Cardiovascular

Acute coronary syndrome: NSTEMI risk stratification and antithrombotic therapy

Clinical Overview and When to Suspect NSTEMI

— Anginal chest pain >10 min at rest, crescendo pattern, or new-onset CCS class III/IV angina within 2 months

— Anginal equivalents in women, elderly (>75), diabetics, CKD: dyspnea, epigastric pain, fatigue, syncope, diaphoresis

— Post-CABG or post-PCI patient with recurrent pain

— Type 1: primary plaque event → treat with dual antiplatelet + anticoagulation + revascularization

— Type 2: supply-demand mismatch (sepsis, tachyarrhythmia, anemia, hypoxia, hypertensive crisis) → treat the underlying stressor; routine DAPT/heparin/cath not indicated unless clear plaque event

Acute coronary syndrome (ACS) spans unstable angina (UA), non-ST-elevation MI (NSTEMI), and ST-elevation MI (STEMI). NSTEMI is defined by myocardial necrosis (elevated high-sensitivity troponin with rise/fall pattern) without persistent ST elevation on ECG.

Pathophysiology: most commonly non-occlusive thrombus on a ruptured or eroded coronary plaque → subendocardial ischemia. Less commonly: coronary vasospasm, embolism, SCAD, supply-demand mismatch (type 2 MI).

When to suspect in an outpatient or ED setting:

Initial triage goal: within 10 minutes of arrival — 12-lead ECG, IV access, continuous telemetry, aspirin 162–325 mg chewed if no contraindication.

Universal Definition of MI (4th): troponin rise/fall with ≥1 value >99th percentile URL plus ischemic symptoms, new ischemic ECG changes, pathologic Q waves, imaging evidence of new wall-motion abnormality, or intracoronary thrombus.

Key distinction: UA vs NSTEMI is purely biochemical — both have identical clinical/ECG features, but NSTEMI has positive troponin. With high-sensitivity troponin assays, true UA has become rare; most "UA" reclassifies as NSTEMI.

Type 1 vs Type 2 MI (critical Step 3 concept):

Board pearl: Cocaine-associated NSTEMI — avoid beta-blockers acutely (unopposed alpha → worse vasospasm); use benzodiazepines, nitrates, CCBs first.

Presentation Patterns and Key History

— Pain often lasts longer than typical angina (>20 min) and may occur at rest

— Crescendo pattern over hours to days, not abrupt onset

— May wax and wane — patient may feel "better" between episodes but troponin still rises

— Women: fatigue, sleep disturbance, dyspnea weeks before event

— Elderly >75: confusion, syncope, weakness, falls

— Diabetics: silent ischemia or isolated dyspnea (autonomic neuropathy blunts pain)

— CKD/dialysis: dyspnea, hypotension during HD session

— Postoperative patients: hypotension, tachycardia, troponin bump on POD 1–3

— PQRST of pain

— Cardiac risk factors: HTN, DM, dyslipidemia, smoking, family h/o premature CAD (men <55, women <65), CKD

— Prior CAD: MI, PCI/stent location and date, CABG, EF

— Bleeding history: GI bleed, intracranial hemorrhage, recent surgery, anticoagulant use → critical for antithrombotic decisions

— Medications: aspirin, P2Y12 inhibitor, anticoagulants, ED drugs (sildenafil within 24h → no nitrates)

— Cocaine/methamphetamine use in young patients

— Last meal (relevant if going to cath lab)

Classic anginal pattern: substernal pressure/tightness, radiating to left arm, jaw, or epigastrium, with diaphoresis, nausea, dyspnea. Worse with exertion, partially relieved by rest or nitroglycerin.

NSTEMI-specific clues:

Atypical presentations (overrepresented on Step 3):

Targeted history (5 minutes max):

Step 3 management: In a stable-appearing patient with chest pain, do not delay the ECG for the H&P. Order ECG first within 10 minutes, then complete history while awaiting results and initial troponin.

Board pearl: A patient with known CAD who reports angina at lower threshold than usual or at rest meets criteria for ACS even with a normal initial ECG and troponin — admit and serial troponin.

CCS pearl: On CCS cases, immediately order: ECG, troponin, CBC, BMP, PT/PTT, lipid panel, CXR, telemetry, IV access, aspirin 325 mg chewed, oxygen if SpO2 <90%.

Physical Exam Findings and Hemodynamic Assessment

— Tachycardia + hypotension → cardiogenic shock or RV infarct → upgrade urgency

— Hypertension → increases myocardial O2 demand; treat with IV nitroglycerin or beta-blocker

— Bradycardia + hypotension → inferior/RV ischemia (RCA territory)

— SpO2 <90% → suggests pulmonary edema or alternative dx (PE)

— S4 gallop: stiff ischemic ventricle, classic in active ischemia

— S3 gallop: systolic dysfunction, suggests larger infarct or pre-existing HF

— New systolic murmur: mechanical complication — papillary muscle dysfunction/rupture (MR) or VSR; usually a complication of completed MI (days 3–7), but acute MR can occur with NSTEMI

— Pericardial rub: post-MI pericarditis (Dressler later)

— I: no HF (~6%)

— II: rales, S3 (~17%)

— III: pulmonary edema (~38%)

— IV: cardiogenic shock (~67%)

General appearance: diaphoresis, pallor, anxiety, Levine sign (clenched fist over chest). These are nonspecific but suggest ongoing ischemia.

Vital signs — risk-stratifying:

Cardiac exam:

Pulmonary exam: rales/crackles → Killip class ≥II → worse prognosis

Vascular exam: unequal pulses, BP differential >20 mmHg between arms, interscapular bruit → suspect aortic dissection before giving antithrombotics

Extremities: cool, mottled, delayed cap refill → cardiogenic shock

Killip classification (in-hospital mortality):

Key distinction: A new murmur + acute pulmonary edema several days after NSTEMI should prompt urgent TTE — looking for papillary muscle rupture (posteromedial papillary muscle, supplied by single PDA branch, is most vulnerable). Surgical emergency.

Board pearl: Always check bilateral arm BPs and feel femoral pulses before initiating heparin/antiplatelets — missed aortic dissection treated as ACS is catastrophic. Widened mediastinum on CXR is a clue.

Step 3 management: Do not delay reperfusion decisions waiting for a full exam — but a 60-second focused cardiopulmonary and pulse exam is non-negotiable.

Diagnostic Workup — ECG and Biomarkers

— ST depression ≥0.5 mm in ≥2 contiguous leads (most specific)

— T-wave inversion ≥1 mm in leads with dominant R wave

— Transient ST elevation (<20 min) — treat as NSTE-ACS

— Normal ECG in up to 30% of NSTEMI — does NOT rule out ACS

— High-sensitivity troponin (hs-cTn) I or T is gold standard

— 0/1-hour or 0/2-hour algorithms (ESC): rule-in if hs-cTn very high or significant absolute delta; rule-out if very low at 0h and 1h

— US algorithm typically 0 and 3 hours

— Rise/fall distinguishes acute MI from chronic elevation (CKD, HF, myocarditis)

— CK-MB is obsolete for diagnosis but can detect reinfarction (short half-life ~24h)

12-lead ECG within 10 minutes of presentation; repeat every 15–30 min if initial nondiagnostic and symptoms persist.

NSTEMI ECG findings (any of):

Posterior MI mimic — ST depression in V1–V3 with tall R waves and upright T waves → obtain posterior leads V7–V9; ST elevation ≥0.5 mm there = STEMI equivalent → emergent cath, not NSTEMI pathway.

Wellens syndrome: deep symmetric T-wave inversions or biphasic T waves in V2–V3 in a pain-free patient → critical proximal LAD stenosis; high-risk NSTE-ACS — needs early angiography, avoid stress test.

de Winter T waves: upsloping ST depression at J point with tall symmetric T waves in precordial leads → proximal LAD occlusion equivalent.

aVR ST elevation ≥1 mm with diffuse ST depression → left main or 3-vessel disease.

Cardiac biomarkers:

Key distinction: Elevated troponin ≠ NSTEMI. Differential: myocarditis, PE, sepsis, HF exacerbation, CKD baseline, takotsubo, tachyarrhythmia. The rise/fall pattern + clinical context defines MI.

Board pearl: A single hs-troponin at presentation below the limit of detection (LoD) in a patient with symptoms >3 hours rules out NSTEMI with >99% NPV.

CCS pearl: Order ECG and troponin q3h ×2–3 sets in any chest pain admission until ACS ruled in or out.

Diagnostic Workup — Advanced and Confirmatory Studies

— Obtain in all NSTEMI patients to assess LVEF, regional wall-motion abnormalities, valvular disease, pericardial effusion, RV function

— Urgent TTE if hemodynamically unstable, new murmur, or suspected mechanical complication

— LVEF guides discharge medications (ACEi/ARB, MRA, ICD eligibility)

— Reserved for low-risk patients ruled out for MI (negative serial troponins, no ECG changes, low HEART/TIMI score)

— Exercise treadmill if can exercise and baseline ECG interpretable

— Pharmacologic (dobutamine echo, regadenoson/dipyridamole SPECT/PET, stress CMR) if cannot exercise or uninterpretable ECG (LBBB, paced, LVH with strain, WPW, digoxin)

— Avoid in active ischemia, unstable angina, or recent MI within 2 days

Echocardiography (TTE):

CXR: rule out alternative dx (pneumothorax, dissection, pneumonia), assess for pulmonary edema/cardiomegaly.

Coronary angiography: the definitive anatomic study; timing depends on risk stratification (see chunk 6 and 8).

CT coronary angiography (CCTA): appropriate for low-to-intermediate risk patients with nondiagnostic ECG and negative/borderline troponin, to rule out obstructive CAD. High NPV. Not for high-risk ACS — go to cath.

Stress testing:

Cardiac MRI: evaluates myocarditis vs MI, viability, infiltrative disease — useful when angiography shows nonobstructive CAD ("MINOCA" workup).

MINOCA (MI with non-obstructive coronaries): <50% stenosis on angiography. Workup: CMR, IVUS/OCT for plaque erosion/SCAD, vasospasm provocation, hypercoagulable panel if young.

Key distinction: Stress testing is for rule-out chest pain pathways, not for established NSTEMI. Once NSTEMI is diagnosed, the patient needs angiography, not stress imaging.

Board pearl: A young woman with NSTEMI and "clean" coronaries → think spontaneous coronary artery dissection (SCAD); manage medically (DAPT, beta-blocker) unless ongoing ischemia — avoid stenting unless necessary as wall is friable.

Step 3 management: Order TTE before discharge in every NSTEMI to document LVEF — drives ACEi/ARB, MRA, and ICD-evaluation decisions at 40 days.

Risk Stratification and Invasive Strategy Timing

— TIMI risk score (0–7): age ≥65, ≥3 CAD risk factors, known CAD (≥50% stenosis), ASA use in past 7 days, severe angina (≥2 episodes in 24h), ST deviation ≥0.5 mm, positive biomarker. Score ≥3 = benefits from early invasive strategy.

— GRACE score (more discriminative): age, HR, SBP, Cr, Killip class, cardiac arrest, ST deviation, troponin. >140 = high risk.

— Immediate (<2 h) — "very high risk":

· Hemodynamic instability or cardiogenic shock

· Refractory/recurrent angina despite max medical therapy

· Life-threatening arrhythmias or cardiac arrest

· Mechanical complications (acute MR, VSR)

· Acute heart failure clearly related to NSTE-ACS

· Recurrent dynamic ST/T changes, especially with intermittent ST elevation

— Early invasive (<24 h) — "high risk":

· GRACE >140

· Rise/fall of troponin consistent with MI

· New ST-segment depression

— Delayed invasive (<72 h) — "intermediate risk":

· DM, CKD (eGFR <60), LVEF <40%, early post-MI angina, prior PCI/CABG, GRACE 109–140

— Ischemia-guided (selective) strategy:

· Low-risk (TIMI 0–1, GRACE <109, negative troponin) — stress test before discharge; cath only if positive

Two validated scores in NSTE-ACS:

Invasive strategy timing (2021 ACC/AHA, 2023 ESC):

Key distinction: Early invasive (<24h) reduces recurrent ischemia and rehospitalization vs ischemia-guided, with mortality benefit in higher-risk subsets. Universal early cath is not required for every NSTEMI.

Board pearl: A frail, elderly patient with NSTEMI and multiple comorbidities may derive less benefit and more bleeding harm from early invasive strategy — shared decision-making is appropriate; document goals of care.

Step 3 management: Hemodynamically unstable NSTEMI = emergent cath like a STEMI — page interventional cardiology immediately, don't wait for the morning. Pre-medicate with DAPT and heparin while transferring.

Pharmacotherapy — Antiplatelet and Anticoagulant Regimens

— Ticagrelor 180 mg load → 90 mg BID — preferred over clopidogrel in invasive strategy (PLATO trial); no CYP2C19 metabolism issues. Side effects: dyspnea, bradyarrhythmias, ↑uric acid. Avoid with prior intracranial hemorrhage.

— Prasugrel 60 mg load → 10 mg daily — only after coronary anatomy known (post-PCI); contraindicated if prior stroke/TIA, age ≥75, weight <60 kg

— Clopidogrel 600 mg load → 75 mg daily — acceptable if ticagrelor/prasugrel contraindicated, fibrinolysis, or on chronic OAC

— Unfractionated heparin (UFH): 60 U/kg bolus (max 4000) → 12 U/kg/h infusion, target aPTT 1.5–2.0× control. Preferred if going to early cath.

— Enoxaparin: 1 mg/kg SC q12h (q24h if CrCl <30); avoid switching between UFH and LMWH

— Fondaparinux 2.5 mg SC daily: best safety profile but requires UFH bolus at time of PCI (risk of catheter thrombosis)

— Bivalirudin: alternative at time of PCI, especially if HIT history

Aspirin: 162–325 mg chewed load → 81 mg daily indefinitely. No contraindication other than true allergy or active major bleed.

P2Y12 inhibitor — loading dose:

Timing of P2Y12 loading: 2020 ESC/2021 ACC guidelines discourage routine pre-treatment before angiography in NSTE-ACS (uncertain anatomy → may need CABG → bleeding risk). Load at time of PCI once anatomy known. Clopidogrel/ticagrelor pre-treatment acceptable if delay to angiography expected.

Parenteral anticoagulation (choose one):

GP IIb/IIIa inhibitors (eptifibatide, tirofiban): "bailout" use during PCI for large thrombus burden or no-reflow; routine upstream use no longer recommended.

Adjunctive antianginal: nitroglycerin (avoid with RV infarct or PDE-5 inhibitor use), beta-blocker within 24h if no shock/HF/heart block, high-intensity statin (atorvastatin 80 mg).

Board pearl: Hold morphine if possible — it impairs P2Y12 absorption and is associated with worse outcomes. Use only for refractory pain.

Step 3 management: Document CrCl, weight, and bleeding history before dosing anticoagulant — most ACS bleeding events arise from incorrect renal dose adjustment.

Revascularization — PCI vs CABG and Periprocedural Care

— Drug-eluting stent (DES) is standard — requires minimum 12 months DAPT post-ACS

— Radial access preferred over femoral — lower bleeding, lower mortality

— Indications: 1- or 2-vessel disease, focal LAD lesion, culprit-only PCI in NSTEMI without shock (vs complete revascularization may be considered)

— Left main disease with high SYNTAX score (>32)

— 3-vessel CAD, especially with diabetes (FREEDOM trial: CABG > PCI in DM)

— Reduced LVEF with multivessel disease (STICH)

— Complex anatomy unsuitable for PCI

— Aspirin: continue

— Clopidogrel/ticagrelor: stop ≥5 days before CABG

— Prasugrel: stop ≥7 days

— Cangrelor bridge if urgent CABG needed

— Access site monitoring (hematoma, retroperitoneal bleed → flank pain, drop in Hgb, hypotension → CT abd/pelvis)

— Contrast nephropathy prevention: IV isotonic saline pre/post; hold metformin 48h if eGFR borderline; NAC not effective

— Statin reload (atorvastatin 80 mg) reduces periprocedural MI

— Monitor for stent thrombosis: recurrent chest pain + ST elevation in same territory — emergent re-cath

— Standard: 12 months DAPT, then aspirin monotherapy

— High bleeding risk: consider shorter (1–3 months DAPT, then P2Y12 monotherapy)

— Low bleeding/high ischemic risk: extended DAPT beyond 12 months may be considered

Coronary angiography defines anatomy and informs revascularization strategy.

PCI (percutaneous coronary intervention):

CABG: preferred over PCI in:

Pre-CABG antiplatelet washout:

Post-PCI care:

DAPT duration after PCI for ACS:

Key distinction: STEMI = primary PCI within 90 min (or fibrinolysis if PCI unavailable >120 min); NSTEMI = risk-stratified timing of angiography; fibrinolysis is never indicated in NSTEMI (no benefit, increased bleeding).

CCS pearl: After PCI, order: continuous telemetry, q1h vitals × 6h, distal pulse checks, serial Hgb, BMP at 24h, scheduled DAPT, beta-blocker, ACEi if EF <40% or HTN/DM, atorvastatin 80 mg, ambulate at 6h post-procedure.

Special Populations — Elderly, Renal, and Hepatic Impairment

— More likely atypical presentation: dyspnea, confusion, falls; higher prevalence of multivessel disease

— Benefit from invasive strategy persists but bleeding risk doubles — use radial access, weight-based heparin dosing, lower-intensity DAPT

— Avoid prasugrel (age ≥75 is contraindication unless DM or prior MI with high ischemic risk)

— Clopidogrel or low-dose ticagrelor preferred

— Frailty assessment guides intensity of care; shared decision-making essential

— Polypharmacy review: NSAIDs, anticholinergics, OAC for AF

— Troponin chronically elevated — rise/fall pattern is what diagnoses MI

— Higher mortality at every level of NSTEMI risk

— Underrepresented in trials but benefit from invasive strategy if eGFR >30

— Dose adjustments:

· Enoxaparin: 1 mg/kg q24h if CrCl <30

· Fondaparinux: avoid if CrCl <20

· Bivalirudin: reduce infusion if CrCl <30

· Ticagrelor, prasugrel: no renal adjustment

· Clopidogrel: no adjustment

— Contrast nephropathy: hydrate with isotonic saline 1 mL/kg/h × 12h pre/post; minimize contrast volume; consider iso-osmolar contrast

— Dialysis patients: still benefit from angiography; do not withhold based on CKD alone

— Ticagrelor: avoid in severe hepatic impairment

— Prasugrel: no formal adjustment but caution

— Statin: continue with monitoring; rhabdo risk increases

— Increased bleeding from coagulopathy/thrombocytopenia — UFH preferred (titratable)

Elderly (≥75 years):

CKD (very high yield):

Hepatic impairment:

Key distinction: In a CKD patient with chest pain and "elevated troponin," compare to prior baseline — a stable troponin without rise/fall is not acute MI; a 20% delta with symptoms is.

Board pearl: Metformin doesn't cause contrast nephropathy but should be held 48h post-contrast if eGFR <60 to prevent lactic acidosis if AKI develops.

Step 3 management: In dialysis patients, time PCI/angiography to post-dialysis when possible — better volume status, lower bleeding risk.

Special Populations — Pregnancy, Young Adults, and Sex-Specific Considerations

— Rare but increasing with advanced maternal age; peripartum window highest risk

— Leading cause: SCAD (spontaneous coronary artery dissection) — accounts for ~40% of pregnancy-associated MI

— Other causes: atherosclerosis, coronary thrombosis, embolism, vasospasm

— Management:

· ECG and troponin same as nonpregnant

· Aspirin: safe (low dose)

· Clopidogrel: limited data, use if needed

· Heparin (UFH/LMWH): preferred anticoagulants — do not cross placenta

· Avoid: statins (teratogenic), ACEi/ARB (fetal renal toxicity), ticagrelor/prasugrel (limited data), warfarin first trimester

· Beta-blocker: metoprolol/labetalol safe

— Angiography: minimize fluoroscopy, shield abdomen; PCI feasible

— SCAD often managed conservatively unless ongoing ischemia

— Consider: cocaine/amphetamines, SCAD, familial hyperlipidemia, vasculitis, hypercoagulable state (antiphospholipid syndrome), Kawasaki sequelae, paradoxical embolism (PFO), anomalous coronary

— Workup: tox screen, lipid panel, lipoprotein(a), homocysteine, thrombophilia panel if MINOCA

— More likely atypical symptoms, more likely to have MINOCA, SCAD, microvascular dysfunction

— Underuse of guideline-directed therapy — explicit attention warranted

— Pregnancy-related complications (preeclampsia, GDM, preterm delivery) are CV risk factors — incorporate in long-term prevention

— Benzodiazepines first; nitrates and CCBs for vasospasm

— Avoid beta-blockers acutely (unopposed alpha stimulation); use carvedilol or labetalol if needed

— Angiography if troponin positive — distinguishes vasospasm from plaque disease

Pregnancy-related ACS:

Young adults (<45):

Women:

Cocaine-associated ACS:

Board pearl: Postpartum woman with NSTEMI and minimal CAD risk factors → SCAD until proven otherwise; CT angiogram or invasive angio with IVUS/OCT.

Step 3 management: Discharge counseling for women must include pregnancy-as-stress-test history (preeclampsia, GDM) as part of long-term ASCVD risk stratification per AHA guidelines.

Complications and Adverse Outcomes

— Papillary muscle rupture → acute severe MR → flash pulmonary edema, new harsh systolic murmur, cardiogenic shock; posteromedial papillary > anterolateral (single blood supply from PDA). Emergent surgical repair; IABP as bridge.

— Ventricular septal rupture (VSR) → new harsh holosystolic murmur at left sternal border, step-up in O2 sat from RA to RV on right heart cath; emergent surgical repair.

— Free wall rupture → pulseless electrical activity, tamponade, sudden death; emergent pericardiocentesis and surgery

— LV aneurysm/pseudoaneurysm: late complication; persistent ST elevation weeks later; anticoagulate if mural thrombus

— VF/VT in first 24–48 h: defibrillate, amiodarone/lidocaine; does not affect long-term ICD decision

— VT >48 h post-MI or with persistent EF ≤35% at 40 days → ICD candidate

— AV block: inferior MI → vagally mediated, transient; anterior MI → infranodal, often needs pacing

— Atrial fibrillation: rate control, anticoagulation if persistent

Mechanical complications (typically days 3–7 post-MI, more common with delayed reperfusion):

Arrhythmias:

LV systolic dysfunction → HF: loop diuretic, ACEi/ARB, beta-blocker, MRA if EF ≤40%; SGLT2 inhibitor regardless of DM status (HF guidelines).

Cardiogenic shock: IABP/Impella, inotropes (norepinephrine first, then dobutamine), urgent revascularization. Mortality remains 30–50%.

Recurrent ischemia / stent thrombosis: acute (<24h), subacute (1–30d), late (1mo–1y), very late (>1y). DAPT noncompliance is leading cause — verify.

Bleeding complications: GI > access site > intracranial. Risk-stratify with PRECISE-DAPT or ARC-HBR; adjust DAPT duration.

Dressler syndrome (post-MI pericarditis): weeks later, autoimmune, pleuritic pain, rub, fever, ↑ESR. Treat with high-dose ASA or colchicine (avoid NSAIDs/steroids early post-MI).

Board pearl: New murmur + hypotension days after NSTEMI → emergent TTE; differentiate acute MR from VSR with bedside echo and right heart cath O2 step-up.

Step 3 management: Reassess LVEF at 40 days post-MI (or 90 days post-revascularization) for ICD eligibility — do not implant earlier.

When to Escalate Care — ICU, Consult, and Triage Decisions

— Hemodynamic instability (SBP <90, signs of shock)

— Ongoing/refractory ischemia despite max medical therapy

— Dynamic ECG changes or recurrent ST elevation

— Sustained VT/VF, high-grade AV block

— Acute pulmonary edema or Killip class III–IV

— Mechanical complications

— Post-arrest care, targeted temperature management

— Need for mechanical circulatory support (IABP, Impella, VA-ECMO)

— Stable NSTEMI awaiting cath

— Post-PCI uncomplicated, first 24h

— Mild HF responsive to therapy

— Post-PCI day 2+ without complications, mobilized, tolerating PO meds

— Interventional cardiology: all NSTEMI for risk stratification and cath timing

— Cardiothoracic surgery: left main, 3VD especially with DM, mechanical complications

— Heart failure team: EF <30%, cardiogenic shock — consider advanced therapies, transplant evaluation

— Electrophysiology: sustained VT, ICD candidacy at 40 days

— Pharmacy: complex anticoagulation, DAPT in patient on chronic OAC (triple therapy)

— Palliative care: frail/elderly with high comorbidity burden; goals-of-care alignment

— Hospital without cath lab: transfer all NSTEMI patients with high-risk features for invasive strategy within 24h

— Use standardized handoff (SBAR) and ensure receiving facility has bed/cath capacity

— Send copies of ECG, labs, troponin trend, medication administration record

Cardiac ICU / CCU admission criteria:

Step-down/telemetry unit:

Floor:

Consults to consider:

Transfer decisions:

Key distinction: NSTEMI ≠ STEMI for transfer urgency — most NSTEMI patients can be stabilized and transferred within 24h; very-high-risk NSTEMI (shock, refractory ischemia, electrical instability) is treated like STEMI with emergent transfer.

Step 3 management: When transferring, continue heparin infusion during transport, document last dose of all antiplatelets clearly, and call the receiving cardiologist directly — bad handoffs kill more patients than bad cardiology.

CCS pearl: On CCS, escalate location when vitals or rhythm deteriorate — moving a crashing patient to "ICU" is often the right next-click rather than another medication.

Key Differentials — Other Cardiac Causes of Chest Pain

— Step 3 distinction: NSTEMI is risk-stratified timing; STEMI is emergent reperfusion now.

STEMI: persistent ST elevation ≥1 mm in ≥2 contiguous leads (≥2 mm in V2–V3 for men <40), or new LBBB with Sgarbossa criteria. Requires primary PCI within 90 min door-to-balloon or fibrinolysis within 30 min if PCI unavailable >120 min.

Unstable angina: identical clinical presentation to NSTEMI but negative troponin. With high-sensitivity assays, increasingly reclassified as NSTEMI or noncardiac. Management similar (DAPT, anticoagulation, risk-stratified cath).

Stable angina: predictable, exertional, relieved by rest/nitroglycerin in <5 min. Outpatient workup with stress test; not an ACS.

Prinzmetal (variant) angina: rest pain, often nocturnal, transient ST elevation, normal coronaries; provoked by smoking, cocaine, hyperventilation. Diagnosis: ergonovine or acetylcholine provocation. Treat with CCB and long-acting nitrates; avoid beta-blockers (unopposed alpha vasospasm).

Pericarditis: sharp, pleuritic chest pain, relieved by leaning forward; diffuse ST elevation with PR depression, friction rub. Treat with NSAID + colchicine; do not anticoagulate.

Myocarditis: viral prodrome, troponin elevation, may mimic MI; CMR shows mid-wall late gadolinium enhancement (non-coronary distribution). Supportive care, avoid NSAIDs.

Takotsubo cardiomyopathy: apical ballooning post-emotional/physical stress; normal coronaries; troponin mildly elevated; ECG mimics ACS. Supportive; recovers in weeks.

Aortic stenosis: exertional chest pain, syncope, dyspnea; harsh systolic murmur with delayed carotid upstroke; echo confirms.

Hypertrophic cardiomyopathy: exertional chest pain, syncope; murmur increases with Valsalva; echo confirms.

Aortic dissection: "tearing" pain radiating to back, BP differential, widened mediastinum on CXR. Absolute contraindication to antithrombotics — get CT angio aorta if any suspicion before heparinizing.

Board pearl: Diffuse ST depression + ST elevation in aVR → left main or severe 3VD ischemia OR severe demand ischemia (sepsis, GI bleed); always consider underlying stress before cath.

Key distinction: Treat the rhythm and the patient, not the troponin in isolation — troponin elevation has many causes.

Key Differentials — Non-Cardiac Causes of Chest Pain

— Pleuritic chest pain, dyspnea, tachycardia, hypoxemia, leg swelling, hemoptysis

— ECG: sinus tachy (most common), S1Q3T3, RBBB, T-wave inversion V1–V4 (RV strain — can mimic anterior ischemia)

— Troponin and BNP can be elevated (RV strain)

— Wells/PERC criteria → D-dimer or CT-PA

— Treatment: anticoagulation; thrombolysis if massive (hemodynamically unstable)

— Sudden tearing pain to back, BP differential, pulse deficit, widened mediastinum

— CT angio aorta; type A → emergent surgery; type B → BP control with esmolol then nitroprusside

— Critical: misdiagnosed as ACS → heparin + DAPT → catastrophic; always consider before anticoagulating

— GERD/esophagitis: burning, postprandial, relieved by antacids/PPI

— Esophageal spasm: can be relieved by nitroglycerin (mimics angina!)

— Boerhaave (esophageal rupture): post-emesis, subcutaneous emphysema, Hamman crunch; CT with oral contrast

— Costochondritis: reproducible with palpation; NSAIDs

— Rib fracture: trauma history

— Tietze syndrome: costochondral swelling

— Peptic ulcer: epigastric, related to meals

— Pancreatitis: epigastric radiating to back, lipase

— Biliary colic: RUQ, postprandial, fatty foods

— Pneumonia: fever, productive cough, infiltrate on CXR

— Pleuritis

Pulmonary embolism:

Aortic dissection:

Tension pneumothorax / spontaneous pneumothorax: sudden pleuritic pain, dyspnea, decreased breath sounds, hyperresonance; CXR; needle decompression/chest tube

Esophageal:

Musculoskeletal:

GI:

Pulmonary:

Psychiatric: panic disorder, anxiety — diagnosis of exclusion after appropriate cardiac workup

Herpes zoster: dermatomal pain, vesicular rash appears days later

Board pearl: Nitroglycerin relief is not specific for cardiac ischemia — esophageal spasm and biliary colic also respond. Don't use response to nitrates to rule in ACS.

Step 3 management: Before discharging a "noncardiac chest pain" patient, ensure PE, dissection, and pneumothorax are ruled out based on pretest probability — these are the lethal "can't miss" mimics.

Secondary Prevention — Discharge Medications and Long-Term Plan

— Aspirin 81 mg daily indefinitely + P2Y12 inhibitor (typically 12 months) + ACEi/ARB

— Beta-blocker (metoprolol succinate or carvedilol)

— Cholesterol — high-intensity statin (atorvastatin 80 mg or rosuvastatin 20–40 mg); LDL goal <70 mg/dL (some guidelines <55)

— Diet, Diabetes management, DAPT adherence

— Exercise, Education, Early cardiac rehab referral

— Aspirin 81 mg + ticagrelor/clopidogrel/prasugrel × 12 months post-ACS

— Shorter (1–3 mo) if high bleeding risk (HAS-BLED, PRECISE-DAPT ≥25)

— Longer (>12 mo) if low bleeding/high ischemic risk

— PPI (pantoprazole) if GI bleed history or chronic NSAID/anticoagulant use — avoid omeprazole/esomeprazole with clopidogrel (CYP2C19 interaction)

— Default: DOAC + clopidogrel × 1–6 months, then DOAC + clopidogrel through 12 months, then DOAC monotherapy

— Aspirin only first 1–4 weeks unless very high ischemic risk

"ABCDE" framework for post-NSTEMI:

Dual antiplatelet therapy (DAPT):

Triple therapy (patient with AF + ACS/PCI):

ACEi/ARB: indicated if EF <40%, HTN, DM, CKD — ideally all post-MI patients

MRA (spironolactone/eplerenone): add if EF ≤40% with HF symptoms or DM, on ACEi + beta-blocker, K <5.0, Cr <2.5

SGLT2 inhibitor: consider in all post-MI patients with HFrEF, DM, or CKD (mortality/HF hospitalization benefit; emerging post-MI data)

High-intensity statin: start in hospital; if LDL >70 mg/dL on max statin → add ezetimibe, then PCSK9 inhibitor or inclisiran for very-high-risk ASCVD

Lifestyle: Mediterranean diet, ≥150 min/wk moderate aerobic, smoking cessation (nicotine replacement + bupropion/varenicline), BMI <25, BP <130/80, A1c <7%, alcohol limits

Influenza and pneumococcal vaccines: reduce post-MI cardiovascular events

Board pearl: Patients on chronic NSAIDs after MI have 2–3× higher mortality — discontinue NSAIDs (except aspirin) at discharge; use acetaminophen or topical therapy instead.

Step 3 management: Write all secondary prevention meds on discharge; do not "defer to PCP" — the inpatient stay is the highest-yield moment for initiation.

Follow-Up, Monitoring, and Cardiac Rehabilitation

— Within 1–2 weeks of discharge: PCP or cardiology — medication reconciliation, symptom check, vital signs, side effect screening

— 4–6 weeks post-MI: cardiology — uptitrate ACEi/beta-blocker, repeat lipid panel (assess statin response)

— 3 months: lipid panel (LDL goal <70, ideally <55); BP/A1c check

— 40 days post-MI: reassess LVEF for ICD candidacy if EF was ≤40%

— 6 and 12 months: DAPT decision point, lipid, BP, A1c

— Annual flu vaccine, q5y pneumococcal

— Refer every post-MI patient — reduces mortality 20–30%, recurrent MI, rehospitalization

— Typical program: 36 sessions over 12 weeks, 3×/week

— Components: monitored exercise, nutrition counseling, psychosocial support, risk factor modification

— Underutilized — only ~30% of eligible patients enroll; explicit referral and addressing barriers (transportation, work) improves uptake

— Home-based or hybrid rehab acceptable alternative for patients with access barriers

— Uncomplicated NSTEMI: 1 week

— Post-PCI: 48 hours private; 2 weeks commercial

— ICD: 6 months private (no shocks)

— Document counseling

— BP <130/80, HR 55–70 (titrate beta-blocker)

— LFTs/CK if statin myalgia

— K and Cr at 1–2 weeks after ACEi/MRA initiation

— A1c q3 months if DM

Follow-up schedule (Step 3 board-favorite cadence):

Cardiac rehabilitation (Class I indication):

Driving restrictions (vary by state but typical):

Sexual activity: typically safe at 1–2 weeks if asymptomatic and exercise tolerance ≥3–5 METs (climbing 2 flights of stairs)

Return to work: sedentary work 1–2 weeks; manual labor 4–6 weeks; case-by-case

Monitoring parameters:

Mental health: screen for depression (PHQ-9) at follow-up — present in ~20% post-MI, independently increases mortality; treat with SSRI (sertraline preferred — best cardiac safety data)

Board pearl: Cardiac rehab referral is a Class I recommendation — its absence on a Step 3 vignette discharge plan is often the "wrong answer" distractor.

CCS pearl: Order cardiac rehab referral, smoking cessation counseling, and PHQ-9 screening as explicit discharge items — they earn points.

Ethical, Legal, and Patient Safety Considerations

— Required elements: indication, alternatives (medical therapy, CABG), risks (bleeding, contrast nephropathy, vascular injury, stroke, MI, death ~1%), benefits, recovery

— In emergent cases (hemodynamic instability, ongoing ischemia, cardiac arrest), implied/emergency consent applies — document inability to obtain consent and life-threatening indication

— Surrogate decision-maker hierarchy if patient incapacitated: spouse > adult children > parents > siblings (varies by state)

— Discuss likely benefit (mortality, symptom relief) vs harms (bleeding, procedural complications, post-procedure decline)

— Use validated tools; document the conversation

— A frail nonagenarian with NSTEMI may prefer conservative medical management — this is an ethical and acceptable choice

— Medication reconciliation at every transition (admission, transfer, discharge)

— Discharge summary to PCP within 48–72 hours

— Teach-back method for medication understanding, especially DAPT — premature discontinuation is the #1 cause of stent thrombosis

— Explicit warning: "Do not stop your blood thinners without calling cardiology" — including before any surgery or dental procedure

— Schedule follow-up before discharge, not "as needed"

— Elective non-cardiac surgery should be deferred ≥6 months post-DES if possible (≥30 days minimum)

— Continue aspirin perioperatively if possible

— Bridge with cangrelor or LMWH if P2Y12 must be held

— Women, Black/Hispanic patients, low-SES patients receive less guideline-directed therapy and rehab referral — Step 3 expects clinicians to apply guidelines uniformly

— Some states require physician reporting of drivers with recent MI/ICD; know your state

Informed consent for cath/PCI:

Shared decision-making in elderly/frail patients:

Transitions of care — the single highest patient-safety risk:

Bridging anticoagulation for surgery:

Disparities and equity:

Mandatory reporting / fitness to drive:

Board pearl: A post-PCI patient stopping clopidogrel for elective dental work → dental work can be done on DAPT with local hemostatic measures; do not stop antiplatelets unnecessarily.

Step 3 management: On discharge, call the PCP, send the discharge summary same-day, schedule follow-up in 1–2 weeks, and confirm patient has filled DAPT prescription before leaving — these are explicit patient safety bundle items.

High-Yield Associations and Rapid-Fire Clinical Facts

Aspirin 162–325 mg chewed = first action in suspected ACS (after ECG order).

Door-to-ECG: ≤10 minutes.

NSTEMI never gets fibrinolysis — no mortality benefit, increased bleeding.

Very-high-risk NSTEMI → cath within 2 hours (shock, refractory ischemia, electrical instability, mechanical complication).

High-risk NSTEMI (GRACE >140) → cath within 24 hours.

TIMI ≥3 → benefits from early invasive strategy.

Ticagrelor + aspirin >100 mg/day = worse outcomes — keep aspirin at 81 mg.

Prasugrel contraindicated if prior stroke/TIA, age ≥75, weight <60 kg.

Wellens T waves → critical proximal LAD; no stress test; go to cath.

de Winter T waves = LAD occlusion equivalent.

ST elevation in aVR + diffuse ST depression = left main or 3VD or severe demand ischemia.

Posterior MI = ST depression V1–V3 with tall R waves → posterior leads V7–V9.

Cocaine ACS: benzodiazepines first, avoid beta-blockers.

RV infarct: avoid nitrates, give IV fluids; ST elevation in V4R.

Papillary muscle rupture: posteromedial > anterolateral (single PDA supply).

Mechanical complications: days 3–7 post-MI.

Dressler syndrome: weeks post-MI; high-dose ASA + colchicine, avoid steroids early.

ICD reassessment at 40 days post-MI (or 90 days post-revascularization).

DAPT post-DES for ACS: 12 months minimum.

Stent thrombosis cause #1: premature DAPT discontinuation.

Cardiac rehab: Class I, reduces mortality 20–30%, refer every patient.

PPI choice with clopidogrel: pantoprazole (avoid omeprazole/esomeprazole — CYP2C19).

Atorvastatin 80 mg or rosuvastatin 20–40 mg = high-intensity statin post-MI.

LDL goal post-MI: <70 mg/dL (very high risk: <55).

Add ezetimibe → PCSK9 inhibitor if LDL not at goal.

Avoid NSAIDs post-MI — increased mortality.

SGLT2 inhibitor: consider in all post-MI HFrEF or DM/CKD patients.

Triple therapy (AF + PCI): DOAC + clopidogrel preferred over warfarin + DAPT; minimize aspirin duration.

Pregnancy ACS: SCAD most common cause; conservative management.

Morphine: impairs P2Y12 absorption — minimize use.

Board pearl: Memorize the timing tiers (2h, 24h, 72h, ischemia-guided) — they're the single most testable Step 3 NSTEMI concept.

Board Question Stem Patterns

Pattern 1 — "Next best step" in suspected ACS: Patient with chest pain in ED; vitals given. → ECG within 10 min + aspirin 325 mg chewed. Don't pick CT or stress test first.

Pattern 2 — Timing of angiography: NSTEMI with GRACE >140 or recurrent angina → <24h cath. Hemodynamic instability → <2h cath. Low-risk → ischemia-guided.

Pattern 3 — Wrong drug for NSTEMI: Stem describes 78-year-old NSTEMI patient given prasugrel → recognize prasugrel contraindicated age ≥75. Switch to clopidogrel or ticagrelor.

Pattern 4 — Posterior MI: ST depression V1–V3 with tall R waves → answer: obtain posterior leads V7–V9 before deciding ST-elevation vs non-ST-elevation pathway.

Pattern 5 — Cocaine chest pain: Young patient, positive tox screen, ST changes → benzodiazepines + nitrates + CCBs, not beta-blockers.

Pattern 6 — Mechanical complication: Post-NSTEMI day 4, new harsh systolic murmur + pulmonary edema → emergent TTE; likely papillary muscle rupture; surgery + IABP.

Pattern 7 — RV infarct: Inferior NSTEMI + hypotension after nitroglycerin → RV infarct; IV fluids; check V4R.

Pattern 8 — Discharge medications: Post-NSTEMI patient with EF 30% — must include ACEi, beta-blocker, aspirin, P2Y12, high-intensity statin, MRA, ICD evaluation at 40 days, cardiac rehab referral.

Pattern 9 — DAPT and surgery: Patient on DAPT post-DES needs elective surgery in 2 months → defer surgery if possible (≥6 months ideal, ≥3 months minimum for DES); continue aspirin; bridge if needed.

Pattern 10 — AF + ACS triple therapy: Default → DOAC + clopidogrel; minimize aspirin duration to weeks.

Pattern 11 — MINOCA: Young woman, NSTEMI, clean coronaries → SCAD; conservative management; consider CMR.

Pattern 12 — Statin intolerance: Patient with myalgias on atorvastatin 80 → trial alternate statin, lower dose, or rosuvastatin; if persistent and LDL >70 → ezetimibe + PCSK9 inhibitor.

Pattern 13 — Cardiac rehab referral: "What additional intervention reduces mortality?" → cardiac rehab, often the unpicked correct answer.

Pattern 14 — Aortic dissection mimic: Chest pain with BP differential or widened mediastinum → CT angio aorta, do not give heparin/DAPT.

Pattern 15 — Troponin in CKD: Stable troponin without rise/fall in dialysis patient → not acute MI; look for alternative dx.

Board pearl: When in doubt on Step 3 ACS questions, the answer often involves timing, contraindications, or secondary prevention completeness rather than the diagnosis itself.

One-Line Recap

NSTEMI is a troponin-positive, non-occlusive coronary thrombosis syndrome managed by immediate aspirin and risk-stratified antithrombotic + invasive strategy — timing of angiography (≤2h very-high-risk, ≤24h high-risk, ≤72h intermediate, ischemia-guided low-risk) plus complete guideline-directed secondary prevention is the testable core.

Diagnose with ECG (ST depression, T-wave inversion, or normal) + rise/fall of high-sensitivity troponin; rule out STEMI equivalents (posterior MI, Wellens, de Winter, aVR elevation) and lethal mimics (dissection, PE, pneumothorax) before anticoagulating.

Treat acutely with aspirin 162–325 mg chewed, parenteral anticoagulation (UFH preferred pre-cath; enoxaparin or fondaparinux alternatives), P2Y12 inhibitor (ticagrelor or clopidogrel; prasugrel only after anatomy known and not if age ≥75, weight <60 kg, or prior stroke), beta-blocker within 24h if no shock, high-intensity statin, and nitrates/morphine as needed (minimize morphine — impairs P2Y12).

Risk-stratify with GRACE/TIMI and choose invasive timing: emergent (<2h) for shock/refractory ischemia/electrical instability/mechanical complications; early (<24h) if GRACE >140 or new ST depression; delayed (<72h) for intermediate risk; ischemia-guided for low-risk with stress test before discharge.

Discharge every patient with DAPT × 12 months, high-intensity statin to LDL <70 (add ezetimibe/PCSK9 as needed), ACEi/ARB, beta-blocker, MRA and SGLT2i if EF ≤40%, smoking cessation, cardiac rehab referral (Class I), 1–2 week follow-up, and explicit teach-back on never stopping DAPT without calling cardiology.

Board pearl: The Step 3 NSTEMI question is rarely "what is it" — it is timing of cath, correct drug choice in the right population, completeness of secondary prevention, and safe transitions of care.