- Chest pain in combination with nausea and vomiting, sweating, breathlessness, and particularly a combination of all these symptoms
- Chest pain in combination with dizziness or feeling light-headed
- New onset chest pain, or a sudden deterioration in previously stable angina, with chest pain episodes lasting longer than 15 minutes, recurring frequently, following little or no exertion
When might fibrinolytic therapy be an appropriate revascularisation in STEMi
- if patients with MI - transportation delay
- NZ guidelines: pre-hospital fibrinolysis for STEMI patients if PCI cant be performed within 2 hours (no C/I)
STEMI: initial treatment (on the way/upon arrival to hospital)
○ Sublingual GTN – 1-2 sprays under the tongue at symptom onset; symptom relief for chest pain with a cardiac cause
○ IV morphine – e.g. 5 -10 mg (2.5 – 5 mg for older or frail patients) IV at 1–2 mg/minute, repeat if necessary; effective for severe pain for patients with ACS
○ IV antiemetic, e.g. metoclopramide 10 mg or cyclizine 25 mg, is usually administered at the same time as, or immediately prior to, IV morphine.
○ Dispersible aspirin – 300 mg; should be given to all patients with an ACS, including those already taking aspirin, if enteric coated aspirin is the only formulation available the patient should chew the tablet. Treatment with aspirin 75 – 150 mg, daily, is then continued indefinitely in all patients unless there are contraindications
○ Clopidogrel – 300 mg (75 mg for patients aged over 75 years) given immediately along with aspirin; 300 mg, is recommended for patients with an ACS who also have evidence of ischaemia on ECG or elevated serum troponin levels. Clopidogrel is then continued at a dose of 75 mg, daily (with aspirin), for these patients.
STEMI: acute management
Antiplatelet agents
- Time of first medical contact (all ACS) - non-enteric coated aspirin 162-325mg
- maintenance daily dose: 81mg
- P2Y12 inhibitor (prasugrel or ticagrelor, if C/I use clopidogrel ) - loading dose asap or at time of PCI - followed by daily dose for at least 1 year
- Eptifibatide (Glycoprotein IIb/IIIa inhibitor) IV : if no reflow + thrombotic complication
Anticoagulant agents
- Parenteral: recommended for all patient w ACS/ during primary PCI
- Enoxaparin (more effective than UFH)
- typically discontinued after uncomplicated PCI
Combined OAC + antiplatelet therapy
- elevated risk of AF, mechanical heart valves, venous thromboembolism, hypercoagulable disorders
- triple therapy (vitamin k antagonist + DAPT) = short as possible - risk of bleeding
Coronary reperfusion: PCI or IV fibrinolytic therapy
- PCI (within 90 mins of FMC)
w onset of symptoms within last 12 hrs
STEMI w cardiogenic shock (regardless of timing)
Advantage of primary PCI over fibrinolysis
- lower rates of early death, reinfarction, intracranial haemorrhage
- however: if PCI delayed >120 mins - fibrinolytic therapy should be given
Benefits of antiplatelet therapy before PCI
Pre PCI – Reduces platelet aggregation and thrombosis. This is usually aspirin + another antiplatelet agent (ticagrelor, prasugrel or clopidogrel) as well as an anticoagulant (heparin).
• If there is significant thrombus burden or if on re-opening of the vessel there is suboptimal blood flow
- Glycoprotein IIb/IIIa inhibitors (tirofiban, abciximab or eptifibatide) as an infusion can be added to provide rapid onset of antiplatelet activity before the patient is taken to the catheterization laboratory or for prevention and treatment of periprocedural thrombotic complications.
- However, these are potent antiplatelet agents so there is an associated risk of bleeding that needs to be considered.
• Chewing aspirin a single dose of aspirin 300mg to allow for rapid systemic delivery (pre-hospital setting)
Benefits of antiplatelet therapy post PCI
Post PCI - DAPT (dual antiplatelet therapy) reduces the likelihood of stent thrombosis as the stent is a foreign body that increases the risk of platelet aggregation and eventual thrombus formation.
Clopidogrel: Indication, PK, Antiplatelet effects, Interactions
Indication: Preferred in association with fibrinolytic therapy – given after for a min of 1 month and a max of 1 year
NSTEMI - indicated at the time of presentation for patients treated with either an early invasive strategy or an ischemia-guided strategy
Preferred in patients who have high risk of bleeding
PK: Efficacy relies on its conversion (by the CYP2C19 enzyme) to its active metabolite.
Patients in the pharmacogenetic group who have a reduced function allele (CYP2C19 *2 or *3) are assigned to ticagrelor.
Antiplatelet effects: Less potent and effective than prasugrel and ticagrelor
Interactions: Manufacturers recommend that omeprazole or esomeprazole should not be used with clopidogrel as it can reduce levels of clopidogrel and thus, clopidogrel-induced antiplatelet effects
Prasugrel: Indication, PK, Antiplatelet effects, Interactions
Indication: Preferred in primary PCI
NSTEMI - managed with an early invasive approach at the time of stenting
Preferred in patients who are not at high risk of bleeding (e.g., those without a history of stroke or transient ischemic attack)
Not indicated in patients with ACS in whom coronary anatomy is not known and an indication for PCI is not clearly established, with the exception of STEMI patients scheduled to undergo immediate coronary catheterization and PCI, if clinically indicated.
PK: Achieves a faster, greater, and more consistent degree of P2Y12 inhibition as compared to clopidogrel.
Prasugrel requires two metabolic steps for formation of its active metabolite, which is chemically similar to the active metabolite of clopidogrel.
Antiplatelet effects: More potent and effective than clopidogrel
Interactions: No interaction between concomitant use of PPIs and prasugrel has been observed.
Ticagrelor
Indication: Preferred in primary PCI
NSTEMI - indicated at the time of presentation for patients treated with either an early invasive strategy or an ischemia-guided strategy
Preferred in patients who are not at high risk of bleeding (e.g., those without a history of stroke or transient ischemic attack)
PK: Belongs to a novel chemical class, cyclopentyl triazolopyrimidine, and is a direct oral, reversibly binding P2Y12 inhibitor with a plasma half-life of ∼12 h.
Antiplatelet effects: More potent and effective than clopidogrel
Interactions: No interaction between concomitant use of PPIs and ticagrelor has been observed.
Secondary prevention recommended for patient post STEMI - how can pharmacist support this?
Recommendation: - post STEMI
• DAPT (aspirin + P2Y12 inhibitor) for a year following discharge
• ACE inhibitor to reduce his BP; if contraindicated or not tolerated, then an ARB
• Beta blocker to reduce his BP and slow HR
• High intensity statin to reduce his cholesterol levels – atorvastatin 80mg or rosuvastatin 20mg or 40mg
• Sublingual glyceryl trinitrate (GTN) to provide immediate relief of chest pain
Pharmacist support:
- how to take medicines
- why they need to take medicines (any specific monitoring or blood tests required)
- info about other medicines - OTC to avoid, herbal remedies, slidenafil - referred to doctor for more info - risk of hypotension + avoid use of GTN spray for 12-24 hrs after dose of slidenafil
- common adverse effects + action
- how to obtain further medicine supply
- missed doses
- lifestyle changes - smoking cessation, diet, exercise, weight loss, sensible alcohol intake
