Molecular structure pattern

Myocardial Infarction w/ ST-Segment Elevation Initial Assessment

Last updated: 08 September 2026
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Clinical Presentation

Characteristics of Ischemic-type Chest Discomfort

Ischemic-type chest discomfort is commonly described as heaviness, pressure, dull, sharp, stabbing, squeezing, tearing, tightness, or burning in nature and may not be severe. Because symptom severity is not reliably associated with a diagnosis of MI, chest discomfort may be a more appropriate term than chest pain for the main symptom of myocardial ischemia. Chest discomfort is considered acute when it has a sudden onset or change in intensity, duration, or overall pattern, and is stable when symptoms are chronic and consistently triggered by exertion or emotional stress. Discomfort is usually central or left-sided, diffuse and non-localized, and is not positional or affected by movement of the region; it may radiate to the jaw, neck, left arm, back, or shoulder. It may occur at rest or during activity, lasts 10–20 minutes or longer, and may not fully respond to Glyceryl trinitrate (GTN). Occasionally, symptoms are mistaken for indigestion or heartburn if pain occurs in the epigastric region. 



Myocardial Infarction w ST-Segment Elevation_Initial Assesment 1Myocardial Infarction w ST-Segment Elevation_Initial Assesment 1




Associated symptoms may include nausea, vomiting, dyspnea, diaphoresis, palpitations, lightheadedness, dizziness, confusion, syncope, fatigue, and weakness. Women, older adults, and people with diabetes may present with epigastric, interscapular, arm, wrist, jaw, or back pain without chest pain or discomfort, and associated symptoms such as nausea or vomiting, dyspnea, or diaphoresis. MI should be suspected especially if the symptoms are severe and occur suddenly, though some patients do not report chest pain at all and present only with associated symptoms (eg breathlessness, palpitations, nausea, or vomiting). MI may present with autonomic nervous system activation (eg pallor, sweating), hypotension or narrow pulse pressure, bradycardia or tachycardia, third heart sound (S3), basal rales, or occasionally syncope in the elderly. 

History

The ischemic-type chest discomfort as described previously may be caused by a cardiac, possible cardiac or non-cardiac etiology. Patients with STEMI are more likely to present with persistent chest discomfort and to experience vomiting, dizziness and diaphoresis compared with patients with non-STEMI (NSTEMI) who are more likely to present with intermittent symptoms. Symptom relief after nitrate administration is not specific for angina, and symptom improvement with proton pump inhibitors (PPIs) and/or antacids should not be considered sufficient to indicate a non-cardiac etiology. Inquire about the patient’s medical, social and family history and assess CV risk factors. It is also important to identify precipitating causes such as uncontrolled hypertension, anemia, thyrotoxicosis or infection.

Physical Examination

The patient may exhibit pallor and diaphoresis or may be completely normal. Basilar rales may indicate heart failure (HF). Apical systolic murmur, S3 or S4 may be present. New-onset murmurs may be due to ventricular septal rupture and mitral regurgitation. Carotid bruits or peripheral vascular disease indicates extensive atherosclerosis.


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Diagnosis or Diagnostic Criteria

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

MI is diagnosed by a rise and/or fall in cTns, with at least one value above the sex-specific 99th percentile of the URL (acute myocardial injury), together with at least one evidence of acute myocardial ischemia:

  • Clinical history consistent with chest pain of ischemic origin lasting >30 minutes
  • Electrocardiogram (ECG) changes of ischemia/infarction and/or development of pathologic Q waves
  • Imaging evidence of an acute coronary pathology, or new loss of viable myocardium or new regional wall motion abnormality consistent with an ischemic etiology
  • Identification of an intracoronary thrombus by angiography or autopsy


When cardiac imaging or biomarker testing is unavailable or non-diagnostic, MI may be presumed in patients with symptoms consistent with acute myocardial ischemia and supportive clinical evidence of new ischemic ECG changes and/or development of pathological Q waves.

Initial Diagnosis of STEMI

The patient presents with a history of prolonged chest pain/discomfort, ie symptoms of acute myocardial ischemia. ECG reveals new ischemic changes, persistent ST-segment elevations, (presumed) new left bundle branch block (LBBB), or pathological Q waves. New or presumed new-onset LBBB is no longer considered as a STEMI equivalent in isolation; however, new non-rate-related LBBB or right bundle branch block (RBBB) is associated with adverse prognosis. A decision to start treatment using percutaneous coronary intervention may be based on the patient’s clinical history and ECG results.  

Acute Coronary Syndrome (ACS)  

Acute Coronary Syndrome with Persistent ST-Segment Elevation  

STEMI presents with elevated levels of cardiac biomarkers. This usually has a completely occluded vessel, resulting in transmural myocardial ischemia and infarction. This is increasingly recognized as more appropriately corresponding to occlusion MI (OMI). 

Acute Coronary Syndrome without Persistent ST-Segment Elevation (Non-ST Elevation ACS [NSTE-ACS])  

Unstable angina (UA) is ischemic discomfort that presents with normal cardiac biomarkers in the blood with or without ischemia-related ECG changes. NSTEMI presents with elevated levels of cardiac biomarkers. This may have a partially occluded coronary artery resulting in subendocardial ischemia. This is increasingly recognized as more appropriately  corresponding to non-occlusion MI (NOMI).  

Please see Acute Coronary Syndrome without Persistent ST-Segment Elevation disease management chart for further information.

Screening

Risk Stratification  

Identifying patients who are at increased risk of further reinfarction or death is essential in order that it can be prevented or intervention can be done accordingly. A referral of high-risk patients to specialty centers should be made for early coronary angiography and revascularization. Risk stratification of post-STEMI patients can be done clinically or by using the Thrombolysis in Myocardial Infarction (TIMI) risk score for a 30-day outcome risk assessment and the Global Registry of Acute Coronary Events (GRACE) risk score for a 6-month outcome risk assessment. Another available risk score post-STEMI is the Killip classification which predicts 30-day mortality. This is relevant for patients who did not receive percutaneous coronary intervention, including those with >48 hours of presentation. Risk assessment should be done repeatedly during hospitalization and at discharge. 

High-Risk Patients  

High-risk patients are those with left ventricular ejection fraction (LVEF) <35%, ischemia that affects >50% of viable myocardium and are post-revascularization (percutaneous coronary intervention or coronary artery bypass graft [CABG]). 

The clinical indicators for high-risk patients include:

  • Advanced age
  • Hypotension and cardiogenic shock
  • Anterior infarction
  • Elevated initial serum creatinine
  • Malignant arrhythmias
  • Early angina on minimal exertion/post-infarct angina
  • Tachycardia
  • Killip class >1
  • Previous infarction
  • History of HF
  • Persistent chest pain
  • Peripheral arterial disease

Medium-Risk Patients  

Medium-risk patients are patients not considered low risk or high risk based on imaging criteria and should be treated based on symptomatic status.  

Low-Risk Patients  

Low-risk patients are those who have LVEF >50% or mild inducible ischemia that affects <20% of viable myocardium.