Medicine

Acute Coronary Syndrome (ACS). Background | by Aayush Pokharel | Sep, 2021

Aayush Pokharel

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.
  • SOB
  • Sweating
  • Nausea and vomiting.
  • Sometimes no symptoms at all: ‘silent MI’.

Signs:

  • HR and BP may be ↑ or ↓.
  • Pallor
  • S3 or S4 heart sounds (especially in STEMI).

ECG:

  • 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.

Other investigations:

  • 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).

Anticoagulation:

  • 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.

NSTEACS:

  • 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.

Other issues:

  • 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.

Electrical:

  • 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.

Structural:

  • 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.

Inflammatory:

  • 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:

  • βblocker.
  • 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.

Territories:

  • 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.

Other findings:

  • 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.
  • PE
  • Brugada syndrome: coved (type 1) or saddle (type 2) ST elevation in V1–3, with T wave inversion.
  • Hyperkalaemia
  • 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.

This information was taken from Medicos PDF app. You can download this app from Google Play Store for free.


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