Unstable Angina (UA) and NSTEMI
Unstable angina (UA) and non–ST-elevation myocardial infarction (NSTEMI) are part of the acute coronary syndrome (ACS) spectrum. Both involve acute myocardial ischemia caused by reduced coronary blood flow—typically from plaque rupture and thrombosis.
The key difference:
Because neither condition presents with persistent ST elevation, diagnosis relies heavily on clinical symptoms, ECG changes, and troponin trends.
Primary References:
Clinical Presentation
Classic ischemic symptoms include:
Chest pressure, tightness, or burning
Radiation to jaw, arm, or back
Shortness of breath
Nausea, diaphoresis, anxiety
Occurs at rest, with minimal exertion, or is worsening compared to baseline
UA is defined by:
Increasing frequency, duration, or severity of angina
New-onset angina (<2 months)
Angina at rest
NSTEMI typically presents similarly but includes measurable troponin elevation.
ECG Findings in Unstable Angina & NSTEMI
The ECG may be normal or show subtle ischemic changes. This makes serial ECGs essential.
Common ischemic changes:
ST-segment depression (horizontal or downsloping)
T-wave inversion (often symmetric and deep)
Transient ST-segment elevation (<20 min)
Pseudonormalization of T waves during pain
Normal ECG does NOT exclude UA/NSTEMI
High-risk features:
Pathophysiology
Both UA and NSTEMI are usually caused by:
Rupture or erosion of an atherosclerotic plaque
Partial coronary artery occlusion
Dynamic thrombus formation
Distal microembolization
Vasoconstriction
Endothelial dysfunction
Whether an event becomes UA or NSTEMI depends on the extent of microvascular obstruction and duration of ischemia.
Differences Between UA and NSTEMI
| Feature | Unstable Angina | NSTEMI |
| Cardiac biomarkers | Normal | Elevated |
| Myocardial necrosis | None | Present |
| ECG | Normal/T-wave inversion/ST depression | Same as UA |
| Chest pain | Present | Present |
| Risk | High-risk ACS | Higher risk than UA |
| Treatment urgency | Urgent | Urgent-to-emergent |
Risk Stratification
Common scoring systems:
High-risk criteria prompting early invasive strategy:
Recurrent chest pain
Dynamic ST/T wave changes
Troponin elevation (NSTEMI)
Hemodynamic instability
Ventricular arrhythmias
CHF symptoms / new MR
Diabetes, renal failure, older age
Reference:
Murphy SP, McCarthy CP, Cohen JA, Rehman S, Jones-O’Connor M, Olshan DS, Singh A, Vaduganathan M, Cui J, Januzzi JL Jr, Wasfy JH. Application of the GRACE, TIMI, and TARRACO Risk Scores in Type 2 Myocardial Infarction. J Am Coll Cardiol. 2025;75(3).
Management
Aspirin
P2Y12 inhibitor (e.g., clopidogrel, ticagrelor)
Anticoagulation (heparin, enoxaparin)
Nitrates (for pain)
Beta blockers (unless contraindicated)
High-intensity statin
Oxygen if needed (SpO2 < 90%)
Treat hypertension or tachycardia contributing to ischemia
Early Invasive Strategy (high-risk patients):
NSTEMI patients with shock or ongoing ischemia may require immediate angiography.
ECG Examples
ST Depression in V4–V6 (Ischemia)
T-Wave Inversion (NSTEMI Pattern)
Widespread ST Depression with STE in aVR (Left Main/Triple Vessel)
Key Points
UA and NSTEMI are caused by partial occlusion of a coronary artery.
NSTEMI is distinguished by troponin elevation, while UA has normal biomarkers.
ECG changes can be subtle or absent—serial ECGs are essential.
High-risk patterns (e.g., widespread ST depression with STE in aVR) require urgent cardiology evaluation.
Treatment focuses on antiplatelet therapy, anticoagulation, beta blockers, statins, and early invasive evaluation.
UA and NSTEMI require rapid recognition to prevent progression to full-thickness MI.