Acute Coronary Syndrome

Acute coronary syndrome (ACS) is a spectrum of conditions caused by acute myocardial ischaemia from a sudden reduction in coronary blood flow, almost always due to atherosclerotic plaque rupture with superimposed thrombosis. It encompasses unstable angina (UA), non-ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI). Mastering the ECG, biomarker kinetics, and the reperfusion decision tree is the single highest-yield cardiology block for NEET PG.

Definition & Classification

ACS is defined by acute myocardial ischaemia, usually presenting as chest pain at rest or with minimal exertion. The three entities are separated using two pivots: the 12-lead ECG (ST elevation vs none) and cardiac biomarkers (rise in troponin vs none).

Entity	ST-elevation on ECG	Cardiac troponin	Underlying lesion
STEMI	Present (persistent)	Elevated	Complete occlusive thrombus (red, fibrin-rich)
NSTEMI	Absent (may have ST depression / T inversion)	Elevated	Subtotal occlusion / transient occlusion
Unstable angina	Absent	Normal	Subtotal occlusion, no necrosis

High-yield: UA and NSTEMI are clinically indistinguishable at presentation — the difference is purely whether troponin rises. UA = ischaemia without necrosis; NSTEMI = ischaemia with necrosis but without transmural infarction.

The Fourth Universal Definition of MI requires a rise and/or fall of cardiac troponin with at least one value above the 99th percentile, plus one of: ischaemic symptoms, new ischaemic ECG changes, new pathological Q waves, imaging evidence of new loss of viable myocardium, or angiographic/autopsy-confirmed coronary thrombus.

Types of MI:

• Type 1 — spontaneous MI from atherothrombotic plaque rupture/erosion. (Classic ACS.)
• Type 2 — supply–demand mismatch without acute plaque event (e.g., sepsis, anaemia, tachyarrhythmia, severe hypertension, coronary spasm).
• Type 3 — cardiac death with ischaemic symptoms before biomarkers could be drawn.
• Type 4a/4b/4c — PCI-related / stent thrombosis / restenosis.
• Type 5 — CABG-related.

Etiology & Pathophysiology

The dominant mechanism is plaque rupture: a lipid-rich plaque with a thin fibrous cap and large necrotic core ("vulnerable plaque") ruptures, exposing the thrombogenic subendothelial collagen and tissue factor. Platelet adhesion, activation and aggregation form a platelet plug, and the coagulation cascade generates a fibrin-rich thrombus.

Plaque rupture → exposure of tissue factor & collagen → platelet adhesion (GPIb–vWF) → activation → aggregation (GPIIb/IIIa cross-linking via fibrinogen) → thrombus → coronary occlusion → ischaemia/infarction.

• A completely occlusive, fibrin-rich (red) thrombus produces transmural ischaemia → ST elevation → STEMI.
• A partially occlusive, platelet-rich (white) thrombus produces subendocardial ischaemia → NSTEMI / UA.

High-yield: Vulnerable plaques are usually non-obstructive (<50% stenosis) before rupture. This is why a "normal" stress test does not exclude future MI — the culprit lesion is often haemodynamically insignificant until it ruptures.

Plaque erosion (no rupture, just endothelial denudation) is increasingly recognised, especially in younger women and smokers. Other non-atherosclerotic causes: coronary spasm (Prinzmetal), spontaneous coronary artery dissection (SCAD — young peripartum women), coronary embolism (AF, endocarditis, prosthetic valve), cocaine, arteritis.

The infarct evolves as a wavefront of necrosis from subendocardium to subepicardium over ~6 hours — the basis for the "time is muscle" reperfusion urgency.

Clinical Features

• Chest pain: retrosternal, heavy/crushing/pressure-like, >20 minutes, radiating to left arm, jaw, or epigastrium; not relieved by rest or nitrates (in MI).
• Associated: diaphoresis (sympathetic), nausea/vomiting (vagal, more in inferior MI), dyspnoea, sense of impending doom (angor animi).
• Examination: S4 gallop, anxiety, pallor; signs of complications — S3 and crepitations (LV failure), new murmur (MR/VSD), raised JVP and clear lungs (RV infarct).

Atypical / silent MI: in diabetics (autonomic neuropathy), elderly, women, and the post-operative patient — may present with dyspnoea, syncope, confusion, or epigastric pain alone.

High-yield: Inferior MI (RCA) often presents with bradycardia, hypotension, nausea and vomiting due to the Bezold–Jarisch reflex (increased vagal tone). Always do right-sided leads (V4R) in inferior STEMI to detect RV infarction.

Diagnosis & Investigations

ECG — the first and most time-critical investigation

STEMI criteria (new ST elevation at the J point in ≥2 contiguous leads):

• ≥1 mm in limb/precordial leads generally, except
• V2–V3: ≥2 mm in men ≥40 yr, ≥2.5 mm in men <40 yr, ≥1.5 mm in women.
• New LBBB in the right clinical setting is treated as a STEMI-equivalent (use Sgarbossa criteria to diagnose MI in pre-existing LBBB/paced rhythm).

ECG evolution: hyperacute peaked T waves → ST elevation → Q wave development → T-wave inversion → ST normalisation with persistent Q waves.

NSTEMI/UA ECG: ST depression (≥0.5 mm) and/or T-wave inversion; may be normal.

ECG localisation of infarct (very high-yield)

Leads with ST elevation	Region	Culprit artery
V1–V2	Septal	LAD (proximal)
V3–V4	Anterior	LAD
V1–V4 (extensive)	Anteroseptal	LAD
I, aVL, V5–V6	Lateral	LCx (or diagonal)
II, III, aVF	Inferior	RCA (80%) or LCx
V4R	Right ventricle	Proximal RCA
V7–V9 (tall R in V1–V2, ST depression V1–V3)	Posterior	RCA / LCx

High-yield: ST elevation in lead III > lead II with reciprocal ST depression in I/aVL points to RCA occlusion. Wellens syndrome (deep biphasic/inverted T waves in V2–V3 during pain-free state) indicates critical proximal LAD stenosis — high risk, do NOT stress test, refer for angiography.

de Winter T waves (upsloping ST depression with tall symmetric T in precordial leads) and aVR ST elevation with diffuse ST depression both signal proximal LAD or left main occlusion — STEMI-equivalents.

Cardiac biomarkers & their kinetics

Cardiac troponin I/T is the biomarker of choice — most sensitive and specific. High-sensitivity troponin (hs-cTn) allows rapid 0/1-hour or 0/2-hour rule-in/rule-out algorithms.

Biomarker	Rises	Peaks	Normalises	Best use
Myoglobin	1–2 h	6–9 h	24 h	Earliest but non-specific
CK-MB	3–6 h	~24 h	48–72 h	Detecting re-infarction
Troponin I/T	3–6 h (hs: ~2 h)	12–24 h	7–14 days	Diagnosis (gold standard)

High-yield: Because troponin stays elevated for up to 2 weeks, CK-MB (normalises by 48–72 h) is preferred to diagnose re-infarction. A re-rise of CK-MB or troponin after initial fall = re-infarction.

Troponin can be elevated without ACS: renal failure, PE, sepsis, myocarditis, heart failure, severe tachyarrhythmia — interpret with clinical context.

Other investigations

• Echocardiography: regional wall-motion abnormality, LV function, mechanical complications.
• Coronary angiography: definitive — identifies culprit lesion and guides PCI.
• Bloods: lipid profile, glucose/HbA1c, renal function, electrolytes (Mg, K).

Risk Stratification

• STEMI prognosis — Killip classification (based on bedside clinical signs of LV failure):

Class	Findings	Approx. mortality
I	No failure (no crepitations, no S3)	~6%
II	Crepitations <50% lung fields, S3, raised JVP	~17%
III	Frank pulmonary oedema (crepitations >50%)	~38%
IV	Cardiogenic shock (SBP <90, hypoperfusion)	~67–80%

• NSTEMI/UA — TIMI score (7 variables: Age ≥65, ≥3 CAD risk factors, known CAD ≥50% stenosis, aspirin use in past 7 days, ≥2 anginal episodes in 24 h, ST deviation ≥0.5 mm, raised biomarkers). Higher score → invasive strategy.
• GRACE score — predicts in-hospital and 6-month mortality; GRACE >140 mandates an early invasive strategy (<24 h).

High-yield: Killip class is for STEMI prognosis; TIMI and GRACE scores guide the timing of an invasive strategy in NSTEMI/UA.

Management

Immediate (all ACS) — "MONA-BASH" with caveats

Stepwise initial approach: Aspirin 300 mg chewed → second antiplatelet (P2Y12 inhibitor) → anticoagulant → oxygen only if SpO₂ <90% → analgesia → reperfusion decision.

• Aspirin 162–325 mg (chewed) loading, then 75 mg OD lifelong.
• P2Y12 inhibitor: ticagrelor 180 mg or prasugrel 60 mg (preferred over clopidogrel in PCI); clopidogrel 300–600 mg if others unavailable / fibrinolysis given.
• Anticoagulation: unfractionated heparin, enoxaparin, fondaparinux, or bivalirudin.
• Oxygen ONLY if SpO₂ <90% (routine O₂ in normoxic patients may be harmful).
• Nitrates for pain/ischaemia — contraindicated in hypotension, RV infarct, and recent phosphodiesterase-5 inhibitor (sildenafil) use.
• Morphine for refractory pain (caution: delays P2Y12 absorption).
• Beta-blocker within 24 h if no contraindication (avoid in acute failure, bradycardia, hypotension, cocaine-induced MI).
• High-intensity statin (atorvastatin 80 mg) for all, early.
• ACE inhibitor within 24 h, especially with LV dysfunction, anterior MI, diabetes.

High-yield: In RV infarction, the patient is preload-dependent — give IV fluids, and avoid nitrates, morphine and diuretics, which drop preload and cause profound hypotension.

STEMI — reperfusion is the priority

The decision is primary PCI vs fibrinolysis, governed by time.

Primary PCI is preferred if it can be delivered within 120 minutes of first medical contact (FMC).

• If at a PCI-capable hospital: door-to-balloon target ≤90 minutes.
• If transfer needed and total FMC-to-device ≤120 min: transfer for primary PCI.
• If PCI cannot be achieved within 120 min: give fibrinolysis within 30 minutes (door-to-needle ≤30 min), ideally within 12 hours of symptom onset, then transfer for angiography (pharmaco-invasive strategy: routine angiography 2–24 h later).

Fibrinolytic agents: tenecteplase (single weight-based bolus, fibrin-specific — most convenient), alteplase, reteplase; streptokinase (cheap, non-fibrin-specific, risk of allergy/hypotension, not repeatable).

Absolute contraindications to fibrinolysis (high-yield): any prior intracranial haemorrhage; ischaemic stroke within 3 months; known cerebral vascular lesion/malignancy; active bleeding (excluding menses); suspected aortic dissection; significant closed head/facial trauma within 3 months.

High-yield: Markers of successful reperfusion after fibrinolysis = >50% resolution of ST elevation at 60–90 min, resolution of chest pain, and reperfusion (accelerated idioventricular) arrhythmia. Failure → rescue PCI.

NSTEMI / UA

• No role for fibrinolysis (may be harmful).
• Antiplatelet + anticoagulant + anti-ischaemic therapy.
• Invasive strategy timing:
  • Immediate (<2 h): haemodynamic instability, refractory angina, life-threatening arrhythmia, mechanical complication.
  • **Early (<24 h):** GRACE >140, rise/fall of troponin, dynamic ST changes.
  • Routine invasive (<72 h): other high-risk features (diabetes, renal dysfunction, prior PCI/CABG).

Secondary prevention (lifelong)

Dual antiplatelet therapy (DAPT) for ~12 months, then aspirin lifelong; high-intensity statin; beta-blocker; ACE-I/ARB; aldosterone antagonist (eplerenone) if EF ≤40% with HF or diabetes; lifestyle — smoking cessation, cardiac rehab, BP and glycaemic control.

Complications

Mnemonic – "DARTH VADER": Death, Arrhythmia, Rupture, Tamponade, Heart failure, Valve disease, Aneurysm, Dressler syndrome, Embolism (mural thrombus), Recurrent infarction.

Complication	Timing	Key point
Ventricular arrhythmia / VF	First hours–days	Commonest cause of pre-hospital death
AV block	Early	Inferior MI → usually transient, atropine-responsive; anterior MI → infranodal, may need pacing
Cardiogenic shock	24–72 h	Killip IV; mortality high
Papillary muscle rupture	2–7 days	Acute severe MR, flash pulmonary oedema; posteromedial muscle most affected (single RCA supply)
Ventricular septal rupture	3–5 days	New pansystolic murmur, step-up in O₂ at RV on catheter
Free wall rupture	3–14 days	Tamponade, PEA, sudden death
LV aneurysm	Weeks	Persistent ST elevation, mural thrombus
Dressler syndrome	2–10 weeks	Autoimmune pericarditis, fever, pleuritic pain — treat with aspirin/NSAID, avoid steroids early

High-yield: A new pansystolic murmur 3–5 days post-MI = papillary muscle rupture (MR) or VSD. Distinguish via echo; both need urgent surgery and may be bridged with an intra-aortic balloon pump.

Key Differentials

• Aortic dissection — tearing pain radiating to back, BP differential between arms, widened mediastinum. (Crucial to exclude — fibrinolysis would be lethal.)
• Pulmonary embolism — pleuritic pain, dyspnoea, S1Q3T3, raised D-dimer, RV strain.
• Pericarditis — sharp, positional, pleuritic pain; diffuse concave ST elevation with PR depression; pericardial rub.
• Myocarditis, Takotsubo (stress) cardiomyopathy — apical ballooning, post-emotional stress, normal coronaries.
• GORD / oesophageal spasm, musculoskeletal pain, biliary/pancreatic pain.

Recently asked / exam angle

• ECG localisation: matching lead groups to culprit arteries (III > II → RCA; aVL/I → LCx; V1–V4 → LAD).
• Biomarker kinetics: "Which marker to diagnose re-infarction?" → CK-MB. "Earliest marker?" → myoglobin. "Most specific?" → troponin.
• Reperfusion logic: PCI within 120 min of FMC vs fibrinolysis within 30 min if PCI unavailable.
• Killip class assignment from a clinical vignette and its mortality implication.
• RV infarction management — fluids in, nitrates/morphine out; V4R lead.
• Mechanical complication timelines (papillary muscle rupture vs VSD vs free wall rupture).
• Wellens syndrome, de Winter T waves, Sgarbossa criteria, aVR elevation = left main.
• Contraindications to nitrates (RV infarct, sildenafil) and to fibrinolysis (prior ICH, recent stroke, dissection).
• Drug of choice questions: antiplatelet loading, high-intensity statin, fibrin-specific lytic (tenecteplase).

Rapid revision

1. ACS = UA + NSTEMI + STEMI; split by ST elevation (ECG) and troponin rise.
2. UA = ischaemia, normal troponin; NSTEMI = troponin up, no ST elevation; STEMI = ST elevation + troponin.
3. STEMI cut-off V2–V3: ≥2 mm men ≥40, ≥1.5 mm women; ≥1 mm elsewhere.
4. Lead III > II elevation with I/aVL depression → RCA (inferior MI).
5. Troponin: rises 3–6 h, peaks 12–24 h, lasts 7–14 days (best for diagnosis).
6. CK-MB normalises in 48–72 h → used to detect re-infarction; myoglobin = earliest marker.
7. Killip IV = cardiogenic shock, mortality ~70%; TIMI/GRACE guide NSTEMI invasive timing.
8. Primary PCI if achievable ≤120 min of FMC; otherwise fibrinolysis ≤30 min (door-to-needle).
9. Door-to-balloon ≤90 min; tenecteplase is the convenient fibrin-specific bolus lytic.
10. RV infarct → give IV fluids; avoid nitrates, morphine, diuretics; check V4R.
11. New pansystolic murmur day 3–5 = papillary muscle rupture (MR) or VSD.
12. Dressler syndrome = autoimmune pericarditis weeks later; treat with aspirin/NSAID, avoid early steroids; secondary prevention = DAPT 12 mo + high-intensity statin + beta-blocker + ACE-I.