Acute Coronary Syndromes — Part 4: NSTEMI/UA Management, Special Populations & Disposition
Early invasive vs conservative strategy, timing of angiography, antiplatelet and anticoagulation for NSTEMI, special populations (women, elderly, diabetes, CKD, cocaine), arrhythmias, and chest pain disposition.
1. NSTEMI/UA — Invasive Strategy Selection
1.1 Early Invasive vs. Initially Conservative Strategy
The fundamental management decision in NSTE-ACS is whether to pursue an early invasive strategy (routine coronary angiography with intent to revascularize) or an initially conservative strategy (ischemia-guided approach with angiography only for recurrent or provocable ischemia). This decision is driven by risk stratification.1 2 3
| Strategy | Definition | Indications |
|---|---|---|
| Immediate invasive (< 2 hours) | Emergent coronary angiography | Hemodynamic instability or cardiogenic shock; recurrent or ongoing chest pain refractory to medical therapy; life-threatening arrhythmias (VT/VF); mechanical complications of MI; acute heart failure clearly related to NSTE-ACS |
| Early invasive (< 24 hours) | Coronary angiography within 24 hours of presentation | GRACE score > 140; rise or fall in troponin consistent with MI; dynamic ST or T-wave changes (symptomatic or silent) |
| Invasive (< 72 hours) | Coronary angiography within 72 hours | GRACE score 109-140; diabetes; renal insufficiency (eGFR < 60 mL/min/1.73m²); LVEF < 40%; early post-infarction angina; prior PCI within 6 months; prior CABG; recurrent symptoms during observation |
| Initially conservative / selective invasive | Medical therapy with angiography only for recurrent ischemia, positive stress test, or high-risk features | Low-risk patients: GRACE score ≤ 108; negative troponins (serial); no recurrent symptoms; no ST changes; no heart failure; no hemodynamic instability; patient preference with informed decision-making |
1.2 Evidence Summary for Invasive Strategy
| Trial | Population | Key Finding |
|---|---|---|
| FRISC II | NSTE-ACS | Early invasive strategy reduced death/MI at 1 and 5 years in intermediate-to-high risk patients |
| TACTICS-TIMI 18 | NSTE-ACS (elevated troponin) | Early invasive reduced 6-month death/MI/rehospitalization (especially in TIMI risk ≥ 3) |
| ICTUS | NSTE-ACS (elevated troponin) | No significant difference in death/MI at 1 year; conservative strategy is reasonable in low-risk troponin-positive patients |
| TIMACS | NSTE-ACS | Early intervention (< 24h) reduced death/MI/stroke at 6 months in GRACE > 140; no benefit in lower-risk patients |
| ACCOAST | Pre-treated with prasugrel vs. placebo before angiography | Pre-treatment with prasugrel INCREASED bleeding without reducing ischemic events; supports NOT pre-treating with prasugrel before angiography |
1.3 Timing of Angiography — Summary by Risk
| Risk Level | Timing | Risk Criteria |
|---|---|---|
| Very high risk | Immediate (< 2 hours) | Hemodynamic instability, cardiogenic shock, refractory angina, life-threatening arrhythmia, acute HF, mechanical complication |
| High risk | Early (< 24 hours) | GRACE > 140, significant troponin rise/fall, dynamic ST/T changes |
| Intermediate risk | Within 72 hours | GRACE 109-140, DM, CKD, LVEF < 40%, prior PCI/CABG, early post-infarction angina |
| Low risk | Selective (if ischemia on non-invasive testing) | GRACE ≤ 108, no troponin rise, no recurrent symptoms, no ECG changes |
2. Antiplatelet Therapy in NSTEMI/UA
2.1 Aspirin
- Loading dose: 162-325 mg chewed (non-enteric-coated), as early as possible (Class I)1
- Maintenance: 81 mg daily indefinitely
2.2 P2Y12 Inhibitor Selection for NSTEMI
| Scenario | Agent | Dose | Notes |
|---|---|---|---|
| NSTEMI — early invasive (going to cath lab) | Ticagrelor preferred | 180 mg load (can be given pre-cath); 90 mg BID maintenance | PLATO trial: ticagrelor reduced cardiovascular death, MI, and stroke vs clopidogrel in ACS with planned invasive strategy; OK to administer before angiography (unlike prasugrel)4 |
| NSTEMI — early invasive (going to cath lab) | Prasugrel | 60 mg load given at time of PCI (NOT before angiography) | ACCOAST showed harm from pre-treatment; load only after coronary anatomy known and PCI planned; contraindicated in prior stroke/TIA |
| NSTEMI — early invasive | Clopidogrel (alternative) | 600 mg load, then 75 mg daily | Appropriate if ticagrelor/prasugrel not available, if high bleeding risk, or if patient is likely to need CABG within 5 days (clopidogrel has shorter washout vs prasugrel) |
| NSTEMI — initially conservative | Ticagrelor or clopidogrel | Ticagrelor: 180 mg then 90 mg BID; Clopidogrel: 300-600 mg then 75 mg daily | Prasugrel should NOT be used without defining anatomy (requires knowledge that PCI will be performed) |
| NSTEMI patient likely to need CABG | Delay P2Y12 if possible | Ticagrelor: hold 3-5 days; Clopidogrel: hold 5 days; Prasugrel: hold 7 days before CABG | Reduces perioperative bleeding; balance bleeding risk vs ischemic risk of withholding |
2.3 Pre-Treatment with P2Y12 Inhibitors
The practice of “pre-treatment” (administering a P2Y12 inhibitor before knowing the coronary anatomy) in NSTEMI is debated:2 3
- Ticagrelor: Pre-treatment is considered reasonable for patients in whom PCI is highly likely and anatomy not yet defined (reversible agent with moderate risk profile; the European cardiology guidelines committee gives a Class IIa recommendation for ticagrelor pre-treatment when PCI is planned)
- Clopidogrel: Pre-treatment is reasonable when early invasive strategy is planned and CABG is unlikely
- Prasugrel: Pre-treatment before coronary anatomy is known is NOT recommended (Class III — harm; ACCOAST trial)
2.4 Glycoprotein IIb/IIIa Inhibitors in NSTEMI
The routine upstream use of GP IIb/IIIa inhibitors is no longer recommended. Their role has been narrowed to:1 2
| Setting | Recommendation |
|---|---|
| Routine upstream use (before angiography) | NOT recommended (Class III — no benefit; increased bleeding) |
| Provisional use during PCI | Class IIa — consider for large thrombus burden, slow/no-reflow, or thrombotic complications |
| Patients on DAPT with potent P2Y12 inhibitor | Generally not needed |
| Patients not yet on P2Y12 inhibitor undergoing PCI | Consider as bridge antiplatelet if P2Y12 not loaded |
3. Anticoagulation in NSTEMI/UA
3.1 Anticoagulation Options
Anticoagulation should be initiated at the time of NSTE-ACS diagnosis and continued until invasive evaluation or for the duration of hospitalization:1 2
| Agent | Dose | Notes | Guideline Class |
|---|---|---|---|
| UFH | 60 units/kg IV bolus (max 4,000 units), then 12 units/kg/h infusion (max 1,000 units/h); target aPTT 50-70 seconds | Most widely used; easily titratable; reversible with protamine; preferred if early invasive strategy planned (< 24-48h) | Class I |
| Enoxaparin | 1 mg/kg SC q12h; if CrCl < 30: 1 mg/kg SC q24h; if CrCl < 15 or on dialysis: use UFH instead | Do not switch between enoxaparin and UFH (increases bleeding); if going to PCI while on enoxaparin: if last dose < 8h ago, no additional anticoagulation needed; if 8-12h, give 0.3 mg/kg IV bolus | Class I |
| Bivalirudin | 0.1 mg/kg IV bolus, then 0.25 mg/kg/h infusion (pre-cath); at PCI: additional 0.5 mg/kg IV bolus and increase infusion to 1.75 mg/kg/h | Direct thrombin inhibitor; useful in HIT; lower bleeding than UFH + GP IIb/IIIa | Class I |
| Fondaparinux | 2.5 mg SC daily | Factor Xa inhibitor; lowest bleeding rates (OASIS-5 trial); must add UFH bolus (85 units/kg, or 60 units/kg with GP IIb/IIIa) at time of PCI due to catheter thrombosis risk; recommended by the European cardiology guidelines committee as preferred anticoagulant for NSTEMI when conservative strategy chosen | Class I (conservative); Class IIa (invasive with UFH supplement) |
3.2 Choosing an Anticoagulant
| Clinical Scenario | Preferred Agent | Rationale |
|---|---|---|
| Early invasive strategy (< 24-48h to cath) | UFH or bivalirudin | Easily managed peri-procedurally; short half-life; can discontinue post-PCI |
| Conservative strategy | Fondaparinux or enoxaparin | Fondaparinux has lowest bleeding rates; enoxaparin does not require aPTT monitoring |
| Heparin-induced thrombocytopenia (HIT) | Bivalirudin | Direct thrombin inhibitor; no cross-reactivity with HIT antibodies |
| Renal impairment (CrCl < 30) | UFH | Renally cleared agents (enoxaparin, fondaparinux) accumulate; UFH is hepatically cleared |
| Planned CABG | UFH | Short half-life allows easy perioperative management |
3.3 Duration of Anticoagulation
- If PCI performed: Anticoagulation generally discontinued after successful PCI unless ongoing indication (LV thrombus, AF, mechanical valve)
- If conservative strategy: Continue anticoagulation for duration of hospitalization or up to 8 days (whichever is shorter), then discontinue
- Transition to oral anticoagulation: Only if separate indication exists (see triple therapy section below)
4. Special Populations
4.1 Women
Women presenting with ACS have important clinical and pathophysiological differences from men:5 6
| Feature | Key Considerations |
|---|---|
| Presentation | Women are more likely to present with atypical symptoms: dyspnea, fatigue, nausea, jaw/neck/back pain, palpitations; less likely to report classic substernal pressure |
| Underdiagnosis | Women are more likely to have normal or non-diagnostic ECGs, lower troponin levels (below male-normed thresholds), and are more likely to be discharged with missed MI diagnosis |
| Sex-specific troponin thresholds | Use sex-specific 99th percentile cutoffs for hs-cTn; women have lower thresholds — using overall thresholds misses approximately 40% of MIs in women |
| Pathophysiology | Higher prevalence of plaque erosion (vs. rupture), SCAD, coronary microvascular disease (INOCA), and takotsubo cardiomyopathy |
| SCAD | Spontaneous coronary artery dissection accounts for up to 35% of MI in women < 50 years; associated with FMD, pregnancy, connective tissue disorders; conservative management preferred in most cases (PCI has high complication rate in SCAD) |
| Treatment disparities | Women receive evidence-based therapies (DAPT, statin, invasive strategy) less frequently than men; outcomes after PCI are comparable when treated equally |
| Bleeding | Women have higher bleeding risk with antithrombotic therapy (lower body weight, lower renal clearance); dose-adjust anticoagulants appropriately |
| Pregnancy | ACS in pregnancy — avoid ACE inhibitors, ARBs, statins; avoid radiation when possible; PCI preferred over fibrinolysis if STEMI |
4.2 Elderly (≥ 75 Years)
| Feature | Key Considerations |
|---|---|
| Presentation | More likely to present atypically (dyspnea as anginal equivalent, confusion, syncope, fatigue); painless MI more common |
| Comorbidities | Higher prevalence of CKD, prior stroke, anemia, frailty — all increase bleeding risk |
| Risk-benefit | Higher absolute ischemic risk → greater absolute benefit from invasive strategy; BUT also higher bleeding risk |
| Antiplatelet therapy | Ticagrelor or clopidogrel preferred over prasugrel (TRITON-TIMI 38 showed no net benefit in ≥ 75 years); if prasugrel used, consider 5 mg maintenance dose |
| Fibrinolysis dose adjustment | Tenecteplase: consider half-dose in patients ≥ 75 years; enoxaparin: no IV bolus, 0.75 mg/kg SC q12h (max 75 mg) |
| Invasive strategy | Age alone should NOT preclude invasive management; frailty assessment more important than chronological age |
| PCI access | Radial access strongly preferred (lower bleeding, lower mortality vs femoral in elderly) |
4.3 Diabetes Mellitus
| Feature | Key Considerations |
|---|---|
| Risk | Diabetes confers 2-4× increased risk of ACS; diabetic patients have higher mortality from MI and more multivessel disease |
| Presentation | “Silent” MI more common (autonomic neuropathy); atypical symptoms (dyspnea, diaphoresis without pain) |
| Invasive strategy | Early invasive strategy recommended (diabetes is an indication for angiography within 72 hours) |
| Revascularization | CABG may be preferred over PCI for multivessel disease in diabetics (FREEDOM trial: CABG superior to PCI with DES for death/MI/stroke at 5 years in diabetic patients with multivessel CAD)7 |
| Antiplatelet | No specific dose adjustments; clopidogrel resistance may be more common in diabetics (favor ticagrelor or prasugrel) |
| Glucose management | Avoid hypoglycemia (associated with worse outcomes in ACS); target glucose 140-180 mg/dL in ICU/acute phase; insulin infusion for glucose > 180 mg/dL; avoid oral sulfonylureas in acute phase |
| Secondary prevention | Aggressive risk factor modification; HbA1c target per diabetes guidelines; statin mandatory; ACE inhibitor/ARB for those with proteinuria or HFrEF |
4.4 Chronic Kidney Disease
| Feature | Key Considerations |
|---|---|
| Risk | CKD is an independent risk factor for ACS and is associated with 2-3× mortality increase; considered CAD equivalent |
| Troponin interpretation | Chronically elevated troponin (especially hs-cTnT) — use dynamic change (rise/fall) for diagnosis, not a single value; see Part 2, Section 6.1 |
| Drug dosing | Enoxaparin: reduce to 1 mg/kg q24h if CrCl < 30; avoid if CrCl < 15 (use UFH); fondaparinux: avoid if CrCl < 20; GP IIb/IIIa: dose adjust (see Part 3); avoid bivalirudin if CrCl < 30 (or use with extreme caution) |
| Contrast nephropathy | Hydrate pre-procedure (isotonic saline preferred); minimize contrast volume (contrast:CrCl ratio < 3.7); hold metformin for 48 hours peri-catheterization; consider iso-osmolar contrast |
| Revascularization | CKD patients benefit from invasive strategy but have higher procedural complications; risk-benefit discussion essential |
| Dialysis patients | Use UFH for anticoagulation; troponin interpretation requires serial testing; higher baseline bleeding risk; higher in-hospital and long-term mortality |
4.5 Cocaine-Associated Chest Pain and ACS
Cocaine use is a common cause of chest pain in young ED patients and can cause true ACS through several mechanisms:8
| Mechanism | Pathophysiology |
|---|---|
| Coronary vasospasm | Alpha-adrenergic stimulation → intense coronary vasoconstriction (most common mechanism) |
| Increased myocardial oxygen demand | Tachycardia, hypertension → supply-demand mismatch |
| Accelerated atherosclerosis | Chronic use promotes endothelial dysfunction and atherogenesis |
| Prothrombotic state | Platelet activation, increased fibrinogen, impaired fibrinolysis |
| Direct myocardial toxicity | Sodium channel blockade → arrhythmias; sympathomimetic excess |
Management of Cocaine-Associated ACS
| Intervention | Recommendation |
|---|---|
| Benzodiazepines | First-line — reduce sympathetic drive, decrease HR, BP, and chest pain; diazepam 5-10 mg IV or lorazepam 1-2 mg IV |
| Nitroglycerin | Safe and effective for cocaine-associated vasospasm; SL or IV as per standard ACS dosing |
| Aspirin | Standard dose — Class I |
| Calcium channel blockers | Second-line vasodilator; verapamil or diltiazem for refractory vasospasm |
| Beta-blockers | CONTROVERSIAL — traditionally contraindicated (concern for “unopposed alpha stimulation” worsening vasospasm); however, recent evidence (meta-analyses and observational studies) suggests no harm and possible benefit, particularly with carvedilol (mixed alpha/beta blocker) or labetalol. The emergency medicine expert consensus panel suggests selective beta-blockers should be avoided initially but may be considered once cocaine effects have resolved (typically > 12-24 hours).8 |
| Phentolamine | Alpha-blocker; 5-10 mg IV for refractory hypertension or vasospasm; theoretical benefit but limited clinical data |
| Fibrinolysis | Higher risk of bleeding in cocaine users; PCI preferred if STEMI |
| PCI | Preferred reperfusion strategy for cocaine-associated STEMI; however, many patients with cocaine chest pain have vasospasm without fixed obstruction — angiography helps distinguish |
4.6 Prior Coronary Artery Bypass Grafting (CABG)
| Feature | Key Considerations |
|---|---|
| Pathology | Graft disease (SVG degeneration, thrombus) vs native vessel progression; SVGs have diffuse atherosclerosis with friable plaque |
| ECG interpretation | Prior CABG may alter expected ECG territories; LBBB common; old MI changes may be present |
| Invasive strategy | Early invasive strategy recommended (within 72 hours); complex anatomy requires experienced operators |
| PCI of SVG | High risk of distal embolization; embolic protection devices recommended; drug-eluting stents preferred |
| Medical therapy | Standard ACS pharmacotherapy applies; higher risk population |
4.7 Patients on Oral Anticoagulation
Patients already on oral anticoagulation (warfarin, DOAC) who develop ACS present a management challenge due to the need for DAPT on top of anticoagulation (“triple therapy”):1 2 3
| Scenario | Recommended Approach |
|---|---|
| Initial management | Hold DOAC or warfarin for procedure; use parenteral anticoagulation for ACS (UFH preferred — allows ACT monitoring) |
| PCI approach | Radial access (lower bleeding); consider bare-metal or latest-generation drug-eluting stent (shorter minimum DAPT duration) |
| Triple therapy duration | Minimize — typically 1 week to 1 month of triple therapy (OAC + aspirin + P2Y12), then transition to dual therapy (OAC + single antiplatelet — usually P2Y12 inhibitor) |
| P2Y12 selection | Clopidogrel preferred over ticagrelor/prasugrel when combined with OAC (lower bleeding; per WOEST, PIONEER AF-PCI, RE-DUAL PCI, AUGUSTUS, ENTRUST-AF PCI trials) |
| Aspirin duration | Discontinue aspirin early (after 1 week to 1 month) while continuing OAC + clopidogrel |
| DOAC vs warfarin | DOAC preferred over warfarin when combined with antiplatelet therapy (lower bleeding; apixaban 5 mg BID or rivaroxaban 15 mg daily with P2Y12 — from AUGUSTUS and PIONEER AF-PCI, respectively) |
5. Chest Pain Disposition Framework
5.1 Admission Criteria (Monitored/Telemetry Bed)
Patients should be admitted to a monitored bed if any of the following are present:9
- Confirmed STEMI or NSTEMI (elevated troponin with ischemic context)
- Ongoing ischemic symptoms despite initial treatment
- Hemodynamic instability
- Significant arrhythmia (new AF, sustained VT, high-grade AV block)
- Signs of heart failure
- HEART score ≥ 7 (high risk)
- GRACE score > 140
- Plans for urgent/emergent cardiac catheterization
- New significant ST-segment or T-wave changes
5.2 Observation Unit Criteria
Patients appropriate for observation (6-24 hour stay with serial monitoring):9
- HEART score 4-6 (intermediate risk)
- Indeterminate initial troponin (slightly above normal, not clearly rising)
- Resolved symptoms with stable hemodynamics
- Normal or non-specific ECG
- Awaiting serial troponin results
- Planned non-invasive stress testing or CCTA
5.3 Safe Discharge Criteria
Patients may be considered for ED discharge with outpatient follow-up if ALL criteria met:9
- HEART score 0-3
- Two negative serial hs-cTn (validated 0/1h or 0/3h protocol) OR single hs-cTn below limit of detection with symptom onset > 3 hours
- Normal or unchanged ECG
- Symptom-free at time of disposition
- No hemodynamic instability during evaluation
- No high-risk features on history (e.g., exertional syncope, rest angina with hemodynamic compromise)
- Reliable follow-up within 72 hours
- Appropriate discharge instructions provided
5.4 Discharge Instructions for Low-Risk Chest Pain
| Component | Details |
|---|---|
| Return precautions | Return to ED immediately for recurrent chest pain, worsening dyspnea, syncope, or palpitations |
| Follow-up | Primary care or cardiology within 72 hours |
| Medications | Aspirin 81 mg daily (if not contraindicated); nitroglycerin SL PRN (if prescribed); continue home medications |
| Lifestyle | Smoking cessation counseling; dietary recommendations; exercise counseling (avoid vigorous exercise until follow-up) |
| Stress testing | Outpatient functional testing or CCTA within 1-2 weeks if clinical suspicion warrants further evaluation |
6. NSTEMI/UA — Additional Management Considerations
6.1 Anti-Ischemic Medical Therapy in NSTEMI
| Agent | Dose and Route | Indications | Contraindications |
|---|---|---|---|
| Nitroglycerin | 0.4 mg SL q5min × 3; then 5-200 mcg/min IV if ongoing ischemia | Ongoing chest pain, hypertension, heart failure | SBP < 90, RV infarction, PDE-5 inhibitor use, severe aortic stenosis |
| Beta-blocker | Metoprolol tartrate 25-50 mg PO q6-12h; carvedilol 6.25 mg PO BID; target HR 50-60 | All NSTEMI patients without contraindications (within 24 hours) | Active HF/pulmonary edema, hypotension, bradycardia, high-grade AV block, severe reactive airway disease, cocaine use (acute) |
| Calcium channel blocker | Diltiazem 30-60 mg PO TID-QID or amlodipine 5-10 mg daily | Beta-blocker contraindicated or refractory angina despite beta-blocker; variant (vasospastic) angina | Diltiazem/verapamil: avoid with severe LV dysfunction (EF < 30%); avoid combining with beta-blocker if concern for heart block |
| Ranolazine | 500-1000 mg PO BID | Refractory angina on maximal medical therapy | QTc > 500 ms; strong CYP3A4 inhibitors; hepatic impairment |
| Statin | High-intensity: atorvastatin 80 mg or rosuvastatin 20-40 mg daily | All ACS patients regardless of baseline LDL | Active liver disease; pregnancy |
| ACE inhibitor | Lisinopril 5 mg, ramipril 2.5 mg, captopril 6.25 mg; titrate to target | Anterior MI, HFrEF (EF ≤ 40%), diabetes, hypertension | SBP < 100, bilateral RAS, K > 5.5, pregnancy |
6.2 Unstable Angina — Contemporary Management
With the widespread adoption of high-sensitivity troponin assays, the incidence of diagnosed “unstable angina” has declined significantly as many patients previously classified as UA are now reclassified as NSTEMI due to detection of minor myocardial necrosis.3 9
For patients with true UA (negative serial hs-cTn with ischemic symptoms and/or ECG changes):
- Risk stratification with HEART score, TIMI score, or GRACE score
- Anti-ischemic medical therapy
- Disposition based on risk score:
- Low risk (HEART 0-3, negative troponins, non-ischemic ECG): consider discharge with outpatient functional testing
- Intermediate risk (HEART 4-6 or recurrent symptoms): observation, serial troponin, non-invasive testing or invasive evaluation
- High risk (HEART ≥ 7, dynamic ECG changes, rest angina): admission and invasive strategy
7. Arrhythmia Management in NSTEMI
7.1 Atrial Fibrillation in ACS
New-onset atrial fibrillation occurs in 10-20% of ACS patients and is associated with higher in-hospital mortality, stroke, and heart failure.1
| Management | Details |
|---|---|
| Hemodynamically unstable AF | Immediate synchronized cardioversion (biphasic 120-200J) |
| Rate control (first-line) | Beta-blocker (metoprolol 5 mg IV q5min × 3, then PO) if no HF/hypotension; amiodarone (150 mg IV over 10 min, then 1 mg/min × 6h, then 0.5 mg/min × 18h) if HF present or beta-blocker contraindicated; diltiazem 0.25 mg/kg IV over 2 min, then 5-15 mg/h infusion (avoid with severe LV dysfunction) |
| Anticoagulation | Therapeutic anticoagulation for AF in ACS (already on parenteral AC for ACS — continue); address long-term anticoagulation need with CHA2DS2-VASc scoring before discharge |
| Rhythm control | Amiodarone is preferred antiarrhythmic in the ACS setting; flecainide/propafenone contraindicated in structural heart disease |
7.2 Ventricular Arrhythmias in NSTEMI
- Less common than in STEMI but still significant
- Sustained VT/VF: Treat per ACLS; amiodarone or lidocaine; emergent revascularization; electrolyte correction
- NSVT: Common; does not typically require antiarrhythmic therapy; optimize beta-blockade and electrolytes
- Polymorphic VT/torsades: Check QTc; magnesium 2g IV; overdrive pacing; discontinue QT-prolonging medications; if due to ischemia (normal QT), treat as ischemic VF
References
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Collet JP, Thiele H, Barbato E, et al. “2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation.” Eur Heart J. 2021;42(14):1289-1367. DOI: 10.1093/eurheartj/ehaa575 ↩︎ ↩︎ ↩︎ ↩︎ ↩︎
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Wallentin L, Becker RC, Budaj A, et al. “Ticagrelor versus Clopidogrel in Patients with Acute Coronary Syndromes (PLATO).” N Engl J Med. 2009;361(11):1045-1057. DOI: 10.1056/NEJMoa0904327 ↩︎
Mehta LS, Beckie TM, DeVon HA, et al. “Acute Myocardial Infarction in Women: A Scientific Statement From the American Heart Association.” Circulation. 2016;133(9):916-947. DOI: 10.1161/CIR.0000000000000351 ↩︎
Gulati M, Levy PD, Mukherjee D, et al. “2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for the Evaluation and Diagnosis of Chest Pain.” Circulation. 2021;144(22):e588-e637. DOI: 10.1161/CIR.0000000000001029 ↩︎
Farkouh ME, Domanski M, Sleeper LA, et al. “Strategies for Multivessel Revascularization in Patients with Diabetes (FREEDOM).” N Engl J Med. 2012;367(25):2375-2384. DOI: 10.1056/NEJMoa1211585 ↩︎
McCord J, Jneid H, Hollander JE, et al. “Management of Cocaine-Associated Chest Pain and Myocardial Infarction: A Scientific Statement From the American Heart Association.” Circulation. 2008;117(14):1897-1907. DOI: 10.1161/CIRCULATIONAHA.107.188950 ↩︎ ↩︎
Writing Committee Members, Gulati M, Levy PD, et al. “2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for the Evaluation and Diagnosis of Chest Pain: Executive Summary.” J Am Coll Cardiol. 2021;78(22):2218-2261. DOI: 10.1016/j.jacc.2021.07.053 ↩︎ ↩︎ ↩︎ ↩︎