Non-ST-Segment Elevation Acute Coronary Syndrome (Non-ST-Segment Elevation Myocardial Infarction and Unstable Angina)¶
Chapter 285 | Part 6: Disorders of the Cardiovascular System
KEY CLINICAL POINTS¶
- NSTE-ACS includes NSTEMI (with myocyte necrosis) and unstable angina (UA, no necrosis).
- High-sensitivity troponin (hs-cTn) is the preferred biomarker for diagnosing myocardial necrosis.
- Antiplatelet therapy (aspirin + P2Y inhibitor) and anticoagulation are core treatments.
- Invasive strategy is favored for high-risk patients (e.g., GRACE score >140, cardiogenic shock).
- Long-term management includes lipid-lowering (LDL-C <55 mg/dL), beta-blockers, and statins.
1. DEFINITION & OVERVIEW¶
Non-ST-segment elevation acute coronary syndrome (NSTE-ACS) encompasses non-ST-segment elevation myocardial infarction (NSTEMI) and unstable angina (UA). NSTEMI is defined by evidence of myocyte necrosis (elevated troponin), while UA lacks necrosis but has ischemia. NSTE-ACS is distinguished from STEMI by the absence of ST-segment elevation on ECG.
TIMI Risk Score for NSTE-ACS¶
| RISK MARKERS | INCIDENCE OF ADVERSE CARDIAC EVENTS (% ) |
|---|---|
| Age ‡65 years | 5 |
| Known CAD (‡50% stenosis) | 8 |
| ST deviation >0.5 mm on ECG | 13 |
| › cardiac markers | 20 |
| ‡2 episodes in 24 h | 26 |
| Prior angina | 41 |
| ‡3 CAD risk factors | 41 |
1.1 Classification¶
NSTE-ACS is divided into NSTEMI (with troponin elevation) and UA (no troponin elevation). The spectrum includes asymptomatic ischemia, silent MI, and acute coronary syndromes with varying degrees of myocardial injury.
1.2 Diagnostic Criteria¶
Diagnosis combines clinical history, ECG findings (ST-T changes), and troponin levels. NSTEMI requires troponin elevation with no alternative explanation for myocardial necrosis.
2. EPIDEMIOLOGY¶
Incidence of NSTEMI is rising due to obesity, diabetes, and CKD, while STEMI is declining from aspirin/statin use. NSTE-ACS accounts for ~80% of ACS cases. Mortality ranges from 1–10% in 30 days and 5–15% in the first year.
2.1 Risk Factors¶
Obesity, diabetes, chronic kidney disease, older age, and male sex are major risk factors. Women and minorities have poorer outcomes despite similar risk profiles.
2.2 Demographics¶
NSTEMI is more common in older adults, while UA is more frequent in younger patients. Racial disparities exist, with worse outcomes in minorities and low-income populations.
3. ETIOLOGY & PATHOPHYSIOLOGY¶
NSTE-ACS results from an imbalance between myocardial oxygen supply and demand. Key mechanisms include plaque rupture/fissure, erosion, and coronary spasm. Vulnerable plaques with lipid cores and thin fibrous caps are prone to disruption.
3.1 Plaque Mechanisms¶
Three main processes: (1) plaque fissure with inflammation, (2) plaque fissure without inflammation, (3) plaque erosion. Vulnerable plaques show eccentric stenosis, scalloped edges, and lipid-rich cores.
3.2 Coronary Spasm¶
Epicardial or microvascular spasm can cause ischemia, especially in patients with fixed coronary obstruction. Spasm is more common in vasospastic angina (VA).
4. CLINICAL FEATURES¶
Chest pain is typically substernal, radiating to left arm/shoulder, and may be at rest. Anginal equivalents (dyspnea, epigastric discomfort) are common in women, diabetics, and the elderly. Physical exam may show diaphoresis, tachycardia, or signs of heart failure.
4.1 Symptomatology¶
Chest pain lasts >10 min, occurs at rest, or has crescendo pattern. Anginal equivalents (e.g., dyspnea, nausea) are more common in women and diabetics.
4.2 ECG Findings¶
ST-segment depression is common; T-wave inversions (>0.3 mV) are more specific. New ST elevation may indicate evolving MI.
5. DIFFERENTIAL DIAGNOSIS¶
Differential diagnoses include pulmonary embolism, aortic dissection, cardiac tamponade, and myocarditis. Anginal equivalents (e.g., dyspnea, epigastric pain) must be distinguished from non-cardiac causes.
6. INVESTIGATIONS & DIAGNOSIS¶
Diagnosis combines history, ECG, and troponin. The HEART score (History, ECG, Age, Risk factors, Troponin) and TIMI score guide risk stratification. hs-cTn levels are used to rule out MI within 1–3 hours.
HEART Score for NSTE-ACS¶
| HEART Score Component | Points |
|---|---|
| History of chest pain | 1 |
| ECG abnormalities (ST-T changes) | 1 |
| Age ‡65 years | 1 |
| Risk factors (e.g., diabetes, CKD) | 1 |
| Troponin ‡99th percentile | 1 |
6.1 Biomarkers¶
hs-cTn is the preferred marker. NSTEMI shows progressive troponin rise peaking at 12–24 h. UA may have transient troponin elevation or no elevation.
6.2 Imaging¶
Coronary angiography identifies epicardial stenosis. Stress testing (exercise or pharmacologic) assesses ischemia. Radionuclide ventriculography evaluates LV function.
7. MANAGEMENT & TREATMENT¶
Acute management includes anti-ischemic drugs (nitrates, beta-blockers), antithrombotics (aspirin + P2Y inhibitor), and anticoagulation. Invasive strategy is preferred for high-risk patients; conservative management for low-risk.
Anti-Ischemic Drug Recommendations¶
| Drug | Use | Contraindications |
|---|---|---|
| Nitrates | Relieve angina | Hypotension, PDE-5 inhibitors <24 h |
| Beta-blockers | Reduce ischemia | Heart failure, bradycardia |
| Calcium channel blockers | Vasospastic angina | Hypotension, pulmonary edema |
7.1 Anti-Ischemic Therapy¶
Nitrates (sublingual/IV) relieve angina. Beta-blockers reduce myocardial oxygen demand. Calcium channel blockers are used for vasospastic angina or beta-blocker contraindications.
7.2 Antithrombotic Therapy¶
Aspirin (150–325 mg loading, 75–100 mg/d maintenance) + P2Y inhibitor (clopidogrel, prasugrel, ticagrelor). DAPT duration depends on bleeding vs. ischemic risk.
7.3 Invasive vs. Conservative Strategy¶
Invasive strategy (PCI/CABG) is favored for high-risk patients (GRACE score >140, cardiogenic shock). Conservative management is used for low-risk patients with stable symptoms.
8. PROGNOSIS & COMPLICATIONS¶
Mortality is 1–10% in 30 days and 5–15% in the first year. Complications include recurrent ACS, heart failure, arrhythmias, and sudden cardiac death. Long-term outcomes are excellent (~90–95% survival at 5 years).
8.1 Risk Factors¶
High-risk features include cardiogenic shock, GRACE score >140, and recurrent ischemia. Patients with severe coronary disease have higher mortality.
8.2 Long-Term Outcomes¶
LDL-C <55 mg/dL, beta-blockers, and statins improve prognosis. Patients with no fixed coronary obstruction have lower risk of MI/death.
9. SPECIAL CONSIDERATIONS¶
Women and minorities have poorer outcomes despite similar risk profiles. VA (vasospastic angina) is more common in younger patients with no traditional risk factors. Pregnancy requires careful anticoagulation management.
9.1 Vasospastic Angina¶
Diagnosed by transient ST-segment elevation with rest pain. Provocative testing with acetylcholine or intravenous ergonovine confirms diagnosis. Calcium channel blockers are first-line.
9.2 Racial and Socioeconomic Disparities¶
Minorities and low-income populations have worse outcomes due to delayed care, comorbidities, and limited access to advanced therapies.
10. KEY POINTS & CLINICAL PEARLS¶
- NSTE-ACS includes NSTEMI (troponin elevation) and UA (no necrosis). 2. hs-cTn is the preferred biomarker. 3. Antiplatelet therapy (aspirin + P2Y inhibitor) is essential. 4. Invasive strategy is favored for high-risk patients. 5. Long-term lipid-lowering (LDL-C <55 mg/dL) and beta-blockers improve outcomes.