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Cardiology›Condition·Updated Apr 17, 2026·v1

Acute Myocardial Infarction

Acute Myocardial Infarction is a critical emergency requiring a coordinated "systems of care" approach. Diagnosis relies on the Universal Definition (troponin elevation + ischemia). STEMI mandates immediate reperfusion (PCI < 90 min), while NSTEMI is risk-stratified. Long-term survival depends on the prevention of adverse remodeling through DAPT, statins, ACE inhibitors, and beta-blockers.

High Evidence171 references·5,639 words·23 min read·v1
CardiologyEmergency MedicineIschemic Heart DiseaseSTEMINSTEMI

Quick Reference

RxDrug of choiceAspirin (324 mg load) + Ticagrelor (180 mg load) or Prasugrel (60 mg load)
AltAlternativesClopidogrel (600 mg load) if high bleeding risk or if fibrinolysis is used
⊘AvoidNSAIDs (except Aspirin), Nitrates in RV infarction, Fibrinolytics in NSTEMI
DxTest of choiceCoronary Angiography (Definitive); High-sensitivity Troponin (Biomarker)
ScKey scoreGRACE Score (Mortality), Killip Class (Heart Failure), SCAI Stage (Shock)
→When to referImmediate referral to Cardiology/Interventional Cardiology for all suspected AMI
AMI requires rapid diagnosis via ECG and troponin, followed by immediate revascularization (PCI) and dual antiplatelet therapy to minimize myocardial necrosis.
Acute myocardial infarction (AMI) is the clinical manifestation of myocardial cell death resulting from prolonged ischemia. It is defined by a rise and/or fall of cardiac troponin (cTn) with at least one value above the 99th percentile upper reference limit, accompanied by clinical evidence of ischemia such as symptoms, new ECG changes, or imaging evidence of wall motion abnormalities. AMI is broadly categorized into ST-elevation myocardial infarction (STEMI), typically indicating complete coronary occlusion, and non-ST-elevation myocardial infarction (NSTEMI). Management centers on rapid reperfusion—ideally via primary percutaneous coronary intervention (PCI) within 90 minutes for STEMI—and aggressive antithrombotic therapy. Despite advances in care, AMI remains a leading cause of morbidity and mortality, particularly when complicated by cardiogenic shock, which carries a mortality rate approaching 50%.

Overview and Recommendations

Background

  • •Understand the Fourth Universal Definition of Myocardial Infarction, which classifies AMI into five types based on pathophysiology. Type 1 is spontaneous MI due to plaque rupture or erosion; Type 2 results from supply-demand imbalance (e.g., anemia, tachycardia); Type 3 is sudden cardiac death; Type 4 is related to (PCI); and Type 5 is related to coronary artery bypass grafting (CABG).
  • •Distinguish between and based on the initial electrocardiogram (ECG). STEMI requires immediate reperfusion due to transmural ischemia, while NSTEMI involves subendocardial ischemia and is managed with urgent or early invasive strategies depending on risk stratification.
  • •Recognize the significance of (CS), the most lethal complication of AMI. It is characterized by systemic hypoperfusion due to cardiac pump failure and is staged from A (at risk) to E (extremis) using the SCAI classification system.
  • •Identify non-atherosclerotic causes of MI, particularly in younger patients and women. (SCAD) is the leading cause of pregnancy-associated MI, while (Myocardial Infarction with Non-Obstructed Coronary Arteries) occurs in 5-10% of cases and requires specialized imaging like Cardiac MRI for diagnosis.
  • •Appreciate the time-dependent nature of myocardial necrosis. The "progressive phase" of active necrosis begins at symptom onset, making the "door-to-balloon" time (target < 90 minutes) the most critical metric for improving survival in obstructive cases.

Evaluation

  • •Suspect AMI in any patient presenting with acute chest pain, pressure, or discomfort, particularly if it radiates to the left arm, neck, or jaw. Be vigilant for atypical presentations in women, the elderly, and patients with diabetes, who may present with isolated dyspnea, nausea, or epigastric pain.
  • •Obtain a 12-lead ECG within 10 minutes of first medical contact. Look for persistent ST-segment elevation in two contiguous leads (≥1 mm in most leads, or age/sex-specific thresholds in V2-V3) to diagnose STEMI.
  • •Identify "Occlusion Myocardial Infarction" (OMI) patterns that may not meet formal STEMI criteria but indicate acute occlusion. These include de Winter T-waves (upsloping ST-depression with tall, symmetric T-waves), hyperacute T-waves, and Wellens' syndrome (biphasic or deeply inverted T-waves in V2-V3).
  • •Order high-sensitivity cardiac troponin (hs-cTn) immediately at presentation (H0). Utilize the H0/H1 or H0/H2 rapid rule-out/rule-in algorithms; a very low H0 value in a patient symptomatic for >3 hours can often rule out AMI, while a significant absolute delta (change) at 1 or 2 hours suggests acute injury.
  • •Perform a targeted physical examination to assess for hemodynamic stability and complications. Use the Killip classification: Class I (no heart failure), Class II (rales, S3 gallop), Class III (pulmonary edema), and Class IV ( with hypotension and hypoperfusion).
  • •Rule out life-threatening mimics using the "Triple Rule Out" approach if the diagnosis is ambiguous. Consider (tearing pain, BP discrepancy), (pleuritic pain, tachycardia), and tension pneumothorax.
  • •Calculate the GRACE or TIMI risk score to guide the urgency of intervention in NSTEMI. High-risk features (GRACE >140, dynamic ST changes) warrant an early invasive strategy within 24 hours.
  • •Utilize point-of-care to identify regional wall motion abnormalities, which support the diagnosis of AMI and help exclude mechanical complications like papillary muscle rupture or ventricular septal defects.
  • •Screen for metabolic mimics such as severe , which can produce "pseudo-infarction" ST-elevation patterns on ECG, especially in patients with known renal failure.
  • •Consider Cardiac Magnetic Resonance (CMR) imaging within 7-14 days for patients with suspected . CMR is the gold standard for differentiating MI from or by identifying specific patterns of late gadolinium enhancement (LGE).

Management

  • •Administer Aspirin 324 mg (chewed) immediately to all patients with suspected ACS unless a true allergy exists. This provides rapid platelet inhibition and is a cornerstone of early therapy.
  • •Initiate a second antiplatelet agent (P2Y12 inhibitor) as soon as possible. For STEMI or high-risk NSTEMI, preferred agents include Ticagrelor 180 mg loading dose followed by 90 mg BID, or Prasugrel 60 mg loading dose (only if coronary anatomy is known and no history of stroke/TIA).
  • •Provide anticoagulation with Unfractionated Heparin (UFH) 60 U/kg bolus (max 4000 U) followed by 12 U/kg/hr infusion, or Enoxaparin 1 mg/kg SC BID. UFH is preferred if the patient is proceeding immediately to the cath lab.
  • •Activate the cardiac catheterization laboratory immediately for any patient with STEMI. The goal is primary PCI with a door-to-balloon time of < 90 minutes at PCI-capable centers or < 120 minutes if transfer is required.
  • •Administer Fibrinolytic therapy (e.g., Tenecteplase weight-based bolus) only if primary PCI cannot be performed within 120 minutes of diagnosis and there are no contraindications (e.g., recent intracranial hemorrhage, active bleeding).
  • •Restrict supplemental oxygen to patients with SaO2 < 90% or PaO2 < 60 mmHg. Routine oxygen in normoxic patients may cause coronary vasoconstriction and increase infarct size.
  • •Manage ischemic pain with Sublingual Nitroglycerin 0.4 mg every 5 minutes (up to 3 doses). Avoid nitrates in patients with right ventricular infarction (leads V3R/V4R elevation) or recent phosphodiesterase inhibitor use (e.g., sildenafil).
  • •Stabilize by maintaining a Mean Arterial Pressure (MAP) ≥ 65 mmHg. Use Norepinephrine 0.05–1.0 µg/kg/min as the first-line vasopressor; add Dobutamine 2.5–20 µg/kg/min if hypoperfusion persists despite adequate MAP.
  • •Consider early mechanical circulatory support (MCS) with a microaxial flow pump (e.g., Impella) in patients with refractory cardiogenic shock (SCAI Stage D/E) to provide left ventricular unloading.
  • •Initiate high-intensity (e.g., Atorvastatin 80 mg daily) as soon as possible, regardless of baseline LDL levels, for their pleiotropic plaque-stabilizing effects.
  • •Start an ACE inhibitor (e.g., Lisinopril 5 mg daily) within 24 hours in patients with LVEF < 40%, hypertension, or diabetes, provided they are hemodynamically stable without hypotension.
  • •Administer oral Beta-blockers (e.g., Metoprolol succinate 25-50 mg daily) within the first 24 hours only in stable patients. Avoid in those with signs of heart failure, low output states, or risk of cardiogenic shock.
  • •Prescribe Mineralocorticoid Receptor Antagonists (MRA) like Eplerenone 25 mg daily for patients already on ACEi and Beta-blockers who have an LVEF ≤ 40% and either symptomatic heart failure or diabetes.
  • •Refer all AMI survivors to a formal cardiac rehabilitation program. Participation significantly reduces all-cause mortality and improves functional capacity post-discharge.
  • •Discharge criteria include hemodynamic stability for 24-48 hours, successful revascularization, absence of high-grade arrhythmias, and a clear plan for dual antiplatelet therapy (DAPT) adherence, typically for 12 months.

Board Review — High Yield

  • •Type 2 MI — Myocardial injury due to supply-demand mismatch (e.g., sepsis, anemia) rather than primary plaque rupture.
  • •Killip Class IV — Represents cardiogenic shock; the highest mortality risk category in AMI.
  • •de Winter T-waves — Upsloping ST-depression with tall, peaked T-waves in precordial leads; signifies acute LAD occlusion.
  • •SCAD — Spontaneous Coronary Artery Dissection; the most common cause of MI in pregnant and postpartum women.
  • •S1Q3T3 — Classic but non-specific ECG finding for pulmonary embolism, a major differential for AMI.
  • •H0/H1 Protocol — Use of high-sensitivity troponin at 0 and 1 hour to rapidly rule out (low delta) or rule in (high delta) AMI.
  • •Right Ventricular Infarct — Suspect with inferior MI + ST-elevation in V4R; treat with fluids, avoid nitrates/diuretics.
  • •Dressler Syndrome — Post-MI pericarditis occurring weeks later; autoimmune-mediated, treated with NSAIDs/Colchicine.

Deep Dive — Evidence Details

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