What is Non-ST-Elevation Acute Coronary Syndrome (NSTEACS)?

Non-ST-Elevation Acute Coronary Syndrome (NSTEACS) Definition

NSTEACS is a clinical syndrome of acute myocardial ischemia presenting without persistent ST-segment elevation on ECG, encompassing both unstable angina (UA) and non-ST-elevation myocardial infarction (NSTEMI), distinguished solely by the presence or absence of elevated cardiac biomarkers indicating myocardial necrosis. 1

Core Diagnostic Framework

NSTEACS represents one of two major categories of acute coronary syndrome based on ECG presentation 1:

• Patients with persistent ST-elevation → STEMI (requires immediate reperfusion therapy)
• Patients without persistent ST-elevation → NSTEACS (may show ST-depression, T-wave changes, or normal ECG)

Pathophysiological Substrate

The underlying mechanism is atherosclerotic plaque rupture or erosion with superimposed partially occlusive or transiently occlusive thrombus formation, leading to coronary ischemia without complete vessel occlusion 1. This contrasts with STEMI where the thrombus completely occludes the culprit vessel 1.

The process involves 1:

• Disruption of the fibrous cap of an atherosclerotic plaque
• Exposure of highly procoagulant plaque contents to circulating platelets
• Formation of intracoronary thrombus (subtotally occlusive)
• Possible coronary vasospasm contributing to flow reduction

Clinical Distinction: UA vs NSTEMI

The critical differentiator between unstable angina and NSTEMI is the detection of elevated cardiac biomarkers (troponin) 1:

• Unstable Angina: Ischemic symptoms WITHOUT elevated troponin (no myocardial necrosis)
• NSTEMI: Ischemic symptoms WITH elevated troponin (myocardial necrosis present)

Both conditions share identical pathogenesis and clinical presentation but differ only in severity—NSTEMI indicates ischemia sufficiently severe to cause irreversible myocardial damage 1.

Clinical Presentation Characteristics

Typical presentation is pressure-type chest pain occurring at rest or with minimal exertion, lasting ≥10 minutes 1. The pain:

• Most frequently starts retrosternally 1
• May radiate to either/both arms, neck, or jaw 1
• Can occur in these areas independent of chest pain 1

Associated symptoms include 1:

• Diaphoresis
• Dyspnea (most common angina equivalent when presenting as new-onset or increased exertional dyspnea) 1
• Nausea or abdominal pain
• Syncope
• Unexplained fatigue

High-Risk Atypical Presentations

Older patients (≥75 years), women, and those with diabetes mellitus, renal insufficiency, or dementia have increased frequency of atypical presentations 1. Atypical symptoms requiring high suspicion include 1:

• Epigastric pain or indigestion
• Stabbing or pleuritic pain
• Increasing dyspnea without chest pain

Electrocardiographic Findings

By definition, NSTEACS presents WITHOUT persistent ST-segment elevation 1. ECG may show 1:

• ST-segment depression
• T-wave changes (inversion, flattening, or pseudo-normalization)
• No ECG abnormalities (normal ECG does not exclude NSTEACS)

Biomarker Criteria for NSTEMI

NSTEMI requires elevated cardiac troponin with rise and/or fall pattern, with at least one value above the 99th percentile upper reference limit 2. High-sensitivity troponin (hs-cTn) assays are strongly recommended over conventional assays for superior diagnostic accuracy 1.

Epidemiology and Clinical Impact

NSTEACS affects approximately 625,000 patients annually in the United States, representing nearly 70-75% of all ACS presentations 1, 3. Patients with NSTEACS typically have more comorbidities (both cardiac and noncardiac) than STEMI patients 1.

Critical Differential Diagnoses

Must exclude life-threatening non-ACS cardiovascular causes 1:

• Aortic dissection
• Expanding aortic aneurysm
• Pulmonary embolism
• Pericarditis

Non-cardiovascular causes to consider 1, 2:

• Esophageal spasm
• Musculoskeletal pain
• Pneumonia, pleurisy, pneumothorax

Risk Stratification Imperative

Risk assessment is mandatory at initial evaluation to guide management intensity and timing of invasive strategy 1. Validated tools include 1, 2:

• TIMI (Thrombolysis In Myocardial Infarction) risk score
• GRACE (Global Registry of Acute Coronary Events) risk score
• PURSUIT risk score
• NCDR-ACTION registry score

Key Clinical Pitfall

With increasingly sensitive troponin assays, biomarker-negative ACS (unstable angina) is becoming progressively rarer 1. Many cardiac pathologies beyond MI cause troponin elevation, requiring careful clinical context interpretation 1.