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.
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.
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
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:
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 !!!
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