Also known as: ACS, MI, myocardial infarction, STEMI, NSTEMI, unstable angina, heart attack
Overview
Spectrum of clinical syndromes resulting from acute myocardial ischemia, classified by ECG and biomarker findings: ST-elevation MI (STEMI), non-ST-elevation MI (NSTEMI), and unstable angina (UA).
Epidemiology
Leading cause of death in the US. Incidence rises sharply with age; male predominance until ~70 when rates equalize.
Try two board-style Acute Coronary Syndrome questions
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Question 1CardiovascularEasy
A 72-year-old man with ST-elevation myocardial infarction (STEMI) undergoes primary percutaneous coronary intervention (PCI) with placement of a drug-eluting stent in the left anterior descending (LAD) and is started on aspirin and prasugrel. He has no history of bleeding or other high bleeding-risk features. Which of the following is the recommended duration of dual antiplatelet therapy?
ALifelong
B6 months
C1 month
D3 months
E12 months
Reveal answer & full explanation
Correct answer: E — 12 months
ALifelong
B6 months
C1 month
D3 months
E12 months✓
Why 12 months is correct
After acute coronary syndrome (ACS) treated with a drug-eluting stent, dual antiplatelet therapy (DAPT) consisting of aspirin plus a P2Y12 inhibitor is recommended for 12 months as the default in patients who are not at high bleeding risk
The 12-month duration is intended to prevent stent thrombosis and recurrent myocardial infarction (MI)
Ticagrelor or prasugrel is preferred over clopidogrel in ACS
Aspirin is continued indefinitely after DAPT is completed
Why the others are wrong
3 months — a shortened DAPT course followed by P2Y12 inhibitor monotherapy is an option for patients at high bleeding risk, not the default after ACS
1 month — stopping aspirin after 1 month is a bleeding-reduction strategy for high-bleeding-risk patients or, under the 2025 ACC/AHA ACS guideline, a switch to ticagrelor monotherapy in patients tolerating ticagrelor-based DAPT; it does not apply to this prasugrel-treated patient without bleeding risk
Lifelong — dual antiplatelet therapy is not continued indefinitely; aspirin alone is continued after the 12-month course
6 months — the default DAPT duration after drug-eluting stent placement for stable ischemic heart disease, not acute coronary syndrome; after ACS in a patient without high bleeding risk the default is 12 months (the trap is applying the stable-disease duration to an ACS)
Question 2CardiovascularMedium
A 58-year-old man with hypertension and diabetes presents to the emergency department with 45 minutes of crushing chest pain radiating to the left arm. He is diaphoretic and confused. Blood pressure is 88/60 mm Hg and pulse is 112/min. ECG shows ST-segment elevation in leads V1 through V4. Which of the following is the most appropriate immediate intervention?
APrimary percutaneous coronary intervention
BIntravenous beta-blockade with metoprolol
CFibrinolysis with tissue plasminogen activator
DIntravenous analgesia with morphine sulfate
EIntra-aortic balloon pump counterpulsation
Reveal answer & full explanation
Correct answer: A — Primary percutaneous coronary intervention
APrimary percutaneous coronary intervention✓
BIntravenous beta-blockade with metoprolol
CFibrinolysis with tissue plasminogen activator
DIntravenous analgesia with morphine sulfate
EIntra-aortic balloon pump counterpulsation
Why primary percutaneous coronary intervention is correct
Anterior ST-elevation MI (ST elevation in V1–V4) complicated by cardiogenic shock (hypotension 88/60 mm Hg, tachycardia, confusion, diaphoresis) requires immediate reperfusion
Primary PCI is the preferred reperfusion strategy in STEMI with cardiogenic shock and is favored over fibrinolysis whenever it can be performed promptly, per current ACC/AHA STEMI guidance
Early revascularization improves survival in cardiogenic shock; the door-to-balloon target is under 90 minutes
Why the others are wrong
Fibrinolysis with tissue plasminogen activator — reserved for when timely PCI is unavailable and markedly inferior to PCI in cardiogenic shock (right-diagnosis-wrong-step: correct goal of reperfusion, wrong modality here)
Intravenous beta-blockade with metoprolol — beta-blockers are contraindicated in cardiogenic shock and acute decompensated heart failure and can precipitate arrest in a hypotensive patient (anchoring on routine early-STEMI order sets without registering the shock contraindication)
Intravenous analgesia with morphine sulfate — relieves pain but does not reperfuse the occluded artery and can lower blood pressure further (buzzword-matching the "MONA" mnemonic instead of prioritizing reperfusion)
Intra-aortic balloon pump counterpulsation — tempting because it provides mechanical hemodynamic support for a hypotensive patient, but it does not reopen the occluded artery, and in IABP-SHOCK II routine IABP added to early revascularization did not reduce mortality, so it is not recommended routinely in infarct-related cardiogenic shock (right-diagnosis-wrong-step: supporting the pressure instead of reperfusing the artery)
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Other: chronic kidney disease, autoimmune disease, cocaine/methamphetamine use
Pathophysiology
Atherosclerotic plaque rupture or erosion exposes thrombogenic material to circulating blood, triggering platelet aggregation and thrombus formation. Partial occlusion → UA/NSTEMI. Complete occlusion → STEMI. Resulting downstream ischemia → myocyte necrosis if not reperfused.
Clinical presentation
Symptoms
Substernal chest pressure, tightness, or 'heaviness' (classic), often radiating to left arm, jaw, or back
Dyspnea, diaphoresis, nausea/vomiting
Atypical in women, elderly, diabetics: fatigue, epigastric pain, syncope, dyspnea without pain
Symptoms ≥20 min and not relieved by rest/nitrates suggest infarction
Signs / physical exam
Diaphoresis, anxiety, hypotension or hypertension
S4 gallop (LV stiffness from ischemia)
New MR murmur → papillary muscle dysfunction
Crackles → LV failure
Classic findings
Levine's sign (clenched fist over sternum); cool/clammy skin; bradycardia in inferior MI.
Differential diagnosis
Aortic dissection — Sudden tearing or ripping chest pain radiating to the back, BP or pulse differential between arms, widened mediastinum on CXR — DO NOT anticoagulate before excluding
Takotsubo (stress) cardiomyopathy — Postmenopausal women after major emotional/physical stressor; ECG and troponin mimic STEMI; apical ballooning on ventriculogram or echo
Tension pneumothorax — Acute dyspnea, unilateral absent breath sounds, tracheal deviation, hypotension — clinical diagnosis; do not delay decompression for CXR
Esophageal rupture (Boerhaave) — Severe chest/upper abdominal pain after forceful emesis, subcutaneous emphysema, pneumomediastinum on imaging
GERD / esophageal spasm — Burning, postprandial, worse supine; may respond to nitrates and confuse the picture; PPI trial
Costochondritis / musculoskeletal — Reproducible with chest wall palpation, no exertional pattern, normal ECG and troponin
Diagnostic workup
Diagnostic criteria
STEMI: new J-point ST elevation in ≥2 contiguous leads, ≥1 mm in all leads other than V2-V3; in V2-V3 ≥2 mm in men ≥40, ≥2.5 mm in men <40, and ≥1.5 mm in women. With LBBB or a paced rhythm, apply Sgarbossa criteria; LBBB alone is not diagnostic. NSTEMI: rise and/or fall of troponin with ≥1 value above the sex-specific 99th percentile upper reference limit, plus evidence of ischemia (symptoms, ST depression / T-wave inversion); a stable elevation (<20% change on serial draws) suggests chronic injury (CKD, HF), and a borderline value that stays flat needs further serial testing (observe zone). UA: ischemic symptoms with negative troponin. Fifth Universal Definition (2026) replaces numbered MI types: primary MI (acute coronary pathology such as plaque rupture or erosion, spontaneous coronary artery dissection, embolism, or vasospasm; mostly former type 1), secondary MI (supply-demand imbalance from another acute illness such as sepsis, tachyarrhythmia, anemia, or hypotension; former type 2, confirmed by obstructive CAD or a new ischemic wall-motion abnormality), and procedure-related MI (complication within 30 days of a cardiac procedure such as PCI or CABG; former types 4-5). Troponin rise without evidence of ischemia = myocardial injury, not MI.
Labs
Troponin I or T (high-sensitivity) at presentation and 1-3 hours later — single most important biomarker
CBC, BMP, Mg, lipid panel, A1c
Coagulation studies prior to antiplatelet/anticoagulant therapy
Risk scores: HEART score (History, ECG, Age, Risk factors, Troponin) guides ED disposition of possible ACS: 0-3 low risk (discharge with outpatient follow-up), 4-6 moderate (observe with serial troponins and stress testing or CCTA), 7-10 high (early invasive); TIMI or GRACE once NSTE-ACS is diagnosed
Imaging
12-lead ECG within 10 minutes of arrival — repeat every 15-30 min if initial nondiagnostic
Portable CXR (look for pulmonary edema, widened mediastinum to exclude aortic dissection)
Bedside echo if hemodynamic instability or mechanical complication suspected
Diagnostic algorithm
flowchart TD
A[Chest pain<br/>≥10 min, suggestive] --> B[12-lead ECG<br/>within 10 min]
B --> C{ST elevation?}
C -->|Yes| D[STEMI]
D --> E[Primary PCI<br/>≤90 min]
D --> F[Fibrinolysis<br/>if PCI delay]
C -->|No| G[Troponin<br/>0 and 1-3 h]
G --> H{"Troponin rise/fall<br/>above 99th percentile?"}
H -->|Yes| I[NSTEMI]
H -->|No| L{Ischemic<br/>symptoms?}
L -->|Yes| M[Unstable Angina]
L -->|No| O["Evaluate other causes<br/>(risk-stratify, e.g., HEART score)"]
I --> J{Risk stratify<br/>GRACE / TIMI}
M --> J
J -->|Very high risk| K1["Immediate invasive (<2 h):<br/>refractory angina, shock,<br/>arrhythmia, acute HF"]
J -->|High risk| K2["Early invasive (<24 h):<br/>e.g., GRACE >140"]
J -->|Intermediate or low risk| K3["Intermediate: invasive in 24-72 h<br/>Low: noninvasive testing,<br/>cath if positive"]
ACS triage algorithm — decision tree from initial chest pain to definitive treatment pathway.
P2Y12 inhibitor (blocks the platelet ADP receptor; clopidogrel and prasugrel are irreversible prodrugs, ticagrelor is reversible) loading dose: ticagrelor 180 mg, clopidogrel 600 mg, or prasugrel 60 mg (prasugrel only if known anatomy proceeding to PCI; contraindicated with prior stroke/TIA; generally not recommended at age ≥75; reduce maintenance dose to 5 mg if weight <60 kg)
Anticoagulation: unfractionated heparin (preferred for PCI), enoxaparin, bivalirudin, or fondaparinux (NSTEMI medical management)
High-intensity statin on admission regardless of baseline LDL — atorvastatin 40-80 mg or rosuvastatin 20-40 mg
Beta-blocker within 24 h (oral): metoprolol tartrate or succinate, carvedilol, or bisoprolol — avoid in acute decompensated HF, bradycardia, hypotension
Sublingual nitroglycerin for ongoing pain (avoid in inferior/RV infarct, hypotension, recent PDE5 inhibitor use)
Supplemental O2 only if SpO2 <90% (routine O2 worsens outcomes in normoxic patients)
STEMI
Primary PCI within 90 min of first medical contact (preferred)
Fibrinolysis (alteplase, tenecteplase) if PCI unavailable within 120 min and symptom onset <12 h
Door-to-needle goal ≤30 min for fibrinolysis
NSTEMI / High-risk UA
Risk-stratify with TIMI or GRACE score
Immediate invasive (cath <2 h) for refractory angina, hemodynamic or electrical instability (cardiogenic shock, sustained VT/VF), or acute HF; early invasive (cath <24 h) for stabilized high-risk patients (e.g., GRACE >140, new ST depression)
Delayed invasive (cath 24-72 h) for intermediate risk
Low-risk UA
Conservative strategy: medical optimization + stress testing prior to discharge
Cath if stress test positive or symptoms recur
Second-line / adjunct
ACEi/ARB within 24 h if LV dysfunction, anterior MI, HTN, diabetes, or CKD
Aldosterone antagonist (spironolactone, eplerenone) if EF ≤40% + symptoms or diabetes
Cardiac rehab referral at discharge
Dual antiplatelet therapy (aspirin 81 mg + P2Y12 inhibitor) for 12 months is the default after ACS, with ticagrelor or prasugrel preferred over clopidogrel for PCI; the 2025 ACC/AHA guideline also endorses switching to ticagrelor monotherapy after ≥1 month in patients tolerating ticagrelor-based DAPT to reduce bleeding; single antiplatelet therapy continues indefinitely afterward
Complications
Arrhythmias: ventricular fibrillation (early, most common cause of death pre-hospital), AV blocks (especially inferior MI), atrial fibrillation
Heart failure (acute or chronic); cardiogenic shock (SBP <90 with hypoperfusion: cold extremities, oliguria, confusion, rising lactate; low EF), treated with emergent PCI of the culprit artery before diuresis, norepinephrine for hypotension, and no beta-blockers; routine intra-aortic balloon pump is not recommended
LV thrombus → embolic stroke (especially large anterior MI)
Posterior MI = ST depression in V1-V3 with prominent R wave (mirror image). Obtain posterior leads V7-V9.
Inferior MI (II, III, aVF) with RV involvement (V4R) — preload-dependent. NITRATES AND DIURETICS ARE CONTRAINDICATED. Give IV fluids.
Wellens syndrome: biphasic or deep symmetric T-wave inversions in V2-V3 = critical proximal LAD stenosis. Often pain-free at presentation. Stress testing contraindicated; cath directly. De Winter T waves (upsloping J-point ST depression with tall, symmetric precordial T waves, no ST elevation) = acute proximal LAD occlusion, a STEMI equivalent; activate the cath lab.
LBBB or paced rhythm (new or old) with ischemic symptoms: apply Sgarbossa criteria, namely concordant ST elevation ≥1 mm in any lead, concordant ST depression ≥1 mm in V1-V3, or discordant ST elevation ≥5 mm (modified Sgarbossa: discordant ST elevation ≥25% of the preceding S-wave depth). Any positive criterion, or persistent ischemic symptoms or hemodynamic instability, is managed like STEMI with emergent cath lab activation.
ECG localization: anterior/septal (V1-V4) = LAD; lateral (I, aVL, V5-V6) = left circumflex; inferior (II, III, aVF) = RCA in most patients (circumflex if left-dominant); posterior (ST depression with tall R waves in V1-V3) = RCA or circumflex.
Images
Anterior STEMI — ST-segment elevation in V1-V4 with reciprocal changes inferiorlyInferior STEMI — ST elevation in II, III, aVF; reciprocal depression in I and aVLNSTEMI — ST-segment depression and T-wave inversion without ST elevation
References
ACC/AHA/SCAI 2021 — 2021 ACC/AHA/SCAI Guideline for Coronary Artery Revascularization (Lawton et al., Circulation 2022)
ACC/AHA/ACEP/NAEMSP/SCAI 2025 — 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes (Rao et al., Circulation 2025;151:e771-e862)
Universal Definition — Fifth Universal Definition of Myocardial Infarction (2026) (Mills, Newby, Zaman et al., ESC/ACC/AHA/WHF Task Force; Global Heart 2026;21:64, co-published in Eur Heart J, JACC, and Circulation)
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