Acute Coronary Syndrome: Overview

Acute Coronary Syndrome (ACS) NSTEMI USA ❤️

📊 Risk Scores Quick Links

• 🧮 TIMI Risk Score (MDCalc)
• 📊 GRACE Risk Score (MDCalc)

🖼️ Illustrations

💡 Teaching Pearl: NSTE-ACS is risk-based medicine.
🔹 Unstable physiology → immediate cath lab.
🔹 Stable but >3% 6-month mortality (GRACE) → angiography within 72 hours.
🔹 Low risk (≤3%) → conservative strategy is reasonable, but ensure LV function assessment and appropriate ischaemia testing/follow-up.

📚 References (guidelines)

• NICE NG185: Acute coronary syndromes (overview)
• NICE NG185: Recommendations (UA/NSTEMI antithrombin, DAPT, GRACE risk, invasive strategy)
• NICE NG185: Visual summary - NSTEMI/Unstable angina early management (PDF)
• ESC 2023: Acute Coronary Syndromes guideline (ACS including NSTE-ACS)

Acute Coronary Syndrome (ACS) STEMI ❤️

📊 Initial Management of Acute STEMI

Site of Coronary Artery Occlusion in STEMI

1. Right coronary artery occlusion
   • ST depression in lead I
   • ST elevation in lead III greater than in lead II
   a. Proximal occlusion

   • ST elevation more than 1 mm with positive T wave in lead V₄R
   b. Distal occlusion

   • ST isoelectric with a positive T wave in lead V₄R
2. Left circumflex artery occlusion
   • ST elevation in lead II greater than lead III
   • ST isoelectric or elevated in lead I
   • ST isoelectric or depressed with negative T wave in V₄R
   a. Extension to posterior wall

   • ST depression in precordial leads
   b. Extension to lateral wall

   • ST elevation in leads I, aVL, V₅, and V₆
3. Left anterior descending artery occlusion
   a. Proximal to first septal branch and first diagonal branch

   • ST elevation in leads aVR and aVL
   • ST depression in leads II, III, and aVF
   • ST elevation in lead V₁ (> 2 mm) and leads V₂ to V₄
   • ST isoelectric or depressed in leads V₅ and V₆
   • Acquired intra-Hisian or RBBB may occur
   b. Distal to first septal branch, proximal to first diagonal branch

   • ST elevation in lead I and aVL
   • ST depression in lead III (lead II is isoelectric)
   • ST elevation in leads V₂ to V₆ but not in lead V₁
   c. Distal to first diagonal branch, proximal to first septal branch

   • ST depression in lead aVL, highest in lead III
   • ST elevation in inferior leads, highest in lead III
   • ST elevation in leads V₁ to V₄
   d. Distal LAD

   • ST depression in aVR
   • ST elevation in inferior leads, highest in lead II
   • ST elevation in leads V₃ to V₆
4. Left main coronary artery occlusion
   • ST elevation in lead aVR
   • ST elevation in lead V₁ (lower than that of lead aVR)
   • ST depression in leads II and aVF
   • ST depression in the precordial leads to the left of V₂

The ECG + Chest Pain or can be silent is diagnostic

🫀 Management of Acute STEMI (Chest Pain + ECG) - NICE NG185 + ESC 2023 aligned

🚨 Key principle: STEMI is a time-critical reperfusion emergency. Do not delay reperfusion for CXR, routine bloods, or waiting for troponin.
NICE timing logic: offer primary PCI if it can be delivered within 120 minutes of the time fibrinolysis could have been given; otherwise offer fibrinolysis (if within 12 hours and no contraindications).
Time = myocardium ⏱️

⚡ Pathophysiology (why speed matters)

• Cause: usually plaque rupture/erosion → platelet activation + thrombin → acute coronary thrombotic occlusion.
• Wavefront necrosis: infarction spreads from endocardium → epicardium over hours; early reperfusion salvages myocardium and preserves LV function.
• Electrical instability: ischaemia triggers VT/VF risk early; hence monitoring and defib readiness.

🩺 Clinical features (typical + atypical)

• Typical pain: central crushing/tight chest pain >20 min ± radiation to jaw/left arm/neck/back.
• Associated symptoms: dyspnoea, diaphoresis 😰, nausea/vomiting, palpitations, syncope, sense of doom.
• Atypical presentations: older adults, women, diabetes, CKD: dyspnoea, collapse, epigastric discomfort, confusion.
• Examination clues: hypotension/shock, pulmonary oedema, new pansystolic murmur (papillary muscle rupture), bradycardia (inferior/RV MI), arrhythmia.

📉 ECG diagnosis (STEMI + STEMI equivalents)

• ST elevation in ≥2 contiguous leads:
  • V2–V3: ≥2 mm (men) or ≥1.5 mm (women)
  • Other leads: ≥1 mm
• Posterior MI: ST depression V1–V3 with tall R waves → record V7–V9 (posterior ST elevation supports STEMI pathway).
• Right ventricular MI: consider with inferior STEMI + hypotension → record V3R/V4R (avoid nitrates if RV infarct suspected).
• LBBB: new/presumed new LBBB with ischaemic symptoms is high risk; use clinical picture + ECG criteria (e.g., concordant changes) and act early if STEMI suspected.
• Repeat ECGs: if symptoms persist or evolve (dynamic STEMI can be missed on first trace).

🧪 Troponin (do not wait for it)

• Troponin supports diagnosis and risk, but STEMI is a clinical + ECG diagnosis requiring immediate action.
• High-sensitivity troponin typically rises within hours; repeating at 3 hours is useful when ECG is non-diagnostic.
• Bedside echo can help if diagnosis unclear (regional wall motion abnormality), but should not delay reperfusion when STEMI is clear.

🚑 Immediate actions (first 5–10 minutes)

• ABCDE, call cath lab / STEMI pathway early; senior decision-maker involved early.
• Cardiac monitor + defib ready ⚡; treat VT/VF per ALS.
• 12-lead ECG and repeat if evolving; consider posterior/right-sided leads when indicated.
• IV access x2; point-of-care glucose; bloods (FBC, U&E, clotting, troponin) but do not delay reperfusion.
• Oxygen only if hypoxaemic: target 94–98% (or 88–92% if risk of hypercapnic respiratory failure).
• Do not delay reperfusion for CXR unless you strongly suspect dissection/other alternative diagnosis needing immediate imaging.

💊 Symptom relief (analgesia + anti-ischaemic)

• Opioid analgesia: IV morphine/diamorphine titrated to pain, plus antiemetic (e.g., metoclopramide/ondansetron) as needed.
• GTN (sublingual or IV) for ongoing pain and hypertension if no contraindications:
  • Avoid in hypotension, suspected RV infarct, severe aortic stenosis, or recent PDE5 inhibitor use.
• Positioning: upright if pulmonary oedema; supine/legs elevated if hypotensive (and treat shock protocol).

🩸 Antiplatelet therapy (NICE NG185)

✅ Core: Aspirin + a P2Y12 inhibitor (dual antiplatelet therapy, DAPT).
NICE specifies prasugrel + aspirin as the preferred option for STEMI undergoing primary PCI in those not on an oral anticoagulant, with age/bleeding cautions.

• Aspirin: 300 mg loading ASAP (chewed/crushed if needed), then 75 mg daily long-term unless contraindicated.
• If primary PCI planned (and not on an oral anticoagulant): offer prasugrel + aspirin.
  • Prasugrel cautions: avoid if prior stroke/TIA; consider alternatives if age ≥75 or weight <60 kg (bleeding risk).
  • If bleeding risk outweighs benefit (often ≥75): offer ticagrelor or clopidogrel instead (with aspirin).
• If already taking an oral anticoagulant: offer clopidogrel + aspirin (avoid prasugrel/ticagrelor in this setting per NICE pathway).
• If STEMI not treated with primary PCI (including after fibrinolysis): NICE supports ticagrelor + aspirin unless bleeding risk high (then consider clopidogrel + aspirin).

🧬 Antithrombin / anticoagulation (match to strategy - NICE NG185)

• Primary PCI with radial access: offer unfractionated heparin (UFH) with bailout glycoprotein IIb/IIIa inhibitor (not routine upfront).
• If femoral access needed: consider bivalirudin with bailout glycoprotein IIb/IIIa inhibitor.
• If fibrinolysis is given: give an antithrombin at the same time (agent per local protocol).
• Avoid routine pre-hospital fibrinolysis or routine GP IIb/IIIa inhibitor use when primary PCI is planned.
• Renal function: adjust dosing where relevant and monitor bleeding risk closely.

⚡ Reperfusion strategy (NICE NG185 + ESC 2023 framing)

• Primary PCI (preferred): offer coronary angiography with follow-on primary PCI if indicated when:
  • presentation is within 12 hours of symptom onset, and
  • primary PCI can be delivered within 120 minutes of the time fibrinolysis could have been given.
• Fibrinolysis: offer if within 12 hours and timely primary PCI (as above) is not achievable and no contraindications.
• Cardiogenic shock: offer urgent coronary angiography with follow-on PCI if indicated (within 12 hours; and consider even later if ongoing ischaemia/shock).
• Late presenters (>12 hours): consider angiography/PCI if ongoing ischaemia, haemodynamic instability, malignant arrhythmias, or shock.
• ESC practical emphasis: bypass non-PCI centres where possible; move directly to cath lab in confirmed STEMI to reduce system delay.

💉 If fibrinolysis is used (what to do next - NICE)

• Give antithrombin at the same time as fibrinolysis.
• Repeat ECG at 60–90 minutes after fibrinolysis.
• Failed reperfusion (e.g., persistent ST elevation): offer immediate coronary angiography with follow-on PCI if indicated; do not repeat fibrinolysis.
• Recurrent ischaemia after fibrinolysis: seek urgent cardiology advice and consider angiography/PCI.
• If clinically stable after successful fibrinolysis: consider angiography during the same admission.

🩻 Cath lab / in-hospital strategy (NICE NG185)

• Access: radial preferred when feasible (lower bleeding/vascular complications).
• Stent choice: offer drug-eluting stent if stenting is indicated.
• Multivessel disease:
  • If no shock: offer complete revascularisation (often during index admission; may be staged).
  • If cardiogenic shock: consider culprit-only revascularisation during index procedure.
• LV function: assess LV function in all STEMI patients (echo before discharge or early follow-up).

🧠 Special situations (high yield)

• Inferior STEMI + hypotension: think RV infarct; record right-sided leads; avoid nitrates; treat with cautious fluids and urgent reperfusion.
• Posterior MI: record V7–V9; treat as STEMI equivalent if posterior ST elevation present.
• Cardiac arrest with ROSC: if ECG/clinical picture suggests acute coronary occlusion, urgent cath lab discussion is warranted (local network protocol).
• Suspected aortic dissection: tearing pain radiating to back, pulse/BP differential, new AR murmur, mediastinal widening - avoid anticoagulants/thrombolysis and image urgently.

💓 Beta-blockers, ACEi/ARB, MRA (inpatient + discharge)

• ACEi/ARB: start when haemodynamically stable, especially with LV dysfunction, anterior MI, diabetes, or hypertension; titrate to target doses.
• Beta-blocker: offer particularly if LV dysfunction or heart failure; avoid/withhold in shock, acute pulmonary oedema, severe bradycardia/heart block, or severe asthma.
• Aldosterone antagonist (eplerenone): consider if LVEF ≤40% with heart failure or diabetes after MI (monitor K+ and renal function closely).
• High-intensity statin: start early unless contraindicated (dose per local post-MI pathway).

🩹 Secondary prevention (what saves lives long-term)

• DAPT: aspirin + P2Y12 inhibitor as directed (often up to 12 months; shorter if bleeding risk high; longer in selected high-ischaemic-risk cases - specialist decision).
• Statin: high-intensity statin long-term; consider add-on lipid therapy in very high risk if targets not met (cardiology/lipid clinic pathway).
• BP, diabetes, smoking: aggressive risk factor control (smoking cessation has one of the biggest absolute benefits).
• Cardiac rehab: structured rehab improves outcomes and adherence; include exercise prescription, education, psychosocial support.
• Vaccination: influenza (and other vaccinations per risk group policy) to reduce infection-triggered events.

📅 Inpatient monitoring and complications to watch for

• Arrhythmias: VT/VF early; AF; bradyarrhythmias (inferior MI); monitor and treat per ALS/cardiology.
• Heart failure / pulmonary oedema: diuretics, nitrates (if BP allows), ventilatory support as needed; assess LVEF.
• Mechanical complications (2–7 days): papillary muscle rupture (acute MR), VSD, free wall rupture (tamponade); suspect if sudden shock/new murmur.
• Pericarditis: pleuritic pain, pericardial rub (early); Dressler syndrome later.

📊 “Risk stratification” (use the right tools)

• Reperfusion decisions in STEMI are ECG + time + clinical status driven (not GRACE/TIMI).
• After reperfusion, prognosis is guided by:
  • Killip class / heart failure severity
  • LVEF (echo)
  • Extent of coronary disease and success of revascularisation
  • Bleeding risk, renal function, frailty, and complications during admission
• GRACE is primarily a NSTEMI/UA risk tool and is not the main determinant for acute STEMI reperfusion.

💡 Teaching pearl: A “normal” early troponin and a “normal” early CT head/chest X-ray do not exclude STEMI. The life-saving decision is whether the ECG/clinical picture demands immediate reperfusion.

📚 References (guidelines)

• NICE NG185: Acute coronary syndromes (overview)
• NICE NG185: Recommendations (STEMI pathway, antiplatelets, anticoagulation, reperfusion timings)
• NICE NG185: STEMI visual summary (PDF)
• ESC 2023 Guidelines: Acute Coronary Syndromes (ACS) (includes STEMI and NSTE-ACS)
• ESC 2023 ACS Guidelines (Eur Heart J) - PubMed record

Secondary prevention Post Acute Coronary Syndrome

🫀 Secondary Prevention Post-ACS / IHD

Secondary prevention aims to reduce recurrent cardiovascular events and improve long-term survival. It should be initiated prior to discharge.

📋 Prior to Discharge – Risk Assessment

• Assess LVEF, residual ischaemia, completeness of revascularisation.
• Check risk markers: LDL-C, HDL-C, triglycerides, fasting glucose, renal function.
• ⚠️ LDL-C should be measured on admission (levels may fall post-ACS).

💊 Antithrombotic Therapy

• Dual Antiplatelet Therapy (DAPT): Aspirin (75–100 mg OD) + P2Y12 inhibitor (e.g. ticagrelor, prasugrel, or clopidogrel). Continue ≥12 months if low bleeding risk.
• Triple Therapy: For AF / prosthetic valves: triple therapy ≤1 week, then anticoagulant + single antiplatelet up to 12 months.
• After 12 months → usually aspirin monotherapy.

🩸 Anticoagulation (selected cases)

• AF with CHA₂DS₂-VASc ≥2 → anticoagulant ± antiplatelet (guided by bleeding risk).
• LV thrombus post-MI → LMWH bridging to warfarin (or DOAC if appropriate).
• Prolonged immobility post-MI → LMWH prophylaxis.

🧬 Lipid Management

• LDL-C target: <1.4 mmol/L and ≥50% reduction from baseline.
• Statins: High-dose (Atorvastatin 80 mg nocte). Proven mortality reduction post-ACS.
• Consider ezetimibe or PCSK9 inhibitor if LDL-C target not achieved.

💊 Key Medications

• Beta-blockers: Indicated if LVEF ≤40% (Class I, LOE A).
• ACE inhibitors: Ramipril 2.5 mg → titrate to 10 mg daily. If intolerant → ARB (valsartan/losartan).
• Aldosterone antagonist: Eplerenone 25 mg OD in STEMI + LVEF ≤40% with DM or HF symptoms.
• Polypill strategy: Fixed-dose combinations may improve adherence.

🚭 Lifestyle & Risk Modification

• Smoking cessation: Offer NRT, varenicline/bupropion if appropriate. Refer to NHS stop-smoking services.
• Diet: Mediterranean diet (fish, nuts, 5-a-day, low sat fat, ↑ soluble fibre).
• Exercise: Mobilise early; target 150 min/week moderate intensity. Enrol in cardiac rehabilitation.

📊 Quick Summary Table

💡 Exam tip: Post-ACS secondary prevention is about “Drugs + Lifestyle + Rehab”. Always mention cardiac rehabilitation and HCC surveillance in cirrhotics.

Acute Coronary Syndrome (ACS): Complications

⚡ Arrhythmias

• ❤️‍🔥 Ventricular tachycardia: Often seen acutely during ischaemia or infarction. Treat persistent VT with IV amiodarone or lidocaine according to local/ALS guidance. Correct potassium and magnesium. Use synchronised DC cardioversion if haemodynamically compromised.
• 💓 Accelerated idioventricular rhythm: Wide-complex regular rhythm, usually rate <120/min. Often stable and may be a sign of reperfusion. Correct potassium and magnesium. Usually settles without treatment.
• 🚨 Ventricular fibrillation: Usually occurs early after MI and requires immediate defibrillation. Early VF does not always imply long-term ICD need, but VF after the first 24–48 hours is more concerning. Start beta-blockade if not contraindicated and seek cardiology advice for late or recurrent arrhythmias.
• 🫀 Atrial fibrillation: Not uncommon after ACS. Treat rate/rhythm depending on haemodynamic status, LV function and symptoms. Options include beta-blocker, digoxin or amiodarone depending on context. Consider anticoagulation according to stroke and bleeding risk.
• 🐢 Sinus bradycardia: Common with inferior MI. Withhold beta-blockers if significant bradycardia or hypotension. Give atropine if symptomatic. Consider temporary pacing if persistent compromise.
• ⛔ Third-degree AV block: Consider atropine, external pacing and urgent cardiology review. Temporary pacing may be needed, especially if haemodynamic compromise persists. A permanent pacemaker may be required if block does not resolve.
• ⚠️ Second-degree AV block: Mobitz II or 2:1 / 3:1 block is more concerning than Wenckebach and may progress to complete heart block. Seek cardiology advice; temporary pacing may be required.
• 🟡 First-degree AV block: Often needs no treatment. If associated with new bundle branch block or anterior MI, it may suggest more extensive conduction-system disease and requires close monitoring.

🩸 Thromboembolic Complications

• 🧠 Systemic embolism: LV thrombus or atrial fibrillation may lead to embolic stroke or peripheral embolism. Risk is higher after large anterior MI and severe LV impairment. Consider echocardiography and anticoagulation where indicated.
• 🫁 DVT and pulmonary embolism: Immobility, inflammation and acute illness increase venous thromboembolism risk. Use VTE assessment and thromboprophylaxis according to local policy, balancing bleeding risk and antiplatelet/anticoagulant therapy.

🏗 Structural Complications

• 💥 Free wall rupture: Rupture into the pericardium can cause tamponade, pulseless electrical activity and sudden death. Classically occurs several days after a large transmural MI as necrotic myocardium softens.
• 🌊 Severe LV dysfunction / pump failure: Loss of viable myocardium may cause pulmonary oedema and cardiogenic shock. Treat pulmonary oedema with oxygen, nitrates if blood pressure allows, IV diuretics and urgent senior/cardiology input.
• 🫀 Papillary muscle rupture: Presents with acute breathlessness, pulmonary oedema and a new loud pansystolic murmur from acute severe mitral regurgitation. Confirm with urgent echocardiography. Needs urgent cardiac surgical assessment.
• 🧱 Ventricular septal rupture: Presents with acute heart failure, shock and a new harsh pansystolic murmur. Confirm with urgent echocardiography. Requires urgent cardiology/cardiac surgery input.
• 🔁 Ventricular remodelling: Harmful thinning and dilatation after a large transmural MI. ACE inhibitors/ARBs, beta-blockers and mineralocorticoid receptor antagonists where indicated reduce adverse remodelling.
• ➡️ Right ventricular MI: Suspect with inferior STEMI, hypotension, raised JVP and clear lung fields. Check right-sided ECG leads, especially V4R. Avoid excessive nitrates/diuretics; cautious fluid loading may improve RV filling.

🔁 Recurrent Ischaemia and Reinfarction

• 🚨 Reinfarction: Suspect if recurrent chest pain, new ECG changes, haemodynamic deterioration or recurrent troponin rise. Discuss urgently with cardiology for repeat angiography/PCI or reperfusion strategy.
• ➡️ Right ventricular infarction: Presents with hypotension, raised JVP and clear lung fields, usually with inferior MI. ECG may show ST elevation in V4R. Echo is useful. Treat hypotension with cautious fluids and avoid preload-reducing drugs if unstable.

🔥 Inflammatory Complications

• 🫀 Early post-MI pericarditis: Usually occurs within the first few days. Chest pain may be sharp, pleuritic or positional. Avoid routine NSAIDs early after MI unless specialist advice supports use; analgesia and cardiology guidance may be needed.
• 🛡 Dressler’s syndrome: Immune-mediated pericarditis occurring weeks to months after MI. Features include fever, pleuritic chest pain and pericardial effusion. Treat with anti-inflammatory therapy under specialist guidance.

🧠 Psychological Complications

• 😟 Anxiety and depression: Common after ACS and may reduce quality of life, medication adherence and cardiac rehabilitation engagement.
• 💬 Ask about mood, sleep, fear of exertion, return to work, sexual activity and confidence after discharge.
• 🏃 Cardiac rehabilitation improves physical recovery, education, confidence and psychological adjustment.

📝 Exam Pearls

• 🚨 Early VF after MI needs defibrillation; late VF is more concerning for ongoing scar/ischaemia risk.
• 🐢 Inferior MI commonly causes bradycardia and AV block.
• 💥 New murmur plus pulmonary oedema after MI = think papillary muscle rupture or VSD.
• ➡️ Inferior MI + hypotension + raised JVP + clear lungs = right ventricular infarction.
• 🫀 Chest pain days after MI may be pericarditis; weeks later may be Dressler’s syndrome.