Rupture of atheromatous plaque in coronary artery → thrombus formation → vessel occlusion locally or elsewhere in the heart.
The 3 acute coronary syndromes are:
- ST elevation myocardial infarction (STEMI): ↑troponin and ST elevation on ECG. In practice, the ST elevation alone is sufficient to treat as the troponins take time to rise.
- Non-ST elevation MI (NSTEMI): ↑troponin and ischaemic symptoms or ECG changes.
- Unstable angina: prolonged, severe angina, usually at rest, possibly with ECG changes. NSTEMI and unstable angina are often grouped together as non-ST elevation ACS (NSTEACS)
Classification by cause:
- Type 1: atherosclerotic plaque rupture. Commonest.
- Type 2: imbalance in myocardial O2 supply and demand e.g. because of anaemia, ↑heart rate, ↓BP, arterial spasm, embolism, or arrhythmia. May happen during surgery or illness.
- Type 3: sudden cardiac death with ischaemic features (on ECG, angiography, or autopsy) but before troponin could be checked.
- Type 4: MI during PCI.
- Type 5: MI during CABG.
Evaluate chest pain using SOCRATES:
- Site: central.
- Onset: usually sudden but can be more gradual.
- Character: tight, crushing, but not sharp.
- Radiation: left arm, neck, jaw. Less commonly right arm, epigastrium, back.
- Associated symptoms: sweating, clamminess, SOB, dizziness, faint, angor animi (an impending sense of doom).
- Timing: duration >15 minutes.
- Exacerbating factors: Exertion, Emotion, Eating. Relieving factors: ACS less likely if relieved by GTN
- Severity: high but can atypically be low.
Atypical presentations, more commonly seen in elderly or diabetic patients:
- Little or no chest pain.
- Nausea and vomiting.
- Sometimes no symptoms at all: ‘silent MI’.
- HR and BP may be ↑ or ↓.
- S3 or S4 heart sounds (especially in STEMI).
- Do immediately, and if negative repeat after 20 minutes if pain continues or suspicion is high.
- See ECG findings in acute coronary syndrome.
Troponin T or I:
- Test on admission and at 3–6 hours. Troponin peaks at 12–24 hours, then declines over 10 days.
- Values >99th centile are diagnostic of acute MI. STEMI diagnosis is initially from the ECG alone so as not to delay treatment.
- Causes of ↑troponin, HEART DIES: HF, Embolus (pulmonary), AF, Renal failure (due to ↓clearance), Thrombus (acute MI), Dissection of the aorta, Inflammation (myo/pericarditis), Excercise (very strenuous), Sepsis.
- FBC: ↓Hb may exacerbate heart strain, and baseline Hb and PLT needed before anticoagulation.
- U+E: baseline before anticoagulants and ACEi, and screens for co-morbid renal disease from HTN.
- Glucose: tight control improves outcomes.
- Lipids: check on admission, as cholesterol can dip 24 hours post-MI.
- CXR: rule out other causes and check for HF.
- Exercise tolerance test: consider in ↓risk patients.
Initial medical treatment:
- Dual antiplatelet therapy: aspirin and P2Y12 inhibitor (clopidogrel, ticagrelor, or prasugrel [preferred if undergoing PCI]). Loading dose for both.
- Analgesia PRN: morphine IV and/or nitrates (oral spray, sublingual tablet, or IV infusion in refractory chest pain).
- Other therapies: oxygen if hypoxemic, β-blockers IV if tachycardic/hypertensive (but not if unstable).
- Unfractionated heparin or bivalirudin IV in those going for immediate or early angiography. Glycoprotein IIb/IIIa inhibitor IV (eptifibatide, tirofiban, or abciximab) is sometimes added as an adjunctive antiplatelet, but not routinely.
- Fondaparinux or enoxaparin SC for those without angiography planned.
STEMI presenting within 12 hours of onset:
- Immediate (within 90–120 mins) primary PCI (percutaneous coronary intervention) i.e. dilation of artery with balloon catheter ± stent placement.
- If PCI not available within 120 mins, consider thrombolysis (alteplase, reteplase, or tenecteplase) and transfer to PCI centre.
- Patients presenting beyond 12 hours are essentially managed like NSTEMI.
- Angiography ± revascularisation within 72 hours (‘early invasive strategy’) if 6 month mortality risk >3% as per GRACE or TIMI score. Revascularisation is usually PCI, but sometimes CABG if left main or triple vessel disease.
- Immediate PCI if unstable, refractory chest pain, or acute severe heart failure.
- Conservative management otherwise.
Start BAGS within 24 hours:
- β-blocker PO e.g. metoprolol, atenolol. Started in the acute phase as it prevents recurrent ischaemia and arrhythmias. May initially be given IV (see ‘Initial medical treatment’ above).
- ACEi, especially if ↓LVEF, but even others benefit.
- Maintain Glucose
- Statin. Evidence of short-term benefit is unclear, but it will be needed for secondary prevention anyway.
- Anticoagulation is usually stopped post-PCI, or continued until discharge in those managed without reperfusion. However, it is continued for 3 months in anterior MI.
- Discharge on CVD secondary prevention medication and offer cardiac rehab.
- Avoid NSAIDs, especially diclofenac.
⅓ of MIs are fatal: 20% pre-hospital, and a further 10% within 30 days.
- Heart block or sinus bradycardia following inferior MI (right coronary artery) as supply to the AV and SA node is disrupted.
- Bundle branch block following anterior MI (left anterior descending artery).
- Ventricular fibrillation.
- Acute mitral regurgitation.
- Papillary muscle rupture.
- Ventricular free wall rupture leading to haemopericardium.
- Ventricular septal rupture. Causes pan-systolic murmur. May lead to cardiogenic shock days later.
- Ventricular aneurysm: blood pools under dyskinetic, thin area of LV wall. Causes persistent (>6 weeks) ST elevation.
- Peri-infarction pericarditis.
- Dressler’s syndrome: pericarditis weeks later.
Myocyte death + ↓stroke volume → ↓HR + ↓BP → sympathetic neurohumoral response + LV changes → HF.st
Offered as primary prevention — especially in those with diabetes or >10% 10 year risk of CVD — or as secondary prevention, post ACS, PVD, or stroke.
- The 10 year risk of MI or stroke can be quantified using CVD risk calculators such as QRISK2 (if age <85) or the Framingham risk equation.
- This is appropriate for people with intermediate risk and without previous CVD events, but less useful for people with major risk factors (e.g. severe dyslipidaemia).
- Those with previous CVD (MI, stroke, PVD) automatically have a 10 year risk >30%.
- Weight loss and dietary change. The Mediterranean diet (fruit, veg, olive oil, fish) has the most evidence for CVD prevention. Also recommend reducing sugar intake and replacing starch with wholegrains.
- Physical activity: 150 minutes/week moderate activity.
- Smoking cessation.
- Reduce alcohol intake: ≤14 units/week
Involves modifying risk factors, namely hypertension, dyslipidaemia, and diabetes.
Secondary prevention post-ACS
Block An ACS:
- ACE inhibitor, aiming for BP of 140/90.
- Aspirin for life.
- Clopidogrel or ticagrelor for 1 year after an ACS.
- Statin: high dose e.g. atorvastatin 80 mg.
Changes over time:
- Acute: peaked T waves (
- Within days: Q waves then T wave inversion. Occasionally, transient Q waves appear much earlier.
- Long-term: Q waves, ST changes.
- Inferior MI (right coronary artery): STE in II-III-aVF, with reciprocal ST depression in lateral leads. If there is also STE in V1–2, consider right-sided ECG — with the chest leads flipped across — to look for RV infarction (STE in V5R-6R) due to RCA occlusion proximal to the RV marginal branch. 10% of inferior MIs are due to LCX infarction (inferolateral MI).
- Anterior MI (left anterior descending): STE in V1–4, with V1–2 septal; reciprocal ST depression in inferior leads (especially III and aVF).
- Lateral MI (left circumflex): STE in I-aVL-V5–6. If aVR affected too, suggests left main artery. Inferior leads may have reciprocal ST depression, or STE in inferolateral STEMI.
- Posterior MI: peaked R and ST depression in V1–3. Add posterior leads (V7–9) if found. Often associated with inferior (RCA) or lateral (LCX) MI.
- LBBB with positive modified Sgarbossa criteria.
- Left axis deviation in anterior MI.
- Sinus bradycardia or heart block in inferior MI.
Other causes of ST elevation:
- Benign early repolarisation (BER, aka high take off): concave up (saddle) ST elevation
- Pericarditis: diffuse, concave up ST elevation. Myocarditis: similar to pericarditis, though sometimes ST elevation may be localised and mimic STEMI.
- LVH: LV strain pattern causing ST elevation in V1–3.
- Aortic dissection: can cause MI if it extends proximally to the coronary ostia, the holes in the aortic valve which supply the coronary arteries. Do not thrombolyse, as there is a risk of cardiac tamponade.
- LBBB and RBBB.
- Brugada syndrome: coved (type 1) or saddle (type 2) ST elevation in V1–3, with T wave inversion.
- ST depression and/or T-wave inversion.
- Note that T-wave inversion is normal in aVR, where it is concordant with the QRS complex (dominant S waves). In children they are also seen in V1 and V2, and their persistence in adulthood is the non-pathological ‘persistent juvenile T-wave pattern’.
- Unlike in STEMI, difficult to localise lesion based on ECG.