creation date: 2025-10-20 16:19
tags: Pathologies


ST Elevation Myocardial Infarction

Background

Definitions

STEMI refers to a clinical even in which myocardial injury occurs as a result of myocardial ischemia along with electrocardiographic changes (ST elevation).

Many of the nonspecific elements of acute coronary syndrome are discussed on its main page.

Pathophysiology

Myocardial ischemia in the context of acute STEMI occurs as a result of complete blockage of a coronary artery. This results in transmural (affecting the entire thickness of the wall) ischemia and thus causing myocardial injury or necrosis.

The exact pathophysiology depends on the type of MI, listed here. However, generally involves an acute thrombotic event due to plaque rupture and subsequent blockage.

It should be noted that because the occlusion is complete and severe, management is required immediately.

Diagnosis

Criteria

STEMIs can manifest with new ST-segment elevation in two anatomically contiguous leads with the following thresholds:

  • ≥0.1 mV in any leads except V2 or V3
  • For V2 and V3:
    • ≥0.2 mV in males ≥40 years old
    • ≥0.25 mV in males <40 years old
    • ≥0.15 mV in females
      ECG findings with presence of symptoms is sufficient for presumed diagnosis of STEMI.

The Sgarbossa criteria can be used for diagnosis of STEMI in patients with preexisting LBBB:

  • ST elevation of ≥1 mm concordant with QRS
  • ST depression of ≥1 mm in V1, V2, or V3
  • ST elevation of ≥5 mm discordant with QRS

Work-up

Immediately following the diagnosis of STEMI, evaluation for conditions that can modify the treatment should be done.

This includes:

  • Shock - may require reperfusion
  • Heart failure
  • Aortic dissection
  • Coagulopathy and/or thrombocytopenia - STEMI treatment increases bleeding risk

If STEMI is ruled out
If ECG changes are not found, cardiac biomarkers are critical for confirming diagnosis and other forms of ACS.

Additionally, transthoracic echocardiogram can find signs suggesting ischemia or prior MI. A ECG-gated contrast CT angiogram can rule out a number of ACS-mimetic conditions.

Management

The goal of management is to reduce risk of death and reduce the extent of permanent cardiac injury. This is a time-sensitive task due to the diminishing effectiveness of treatment and as such rapid treatment following identification is crucial.

Management consists of routine therapies to slow the progression of coronary artery thrombus formation and symptom management and reperfusion with either PCI or fibrinolysis.

Routine therapy

Regardless of the selection of PCI or fibrinolysis, these therapies are used routinely:

Aspirin

  • Antiplatelet therapy reduces thrombus formation and thus worsening of occlusion
  • Loading dose of uncoated aspirin 162-325 mg chewed or crushed
  • Continued post-discharge as aspirin 81 mg
  • Administered even if patient is taking oral anticoagulants but evidence is unclear for patients with possible aspirin allergy
    Anticoagulation and additional antiplatelets
  • May be added based on reperfusion strategy
    Nitrates
  • Treatment of symptoms of chest discomfort, HF, and/or hypertension
  • Contraindicated if:
    • Patient is hypotensive (<90 mmHg or ≥30 mmHg below baseline)
    • Bradycardic (<50 bpm) or tachycardic (>100 bpm)
    • Suspected RV infarction
    • PDE-5 inhibitor use in prior 24 hours
    • Hypertrophic cardiomyopathy
      Beta blockers
  • Cardioselective PO preferred (eg. metoprolol or atenolol)
  • Contraindicated if patient has shock, HF, bradycardia, or heart block
    Statins
  • Patients who do not already take one will have one started
    Morphine and oxygen
  • Pain management and supplemental oxygen are used as needed

Reperfusion

Selection of PCI or fibrinolysis
Selection is based on the availability of percutaneous coronary intervention (PCI) within 120 minutes. If that is not possible, patient should be given thrombolytic therapy.

  • Door to PCI ~ 30-60 minutes
  • Door to fibrinolysis ~30 minutes

PCI’s effectiveness diminishes with time. Additional relative contraindications include:

  • Inability to obtain vascular access
  • Severe comorbidities or advanced frailty
  • Technical impossibility (eg. anatomy not amenable)
  • Patient refusal of procedure

Fibrolytic therapy effectiveness also diminishes with time and is ideally administered within 12 hours of symptom onset. Rescue PCI may be indicated following fibrinolysis if there is evidence of failed reperfusion.

Percutaneous coronary intervention (PCI)
PCI is a minimally invasive, non-surgical procedure to open narrowed or blocked coronary arteries via balloon angioplasty and stent placement.

The procedure involves:

  1. Assess and catheterization: a catheter is placed through radial/femoral/brachial artery to access the aorta and coronary arteries
  2. Lesion identification: coronary angiograms determine extent, location, and severity
  3. Balloon angioplasty and stenting: a guidewire, balloon, and stent are used to compress the atherosclerotic plaque against the arterial wall

In rare cases, coronary artery bypass grafting (CABG) is indicated if PCI is not possible but is rare, typically if the extent of the occlusion or time since presentation is great enough to skip fibrinolysis.

Complications include risk of bleeding, vascular damage, risk of stent thrombosis, and stroke (3-5%).

Fibrinolysis
Fibrinolytic therapy is indicated if PCI is not available or too much time as passed for PCI to be effective. This consist of administration of fibrinolytic agents which activate the endogenous fibrinolytic pathway, degrading fibrin and thus the thrombus.

Available agents are:

  • Streptokinase IV infusion
  • Alteplase (tPA) IV infusion
  • Reteplase IV bolus x2
  • Tenecteplase (TNK-tPA) IV bolus

It should be noted that fibronolysis is contraindicated with:

  • Prior intracranial hemorrhage
  • Known structural cerebrovascular lesion (AVM)
  • Intracranial neoplasm
  • Ischemic stroke within 3 months (except acute stroke <3 hours)
  • Suspected aortic dissection
  • Active bleeding or bleeding diathesis
  • Significant head or facial trauma within 3 months
    And relatively contraindicated with:
  • History of uncontrolled hypertension
  • Recent major surgery or prolonged CPR
  • Recent internal bleeding
  • Pregnancy or active peptic ulcer
  • Current anticoagulant use with high INR

In cases were fibrinolysis is not possible, late PCI may be indicated. Additionally, aggressive conservative therapy may be necessary.

Post-reperfusion therapy

PCI
Following PCI, management primarily aims to reduce risk of complications and worsening of disease:

  • Dual anti-platelet therapy
  • Beta-blockers
  • Nitrates
  • Aspirin
  • ACE inhibitor (prevents remodelling)
  • Statin (reduces LDL and anti-inflammatory properties)

References

Tools / Guidelines

Additional Reading