creation date: 2025-10-20 16:19
tags: Pathologies
Non-ST Elevation Myocardial Infarction
Background
Definitions
NSTEMI refers to myocardial infarction without the ECG changes seen with a STEMI.
Many of the nonspecific elements of acute coronary syndrome are discussed on its main page.
Pathophysiology
As with other forms of ACS, the pathophysiology of an MI involves the mismatch of myocardial oxygen demand and supply. In the case of NSTEMI, a partial occlusion of the coronary artery results in the condition. A number of causes can result flow-limitation of blood which includes:
- Stable plaque
- Vasospasm
- Coronary embolism
- Coronary arteritis
Non-coronary injury to the heart can also produce NSTEMI. Other causes including hypotension, pulmonary embolism, and tachycardia can cause increased oxygen demand that cannot be met.
As there is still partial oxygen supply, the ischemia and infarction occurs at the inner one-third of the myocardium (the subendocardium). This is thus called subendocardial infarction.
Diagnosis
Criteria
As NSTEMI does not have characteristic ECG findings, cardiac biomarkers are the mainstay of diagnosis.
A diagnosis of NSTEMI requires:
- Elevated cardiac troponin (cTn) I and T - ≥99th percentile or serial increase
- Clinical history and/or ECG findings (ischemia or pathological Q waves)
It should be noted that early presentation following onset of symptoms may produce a negative test (most patients can be diagnosed within 2-3 hrs). In these cases, serial testing is indicated until 6 hours after presentation. In highly suspicious cases, 12 hour sampling should be done.
Work-up
As with all ACS workup, an ECG should be performed to rule out STEMI.
In general, the approach to troponin measurements is as follows:
- Initial measurement at presentation
- If not elevated, repeat in 3-6 hours; if high-suspicion, repeat sooner
- If patient is presenting late, a change in troponin level between serial measurements may not be noticeable without longer period
In cases where troponin is elevated in the absence of ischemia, workup may be necessary for other causes of cardiac injury.
Differential
A number of causes can result in elevated troponin which includes:
- Heart failure
- Rapid atrial fibrillation
- Myocarditis
- Anthracycline cardiotoxicity
- Subendocardial wall stress
- Myopericarditis
- Sepsis
- Chronic kidney disease
Life threatening causes not relating to coronary artery disease are:
- Pulmonary embolism
- Stress-induced cardiomyopathy
Management
Initial therapy
Initial therapy consists of antiischemic and analgesic therapy:
- Supplemental oxygen as needed based on O2 saturation
- Nitroglycerin - routine for pain management unless contraindicated
- Morphine - for extreme levels of pain but should be avoided due to negative outcomes
- Beta blockers
- Statin therapy
Additional therapy includes:
- Aspirin and platelet P2Y12 receptor blocker
- Anticoagulation
Revascularization
Following diagnosis, angiography and intervention are indicated for early intervention and prevent worse cardiac events.
Decision to revascularize depends on cardiac risk stratification using the TIMI score (score ≥2):
- Age ≥65
- Presence of at least three risk factor for CAD (ie. DM, hypertension, hyperlipidemia, smoking, FHx)
- Previous hx of coronary stenosis of 50% or more
- Presence of ≥2 episodes of angina 24 hours prior to presentation
- Aspirin use in past 7 days
- ST-segment deviations ≥0.05 mV on initial ECG at admission
- Elevated serum cardiac markers of necrosis
Prevention of arrhythmias
Arrhythmias are often seen during and after the acute phase of NSTEMIs. Prophylactic use of beta blockers and treatment of hypokalemia and hypomagnesemia is recommended.