Non-ST elevation myocardial infarction (NSTEMI)


NSTEMI is diagnosed in patients who have symptoms consistent with acute coronary syndrome (ACS) and troponin elevation, but without ECG changes consistent with STEMI.

The differentiation between NSTEMI and unstable angina pectoris (UAP) is usually retrospective, based on the presence or absence of raised cardiac enzymes.

Compared to UAP, patients with NSTEMI have higher risk of death. 

Clinical manifestation 

The “typical” presentation of NSTEMI is a pressure-like substernal pain, occurring at rest. It usually lasts more than 20 minutes, can radiate to the neck, jaw or arm. The pain may be associated with dyspnea, nausea or vomiting, syncope, fatigue, or diaphoresis. 


Non‐occluding thrombus formed on a ruptured plaque in the coronary artery  is the most frequent cause of NSTEMI. Also the reason can be progressive coronary artery narrowing from atherosclerosis or restenosis after cardiac revascularization. Conditions not particularly related to the coronary arteries such as hypotension, hypertension, tachycardia, aortic stenosis, and pulmonary embolism lead to NSTEMI because the increased oxygen demand cannot be met.


The coronary artery is incompletely occluded by platelet-rich “white” thrombus that is recently formed from platelet aggregation at the site of a damaged inner surface of a coronary artery. The trigger for this platelet aggregation is usually rupture of an atherosclerotic plaque in an artery with < 50% stenosis. This white thrombus is in sharp contrast to the mature red blood cell and fibrin-rich “red” or “mature” thrombus, which is the hallmark pathologic finding in patients with STEMI. 

ECG manifestation

  • ST depressions
  • T wave  inversions 

Dynamic changes (different from baseline ECG or changing over time) are strongly suggestive for myocardial ischaemia. With the remission of angina, ST depressions disappear. 

ST depression can be either upsloping, downsloping, or horizontal 

  • Horizontal or downsloping ST depression ≥ 0.5 mm at the J-point in ≥ 2 contiguous leads indicates myocardial ischaemia
  • ST depression ≥ 1 mm is more specific and conveys a worse prognosis
  • ST depression ≥ 2 mm in ≥ 3 leads is associated with a high probability of NSTEMI and predicts significant mortality (6x higher risk of death)

  • Upsloping ST depression is non-specific for myocardial ischaemia.
  • Presence of widespread ST depressions plus ST elevation in aVR > 1 mm is suggestive of left main coronary artery occlusion

ST depression due to subendocardial ischaemia is usually widespread — typically present in leads I, II, V4-6 and a variable number of additional leads.

T wave inversion must fulfill these criteria:

  • be present in ≥ 2 contiguous leads that have dominant R waves (R/S ratio > 1)
  • be dynamic
  • be at least 1 mm deep 

T wave inversion is not a very specific sign if present in leads III, aVR and V1.

Other reported ecg abnormalities include a tall and broad R wave, disappearance of the S wave, a taller T wave, and negative U waves.

!!! You can’t localise NSTEMI and NAP based on ECG !!!


  • coronary angiography/PCI
  • UFH
  • ASA
  • P2Y12 inhibitors
  • nitrates

ECG 1 NSTEMI in a patient with ST depressions in I, aVL, V2-6, negative T waves in I, aVL 

ECG 2  NSTEMI in a patient with repolarization changes in II, III, aVF, V4-V6

ECG 3 NSTEMI in a patient with 1mm ST depression in V5-V6 and negative T waves in I, aVL


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  3. J. Bělohlávek, M. Aschermann. 10.03.2008. Doporučený postup pro diagnostiku a léčbu akutních koronárních syndromù bez elevací ST úsekù na EKG
  5. Michael Simons, MDJeffrey A Breall, MD, PhD. Overview of the acute management of non-ST elevation acute coronary syndromes.