Treatment Guideline Chart
Myocardial infarction is death of cardiac myocytes (necrosis) caused by prolonged ischemia. The term acute "usually" refers to the time 6 hours to 7 days following pathologic appearance of the infarct.
The patient may experience ischemic-type chest discomfort with accompanying symptoms of nausea, vomiting, dyspnea, diaphoresis, lightheadedness, dizziness, syncope, fatigue and weakness.
Rapid diagnosis and risk stratification of chest pain in patients are important to identify acute myocardial infarction patients who will benefit from reperfusion therapy.

Myocardial%20infarction%20w_%20st-segment%20elevation Diagnosis


Rapid diagnosis and risk stratification of chest pain patients are important to identify acute myocardial infarction (AMI) patients who will benefit from reperfusion therapy (ie reopening of the occluded artery)  

Initial Diagnosis of STEMI

  • Patient should present with history of prolonged chest pain/discomfort, ie symptoms of AMI
  • Electrocardiogram (ECG) reveals new ischemic changes, persistent ST-segment elevations, (presumed) new left bundle-branch block (LBBB), or pathological Q waves
    • A decision to start treatment using PCI may be based on the patient’s clinical history and ECG results

Confirmatory Tests for the Diagnosis of MI

  • Elevated biochemical markers of myocardial necrosis
    • Increase and/or decrease of cardiac troponin values with at least 1 value >99th percentile upper reference limit (URL)
    • These can confirm diagnosis in the absence of ECG changes
  • 2D echocardiography and perfusion scintigraphy, if available, can be used to look for (presumed) new regional wall motion abnormalities or loss of viable myocardium consistent with an ischemic cause
  • Intracoronary thrombus identified by angiography or autopsy 


Patient History

  • Ischemic-type chest discomfort as previously described

Laboratory Tests

Electrocardiogram (ECG)

  • Obtain and interpret as soon as possible, preferably within 10 minutes of emergency department (ED) arrival, since even at the early stage, ECG is rarely normal
    • If ECG shows ST-segment elevations or new or presumed new LBBB, then patient should be immediately evaluated for and if with no contraindications, given reperfusion therapy
    • If resting ECG is without ST elevation or is non-interpretable (eg new RBBB, paced rhythm), consider non-ST-segment elevation acute coronary syndromes (NSTE-ACS) (eg NSTEMI or unstable angina)
  • ECG changes of AMI are evolutionary
    • Hyperacute changes of a tall peaked T wave
    • ST-segment elevation followed by development of Q wave
      • In resource-limited settings, development of pathological Q waves can confirm the diagnosis of MI if only the patient’s clinical history and ECG results are available
    • Then return of ST-segment to isoelectric and T-wave inversion
  • ST-segment elevation
    • New or presumed new ST-segment elevation at the J point in 2 or more contiguous leads should be considered at ≥0.2 mV for men ≥40 years, ≥0.25 mV for men <40 years, or ≥0.15 mV for women regardless of age in leads V2-V3, and/or ≥0.1 mV in other leads
  • ST-segment depression and T-wave changes
    • New horizontal or down-sloping ST-segment depression ≥0.05 mV in 2 contiguous leads
    • T-wave inversion ≥0.1 mV in 2 contiguous leads with prominent R wave or R/S ratio >1
  • ECG may be vague in the early hours and may not show ST-segment elevation or new Q waves
    • Repeat or serial ECG should be taken to compare with previous records and detect evolving infarction
    • Additional chest leads (V7-9) and right ventricular leads may be helpful

Biochemical Indicators for Detecting Myocardial Necrosis

  • Blood samples should be taken on 1st assessment and 3-6 hours later
  • Preferred biomarker for myocardial damage is cardiac troponin (T or I)
    • High-sensitivity cardiac troponin (hs-cTn) assays have higher negative predictive value for AMI than standard assays and hs-cTn levels >5-fold the URL have high positive predictive value for acute type 1 MI  
      • hs-cTn assays are associated with a 2-fold increase in identifying type 2 MI, eg tachyarrhythmias, heart failure
  • If cardiac troponin assays are not available, CK-MB assay is the preferred alternative
    • Maximal CK-MB exceeding the 99th percentile of the values for a reference control group on 2 consecutive samples or
    • Maximal value over 2x the upper limit of normal for the specific institution at least once during the 1st hour following the index clinical event
    • Values for CK-MB should rise and fall; if the values remain elevated without change this is typically not due to MI
  • A diagnosis of reinfarction is supported by a value increase of ≥20% between 2 samples of troponins or CK-MB collected 3-6 hours apart 


  • Helpful in detecting wall motion abnormalities or loss of viable myocardium in the presence of elevated biomarker values
  • Without any delay to therapy, obtain chest X-ray
  • Perform chest X-ray, transthoracic and/or transesophageal echocardiography, contrast computed tomographic (CT) scan to differentiate ST-segment elevation myocardial infarction (STEMI) from aortic dissection in a doubtful presentation
  • Perform echocardiography to allow risk stratification of patients with chest pain upon ED arrival and in those whose diagnosis is unclear and ECG is not diagnostic, especially in patients with LBBB or pacing and suspicion of posterior STEMI with anterior ST-segment depressions
  • Transthoracic echocardiography may provide evidence of focal wall motion abnormalities and facilitate triage in patients with ECG findings that are difficult to interpret


  • All patients with ischemic symptoms of ≤12 hours and persistent ST-segment elevation or new or presumed new LBBB should undergo early mechanical (percutaneous coronary intervention or PCI) or pharmacological (fibrinolytic) reperfusion therapy unless they have contraindications
  • Primary PCI is superior to fibrinolysis when done at an appropriate time and at experienced institutions
    • Both appear to have the same benefits in low-risk patients presenting within 3 hours of symptom onset but primary PCI is preferred in those presenting with a symptom duration of 3-12 hours
  • Goal is to administer reperfusion treatment within 30 minutes of patient arriving at hospital for fibrinolytic therapy and within 90 minutes of patient arriving at hospital for PCI  
  • Patients who received primary PCI or fibrinolysis had better survival outcomes than those who did not receive any reperfusion therapy  

Primary PCI should be considered in the following patients with:  

  • Contraindications to IV fibrinolytic therapy
  • High-risk features or presenting with cardiogenic shock
  • Symptom duration of >12 hours and ECG evidence of ongoing ischemia 
    • Consider a routine primary PCI in patients presenting 12-48 hours after onset of symptoms

In institutions that are experienced in PCI (stenting and/or angioplasty)

  • STEMI diagnosis to wire crossing should be within 90 minutes
  • For primary PCI, stenting is recommended over balloon angioplasty

In institutions that are not experienced in PCI 

  • If patient is transferred from a non-PCI-capable center, wire crossing should be performed within 120 minutes from STEMI diagnosis
    • If unable to meet target time for primary PCI (ie >120 minutes), consider pre-hospital or nearest in-hospital fibrinolytic therapy within 12 hours of onset of symptoms then transfer patient to a PCI-capable center for pharmacoinvasive treatment strategy 
  • If there are no contraindications, fibrinolytic therapy should be started within 30 minutes in STEMI patients initially presenting to a hospital without PCI capability and who cannot be transferred to a PCI center in a timely manner
    • Bolus administration of fibrinolytic therapy should be within 10 minutes from STEMI diagnosis 
  • Careful individual assessment needs to be made of the potential benefits of mechanical reperfusion vs risks of treatment delay and transportation to the nearest interventional catheterization lab

Inclusion Criteria for IV Fibrinolytic Therapy

  • Symptoms consistent with AMI
  • ST-segment elevation on ECG 
  • New or presumably new bundle-branch block (that is obscuring ST-segment analysis) and history of MI symptoms
  • Time to therapy from onset of angina: <12 hours; most beneficial if <6 hours (golden hour is <2 hours)
    • No significant benefit if >12 hours, except in patients with ongoing ischemia and ST-segment elevation on ECG 
  • First medical contact in a PCI center of >90 minutes or transfer from a non-PCI center of >120 minutes

Absolute Contraindications

  • Previous hemorrhagic stroke or stroke of unknown origin at any time
  • Ischemic stroke within 3 months except acute ischemic stroke within 4.5 hours
  • Known intracranial neoplasm or central nervous system damage
  • Significant closed-head or facial trauma within 3 months
  • Known structural cerebral vascular lesion (eg arteriovenous malformation)
  • Aortic dissection (confirmed or suspected)
  • GI bleeding within the last month
  • Active bleeding or bleeding diathesis (does not include menses)
  • Surgery within 2 months intracranially or intraspinally
  • Severe uncontrolled hypertension that is unresponsive to emergency therapy
  • For Streptokinase: Prior treatment within the previous 6 months

Relative Contraindications

Risks versus benefits must be considered

  • Uncontrolled or refractory hypertension on presentation (SBP >180 mmHg and/or DBP >110 mmHg); history of severe uncontrolled hypertension
  • Transient ischemic attack within >3 months
  • Taking oral anticoagulants
  • Traumatic or refractory resuscitation
  • For Streptokinase/Anistreplase: Prior exposure (especially within 5 days–12 months) or prior allergic reaction
    • Antibodies may be present and can impair the action of the agent
  • Pregnancy
  • Active peptic ulcer disease
  • Advanced liver disease
  • Infective endocarditis
  • Dementia
  • Major surgery within <3 weeks
  • Internal bleeding within 2-4 weeks
  • Non-compressible vascular punctures


  • Myocardial infarction can be classified clinically as:
    • Type 1: Acute athero-thrombosis is demonstrated post-mortem in the artery supplying the infarcted myocardium
    • Type 2: Myocardial oxygen supply and demand imbalance not related to acute athero-thrombosis
    • Type 3: Cardiac death in patients with symptoms suggestive of myocardial ischemia and presumed new ischemic changes on ECG prior to cardiac troponin values becoming available or abnormal
    • Type 4a: Percutaneous coronary intervention (PCI)-related MI
    • Type 4b: Stent or scaffold thrombosis associated with PCI
    • Type 4c: Restenosis associated with PCI
    • Type 5: Coronary artery bypass grafting (CABG)-related MI
Editor's Recommendations
Special Reports