What is the management of St Elevation Myocardial Infarction (STEMI)?

ST-Elevation Myocardial Infarction (STEMI)

Etiology

STEMI results from acute thrombotic occlusion of a coronary artery, typically following rupture or erosion of an atherosclerotic plaque. 1

• The underlying pathology involves atherosclerotic plaque destabilization, leading to platelet aggregation, thrombus formation, and complete vessel occlusion 1
• Risk factors include smoking, hypertension, diabetes mellitus, dyslipidemia, family history of premature coronary disease, and sedentary lifestyle 2

Epidemiology and Risk Factors

STEMI remains a major cause of cardiovascular morbidity and mortality worldwide, though incidence has declined with improved prevention strategies. 3

• Traditional risk factors include:
  • Smoking (strongest modifiable risk factor requiring immediate cessation) 1
  • Diabetes mellitus (increases risk and worsens outcomes) 1, 2
  • Hypertension (contributes to atherosclerotic burden) 1, 2
  • Dyslipidemia (elevated LDL-C drives plaque formation) 2
  • Age and sex (risk increases with age; males at higher risk at younger ages) 1
  • Prior MI or coronary disease (indicates established atherosclerosis) 1

Pathophysiology

Complete thrombotic occlusion of a coronary artery leads to transmural myocardial necrosis if reperfusion is not achieved within 12 hours. 1

• Plaque rupture or erosion exposes thrombogenic material, triggering platelet activation and coagulation cascade 1
• Thrombus propagation causes complete vessel occlusion, resulting in myocardial ischemia progressing to infarction 1
• Time is myocardium: Irreversible myocardial damage begins within 20-40 minutes of complete occlusion, with infarct size directly correlating with duration of ischemia 4, 3
• Complications include left ventricular dysfunction, heart failure, cardiogenic shock, mechanical complications (ventricular septal rupture, papillary muscle rupture, free wall rupture), arrhythmias, and death 1

Clinical Manifestations

Typical presentation includes severe, crushing chest pain lasting >20 minutes, often radiating to the left arm, jaw, or back, accompanied by diaphoresis, nausea, and dyspnea. 1, 2

• Chest discomfort characteristics: Substernal pressure, tightness, or squeezing sensation not relieved by rest or nitroglycerin 1, 2
• Associated symptoms: Diaphoresis, nausea, vomiting, dyspnea, lightheadedness, syncope 1, 2
• Atypical presentations (more common in elderly, women, diabetics): Isolated dyspnea, epigastric pain, syncope, or fatigue without chest pain 2
• Physical examination findings:
  • Tachycardia, hypotension (suggests cardiogenic shock or right ventricular infarction) 1, 2
  • Pulmonary rales (indicates heart failure) 1, 2
  • Fourth heart sound (S4), new murmur (suggests mechanical complication) 1
  • Signs of cardiogenic shock: Cool extremities, altered mental status, oliguria 1, 2

Diagnostics

A 12-lead ECG must be obtained within 10 minutes of first medical contact in all patients with suspected STEMI. 1

ECG Criteria for STEMI Diagnosis:

• ST-segment elevation ≥0.1 mV (1 mm) in at least two contiguous precordial or adjacent limb leads 1, 2
• New or presumed new left bundle branch block 2
• Right-sided ECG leads (V3R, V4R) should be obtained in inferior STEMI to detect right ventricular infarction 1
• Posterior leads (V7-V9) may identify isolated posterior MI 1

Additional Diagnostic Studies:

• Cardiac biomarkers (troponin I or T, CK-MB): Confirm myocardial necrosis but should not delay reperfusion therapy 1
• Routine echocardiography during hospitalization to assess LV/RV function, detect mechanical complications, and exclude LV thrombus 1, 2
• Chest radiography: Evaluate for pulmonary edema, alternative diagnoses 1

Critical Pitfall:

• Never delay reperfusion therapy waiting for cardiac biomarker results—ECG diagnosis is sufficient to initiate treatment 1

Management

Immediate Pre-Hospital Management

Patients with suspected STEMI should activate emergency medical services (EMS) immediately rather than self-transport, as EMS enables pre-hospital ECG, early diagnosis, and direct triage to appropriate facilities. 1

• Aspirin 162-325 mg (chewable, non-enteric coated) should be administered immediately by EMS or patient if prescribed 1, 2
• 12-lead ECG by EMS personnel at first medical contact enables pre-hospital STEMI diagnosis and activation of catheterization laboratory 1
• Direct transport to PCI-capable hospital bypassing emergency department when STEMI diagnosed pre-hospital 1

Reperfusion Strategy: The Critical Decision

Primary PCI is the preferred reperfusion method when performed by an experienced team within 90-120 minutes of first medical contact. 1

Primary PCI Strategy (Preferred):

• Goal: First medical contact-to-device time ≤90 minutes for patients presenting directly to PCI-capable hospital 1
• Goal: First medical contact-to-device time ≤120 minutes for patients requiring transfer from non-PCI-capable hospital 1
• Patients transferred for primary PCI should bypass the emergency department and go directly to the catheterization laboratory 1
• Absolute indications for primary PCI regardless of time delay:
  • Cardiogenic shock 1
  • Acute severe heart failure 1
  • Contraindications to fibrinolytic therapy 1

Fibrinolytic Therapy Strategy (When Primary PCI Not Feasible):

Fibrinolytic therapy should be administered within 30 minutes of hospital arrival when anticipated first medical contact-to-device time exceeds 120 minutes. 1

• Optimal timing: Most effective when administered within 3 hours of symptom onset, preferably in pre-hospital setting 1, 5
• Fibrin-specific agents recommended (in order of preference): Tenecteplase, alteplase, or reteplase 1, 5
• Tenecteplase dosing (single weight-adjusted IV bolus): 5
  • 30 mg for <60 kg
  • 35 mg for 60-69 kg
  • 40 mg for 70-79 kg
  • 45 mg for 80-89 kg
  • 50 mg for ≥90 kg
  • 50% dose reduction for patients ≥75 years to reduce stroke risk 5

Absolute contraindications to fibrinolytic therapy: 6

• Prior intracranial hemorrhage at any time
• Known structural cerebral vascular lesion
• Ischemic stroke within 3 months
• Suspected aortic dissection
• Active bleeding or bleeding diathesis
• Significant closed-head trauma within 3 months

Pharmacoinvasive Strategy (Post-Fibrinolysis Management)

All patients receiving fibrinolytic therapy must be transferred immediately to a PCI-capable center for either rescue PCI or routine angiography within 2-24 hours. 1, 5

• Rescue PCI indicated immediately when: 1, 5
  • Fibrinolysis fails (<50% ST-segment resolution at 60-90 minutes)
  • Hemodynamic instability develops
  • Electrical instability (ventricular arrhythmias)
  • Worsening ischemia
• Routine angiography and PCI of infarct-related artery recommended 2-24 hours after successful fibrinolysis 1, 5
• Critical timing rule: Angiography should not be performed within first 2-3 hours after fibrinolytic administration unless rescue PCI needed 1
• Emergency angiography indicated for cardiogenic shock or heart failure regardless of fibrinolysis success 1, 5

Antithrombotic Therapy

Antiplatelet Therapy:

Aspirin 150-325 mg oral (chewable) or IV 250-500 mg should be administered immediately, followed by 75-100 mg daily indefinitely. 1, 2

A potent P2Y12 inhibitor (ticagrelor or prasugrel) should be administered before or at the time of PCI and continued for 12 months. 1, 2

• Ticagrelor (preferred in most patients): 1, 2
  • Loading dose: 180 mg
  • Maintenance: 90 mg twice daily for 12 months
• Prasugrel: 1, 6
  • Loading dose: 60 mg
  • Maintenance: 10 mg daily (5 mg daily if <60 kg)
  • Generally not recommended in patients ≥75 years except high-risk patients (diabetes or prior MI) 6
  • Contraindicated in patients with prior stroke or TIA 6
  • Consider ticagrelor over prasugrel in patients with cerebrovascular disease 7
• Clopidogrel (if ticagrelor or prasugrel unavailable or contraindicated): 1
  • Loading dose: 300-600 mg
  • Maintenance: 75 mg daily

Anticoagulation:

For patients undergoing primary PCI: 1

• Unfractionated heparin (weight-adjusted IV bolus followed by infusion) or
• Enoxaparin or
• Bivalirudin
• Fondaparinux not recommended for primary PCI 1

For patients receiving fibrinolytic therapy: 1, 5

• Enoxaparin IV followed by subcutaneous (preferred over unfractionated heparin) 1, 5
• Unfractionated heparin (weight-adjusted IV bolus followed by infusion) 1, 5
• Continue anticoagulation until revascularization or for duration of hospital stay (up to 8 days) 1, 5

Stent Selection in Primary PCI:

Both bare-metal stents and drug-eluting stents are acceptable for primary PCI. 1

• Bare-metal stents preferred in patients with: 1
  • High bleeding risk
  • Inability to comply with 12 months of dual antiplatelet therapy
  • Anticipated invasive or surgical procedures within next year
• Drug-eluting stents contraindicated in patients unable to tolerate or comply with prolonged dual antiplatelet therapy due to increased stent thrombosis risk 1

Special Populations:

Cardiac Arrest Patients:

Immediate angiography and PCI should be performed in resuscitated out-of-hospital cardiac arrest patients whose post-resuscitation ECG shows STEMI. 1, 2

• Therapeutic hypothermia should be started as soon as possible in comatose patients with STEMI and out-of-hospital cardiac arrest caused by ventricular fibrillation or pulseless ventricular tachycardia 1

Late Presenters (12-24 Hours):

Primary PCI is reasonable in patients with ongoing ischemia 12-24 hours after symptom onset. 1

• Routine PCI of totally occluded infarct artery >48 hours after STEMI onset is not indicated in asymptomatic patients 1

Adjunctive Medical Therapy:

• High-intensity statin therapy initiated immediately with target LDL-C <70 mg/dL or ≥50% reduction 2
• Beta-blockers (oral, not IV) within 24 hours in hemodynamically stable patients 1
• ACE inhibitors or ARBs within 24 hours, especially if anterior MI, heart failure, or LVEF <40% 1
• Aldosterone antagonists if LVEF ≤40% and heart failure or diabetes, without significant renal dysfunction or hyperkalemia 1
• Avoid NSAIDs (except aspirin) as they increase mortality, reinfarction, hypertension, heart failure, and myocardial rupture 1

Post-Discharge Management:

Dual antiplatelet therapy (aspirin plus ticagrelor or prasugrel) should be continued for 12 months after PCI unless excessive bleeding risk develops. 1, 2

• Aspirin 75-100 mg daily indefinitely 1, 2
• Smoking cessation with repeated counseling, nicotine replacement, varenicline, or bupropion 1
• Cardiac rehabilitation program participation 1
• Routine echocardiography to assess ventricular function and detect complications 1, 2

Critical Pitfalls to Avoid:

• Never delay primary PCI to obtain additional imaging or wait for biomarkers—ECG diagnosis is sufficient 1
• Never perform PCI of non-infarct arteries during primary PCI in hemodynamically stable patients—this increases harm 1
• Never discontinue dual antiplatelet therapy prematurely—this dramatically increases risk of stent thrombosis, MI, and death 1
• Never administer facilitated PCI with full-dose fibrinolysis followed by immediate PCI—this strategy is harmful 1
• Never perform angiography within 2-3 hours after fibrinolytic administration unless rescue PCI needed 1