Acute Coronary Syndromes

Clinical Snapshot

Acute coronary syndrome (ACS) refers to any clinical presentation compatible with acute myocardial ischemia due to a primary coronary event — plaque rupture, erosion, fissuring, or dissection — and spans a spectrum from unstable angina through non-ST-elevation MI (NSTEMI) to ST-elevation MI (STEMI).^[1] The 2025 ACC/AHA guideline unifies management of type 1 MI (both STEMI and NSTEMI) under shared core principles — dual antiplatelet therapy, anticoagulation, high-intensity statin for every patient, and a strong preference for an invasive strategy — while preserving the fundamentally different time pressure of each: STEMI is a "minutes matter" emergency requiring immediate reperfusion, while NSTE-ACS is risk-stratified (TIMI or GRACE score) to determine how urgently angiography is needed.^[2]

Recognize the Condition

Typical presentation

Substernal chest pain/pressure, often radiating to the arm, jaw, or back, associated with diaphoresis, nausea, or dyspnea, typically lasting more than 20 minutes and not fully relieved by rest or nitroglycerin. Onset at rest or with minimal exertion, new-onset severe angina, or angina that is more frequent, longer, or lower-threshold than a patient's baseline pattern (crescendo angina) all suggest an acute coronary syndrome rather than stable angina.

Atypical presentation

Women, older adults, and patients with diabetes are more likely to present atypically — dyspnea, fatigue, epigastric discomfort, or nausea/vomiting without classic chest pain. A high index of suspicion in these groups avoids missed or delayed diagnosis.

The three ACS categories

Unstable angina

Ischemic symptoms without troponin elevation and without persistent ST elevation.

NSTEMI

Troponin elevation (myocardial injury) without persistent ST elevation.

STEMI

Troponin elevation with persistent ST-segment elevation (or new left bundle branch block) on ECG, indicating a completely occluded coronary artery — the extreme, most time-critical end of the spectrum.

Risk Factors

Traditional cardiovascular risk factors: smoking, diabetes mellitus, hyperlipidemia, hypertension.
Family history of premature coronary artery disease (first-degree relative with MI before age 55 if male, before age 65 if female).
Known coronary artery disease, prior MI, or prior revascularization (PCI or CABG).
Chronic kidney disease.
Cocaine or stimulant use (can cause coronary vasospasm and ACS even without underlying atherosclerosis).

Red Flags & Refer

Any suspected ACS is itself the red flag — this is a time-critical emergency requiring immediate ECG, troponin, and activation of the institution's ACS protocol; there is no "routine" version of this condition.

Escalate to emergency reperfusion/cath lab activation immediately for ST-segment elevation or new left bundle branch block on ECG (STEMI protocol).
Hemodynamic instability or cardiogenic shock.
Sustained ventricular tachycardia or ventricular fibrillation.
Mechanical complications — a new loud murmur suggesting papillary muscle rupture or ventricular septal defect, or sudden hypotension suggesting free wall rupture/tamponade.
Ongoing or recurrent ischemic symptoms despite initial therapy.
For NSTE-ACS specifically, escalate to urgent (rather than routine risk-stratified) angiography for refractory angina, hemodynamic or electrical instability, mechanical complications, acute heart failure, or recurrent ST-segment changes.

Assessment & Diagnosis

Immediate investigations

12-lead ECG within 10 minutes of presentation — the single most important initial test, since it determines the STEMI-vs-NSTE-ACS pathway.
Troponin — a highly sensitive and specific marker of myocardial injury, used both to confirm the diagnosis and to risk-stratify. Note: troponin elevation is not specific to ACS — pulmonary embolism, myocarditis, severe heart failure, cardiac trauma, pericarditis (present in 30-50% of pericarditis cases from epicardial inflammation), sepsis, critical illness, neurologic events, hypothyroidism, chemotherapy-related cardiotoxicity, and renal insufficiency can all elevate troponin. Biotin supplements can cause falsely low troponin results with some assays — ask about biotin use and confirm with the lab if the clinical picture and troponin result are discordant.
CBC, electrolytes, glucose, creatinine, and a fasting lipid profile within 24 hours of presentation.
Portable chest x-ray.
Echocardiography — used early when history/ECG are nondiagnostic (regional wall motion abnormality with chest pain suggests ischemia), and after stabilization to assess left ventricular function; used emergently if a mechanical complication is suspected.

Risk stratification for NSTE-ACS (does not apply to STEMI, which is always treated as maximal urgency)

The TIMI risk score is a simple 7-item point-sum used to estimate the 14-day risk of death, MI, or urgent revascularization in UA/NSTEMI — 1 point for each criterion present, out of a maximum of 7.^[3]

Criterion	Points
Age ≥ 65 years	1
≥ 3 risk factors for CAD (family history, hypertension, hypercholesterolemia, diabetes, current smoker)	1
Known CAD (prior coronary stenosis ≥ 50%)	1
Aspirin use in prior 7 days	1
Severe angina (≥ 2 episodes in prior 24 hours)	1
ST-segment deviation ≥ 0.5 mm on presenting ECG	1
Elevated cardiac markers (troponin or CK-MB)	1

14-day risk climbs steeply with score: 0-1 point = 4.7%; 2 points = 8.3%; 3 points = 13.2%; 4 points = 19.9%; 5 points = 26.2%; 6-7 points = 40.9%. A score ≥3 favors an early invasive strategy; a score ≥4 favors enoxaparin over unfractionated heparin plus a glycoprotein IIb/IIIa inhibitor.

The GRACE risk score is a more complex, continuously-weighted regression model — using age, heart rate, systolic BP, creatinine, Killip class, cardiac arrest at admission, ST deviation, and elevated markers as continuous/graded inputs rather than a simple point-sum — that better discriminates 1-month and 1-year mortality risk and is preferred where available; it requires a validated calculator rather than manual scoring.^[4]

A high-risk patient — TIMI ≥3, positive cardiac markers, ST changes, recurrent ischemia, heart failure, hemodynamic instability, sustained VT, or prior revascularization — should proceed to early invasive angiography rather than a conservative strategy.

Treatment Targets

Decrease mortality and complications.
Reduce or contain infarct size; salvage viable myocardium.
Re-establish and maintain patency of the infarct-related artery (STEMI) or achieve appropriately-timed revascularization (NSTE-ACS).
Prevent recurrent ischemia and reinfarction.
Initiate secondary prevention pharmacotherapy before discharge.

Choose Initial Treatment

Direct treatment rule

Reperfusion strategy

STEMI, 1st line primary PCI at a facility that can achieve first-medical-contact-to-device time ≤90 minutes — preferred over fibrinolysis given lower mortality and intracranial hemorrhage risk, especially in patients over 75.

If primary PCI cannot be achieved within 2 hours, use a pharmacoinvasive strategy — fibrinolysis (door-to-needle ≤30 minutes) followed by transfer for angiography, either immediately or on a more routine timeline.

NSTE-ACS pursue an invasive strategy (angiography ± revascularization) in essentially all patients; timing is urgent (<24h) for high-risk features, and can be more routine (within the same admission) for lower-risk patients per TIMI/GRACE stratification.

Complete revascularization is now recommended over culprit-lesion-only PCI when feasible, and a radial-first approach is preferred over femoral access given lower bleeding/vascular complication rates.^[1]

Antiplatelet therapy

1st line P2Y12 inhibitor ticagrelor or prasugrel — both are Class 1, without a preference between them, for both STEMI and NSTEMI.^[5]

Use clopidogrel only if ticagrelor/prasugrel are contraindicated, not tolerated, unaffordable, or unavailable — clopidogrel is no longer positioned as an equal first-line option.

Do not start prasugrel before coronary anatomy is defined (angiography performed), and avoid in patients with a prior stroke/TIA.

DAPT duration: ASA plus a P2Y12 inhibitor for a default of 12 months in patients without elevated bleeding risk; in high-bleeding-risk patients, a short-DAPT strategy (1 month) followed by P2Y12-inhibitor monotherapy is a reasonable alternative that reduces bleeding without a clear ischemic tradeoff.

Statin therapy

All ACS patients — regardless of baseline LDL — should be started on a high-intensity statin (atorvastatin 40-80 mg or rosuvastatin 20-40 mg) before discharge.

If LDL remains ≥1.8 mmol/L (70 mg/dL) on maximally tolerated statin, add ezetimibe, then a PCSK9 inhibitor if still above target.

Non-Pharmacologic Treatment

Bed rest during active ischemia, with gradual mobilization once symptoms stabilize and no complications are evident.
Continuous ECG monitoring for arrhythmias and ST-segment shifts in all high-risk patients.
Do not give routine supplemental oxygen to a normoxic patient — trial evidence shows this does not improve outcomes and may increase infarct size; reserve supplemental oxygen for documented hypoxemia (SpO2 <90%).^[6]
Radial arterial access preferred over femoral for PCI given lower bleeding and vascular complication rates.
Smoking cessation counselling initiated within 24 hours and reinforced repeatedly — one of the highest-yield secondary-prevention interventions.
Cardiac rehabilitation referral before or shortly after discharge.
Stool softeners in the immediate post-MI period to avoid straining with bowel movements; anxiolytics may be used as needed for anxiety in the acute period.

Pharmacologic Treatment Options

Drug / intervention	Role	Dose / use	Important adverse effects	Teaching points
ASA Preferred	All ACS, immediately and long-term	Loading 160-325 mg chewed, then 81 mg PO daily indefinitely	GI upset, bleeding, rare bronchospasm	Give immediately if not already on ASA. Continue indefinitely alongside the P2Y12 inhibitor.
Ticagrelor Preferred	1st-line P2Y12 inhibitor, STEMI or NSTE-ACS	Loading 180 mg, then 90 mg PO BID	Bleeding, dyspnea (may require switch to another agent), bradyarrhythmias	Co-equal 1st-line choice with prasugrel. Hold 5 days before non-urgent CABG.
Prasugrel Preferred	1st-line P2Y12 inhibitor, after coronary anatomy is known	Loading 60 mg, then 10 mg PO daily	Bleeding — higher risk over age 75, weight under 60kg, prior stroke/TIA	Do not start until angiography has defined the anatomy. Contraindicated with prior stroke/TIA. Hold 7 days before non-urgent CABG.
Clopidogrel Alternative	P2Y12 inhibitor when ticagrelor/prasugrel are not an option	Loading 300-600 mg, then 75 mg PO daily	Bleeding, rash, purpura	Reserve for contraindication/intolerance/unavailability of preferred agents. Hold 5 days before non-urgent CABG.
Enoxaparin Preferred	Anticoagulation, UA/NSTEMI or STEMI adjunct	UA/NSTEMI: 1 mg/kg SC Q12H. STEMI: 30 mg IV bolus then 1 mg/kg SC Q12H (reduced regimen if age >75 or renal impairment)	Bleeding, injection-site hematoma, rare HIT	Preferred over UFH if ClCr >30 mL/min. Never give IM.
Unfractionated heparin Alternative	Anticoagulation when enoxaparin is not appropriate (ClCr ≤30, or post-PCI)	Weight-based bolus and infusion per institutional protocol	Bleeding, HIT	Preferred over enoxaparin in significant renal impairment given no renal clearance dependence.
Tenecteplase Special situation	STEMI fibrinolysis when primary PCI unavailable within 2 hours	Single weight-based IV bolus	Bleeding, intracranial hemorrhage	Greatest benefit within 6 hours of symptom onset. Give with UFH or enoxaparin.
Metoprolol Preferred	Beta-blocker, all ACS without contraindication	Start oral within 24h, titrate to resting HR 50-60 bpm	Bradycardia, hypotension, bronchospasm	IV only if ongoing pain/tachycardia without contraindications; otherwise start oral.
Nitroglycerin Preferred	Symptom relief, all ACS	Sublingual 0.3-0.6 mg PRN; IV if pain persists 15-20 min despite sublingual	Headache, hypotension	Contraindicated with PDE5 inhibitor use (sildenafil/vardenafil under 24h, tadalafil under 48h) or significant hypotension. Avoid in RV infarct.
Atorvastatin (high-intensity) Preferred	All ACS, regardless of baseline LDL	40-80 mg PO daily, started before discharge	Myalgia, transaminase elevation	High-intensity statin is mandatory for every ACS patient, not just those with elevated LDL.
Ramipril Preferred	ACE inhibitor, within 24h if no contraindication	Initial 1.25-2.5 mg PO BID, target 5 mg BID or 10 mg daily	Cough, hyperkalemia, hypotension, angioedema (rare)	Start within 24h unless SBP under 100 mmHg. Continue indefinitely, even with preserved LV function.

Special Populations

Pregnancy

ACS in pregnancy/early postpartum is rare but increasing; coronary artery disease with plaque rupture accounts for only about 40% of cases — spontaneous coronary artery dissection is an important alternative cause to consider. Work up and treat with the same urgency as a non-pregnant patient, with combined obstetric/cardiology management. ASA at usual doses (81 mg/day) is safe. Clopidogrel is the preferred P2Y12 inhibitor (other agents not well studied in pregnancy). UFH and LMWH can be used, with awareness of increased maternal bleeding risk. Beta-blockers and nitrates can be used. ACE inhibitors, ARBs, and statins are contraindicated in pregnancy — hold these regardless of the strength of the non-pregnancy indication. Primary PCI is preferred for STEMI in pregnancy; fibrinolysis may be considered where primary PCI is unavailable.

Breastfeeding

ASA, UFH, LMWH, and beta-blockers are considered safe. Given that other standard ACS medications (statins, some antiplatelet/anticoagulant combinations) are not well characterized in lactation, discontinuing breastfeeding is generally recommended in the acute ACS setting to allow standard, undelayed maternal treatment.

Older adults (over 75)

Primary PCI is preferred over fibrinolysis given higher intracranial hemorrhage risk with thrombolytics in this age group. Reduced enoxaparin dosing applies for STEMI (no IV bolus, lower subcutaneous dose). Prasugrel carries a higher bleeding risk over age 75 and in patients under 60 kg — weigh carefully against ticagrelor.

Renal impairment

Enoxaparin requires dose reduction (or a switch to UFH) at ClCr ≤30 mL/min. Contrast-induced nephropathy risk should be considered before angiography — adequate hydration and minimizing contrast volume are standard mitigations.

Monitoring & Follow-Up

Serial ECGs (STAT, then every 8 hours for 24 hours, then daily for STEMI) and serial troponin until the diagnosis is enzymatically confirmed or excluded. Echocardiography after stabilization to assess LV ejection fraction — this determines the need for a mineralocorticoid receptor antagonist, an ICD referral (EF <30% at 1 month post-MI or 3 months post-revascularization), and the intensity of heart failure therapy. Reinforce secondary prevention at every follow-up: antiplatelet/anticoagulant adherence, statin adherence and LDL target, blood pressure control, smoking cessation, and cardiac rehabilitation attendance. Community pharmacists are well positioned to catch early nonadherence to DAPT, since stopping a P2Y12 inhibitor early after stent placement carries a real stent-thrombosis risk.

Treatment Failure / Next Step

Recurrent or ongoing ischemia: optimize antianginal therapy and consider urgent angiography/revascularization if not already performed.
New heart failure: treat aggressively per standard heart failure management; consider angiography/revascularization if LVEF <40% post-MI.
Arrhythmias: asymptomatic PVCs need no treatment; symptomatic ectopy usually responds to a beta-blocker (avoid Class IC agents); sustained ventricular arrhythmias need investigation for recurrent ischemia and possible electrophysiology referral; new atrial fibrillation needs rate control (beta-blocker, or digoxin if concomitant heart failure) and consideration of anticoagulation.
Pericarditis (usually within 72 hours post-MI): increase ASA to 650 mg PO QID for 1-2 weeks; add colchicine if symptoms persist despite this. Anticoagulants generally do not need to be stopped for early post-MI pericarditis, but use caution if pericarditis presents weeks-to-months later (Dressler syndrome) given pericardial bleeding/tamponade risk.
Suspected mechanical complication (papillary muscle rupture, VSD, free wall rupture): emergency echocardiography and immediate surgical/interventional consultation — these carry very high mortality even with prompt treatment.

Common Errors to Avoid

Giving routine supplemental oxygen to a normoxic ACS patient — no benefit, possible harm (larger infarct size).^[6]
Using immediate-release nifedipine for anginal symptoms — the acute blood pressure drop increases stroke risk; use a beta-blocker or, if contraindicated, a rate-limiting calcium channel blocker instead.
Starting or continuing a calcium channel blocker (especially diltiazem/verapamil) in a STEMI patient with significant LV dysfunction or pulmonary congestion — increases morbidity/mortality; oral diltiazem is specifically contraindicated in this setting.
Combining a non-dihydropyridine calcium channel blocker with a beta-blocker without close monitoring — additive bradycardia, AV block, and negative inotropic risk.
Defaulting to clopidogrel as a routine first choice — ticagrelor or prasugrel are now the preferred P2Y12 inhibitors; clopidogrel is for when those are not an option.
Starting prasugrel before coronary anatomy is known, or in a patient with a prior stroke/TIA.
Stopping DAPT early (before the planned 12-month course, or before the planned short-DAPT transition point) without confirming this was a deliberate, guideline-concordant plan — a common, dangerous, and often unintentional nonadherence pattern pharmacists can catch.
Withholding a high-intensity statin because baseline LDL "looks fine" — every ACS patient gets a high-intensity statin regardless of baseline LDL.
Missing biotin supplement use as a cause of a falsely low troponin in a patient whose clinical picture strongly suggests ACS.

Clinical Decision Algorithm

Algorithm A — Initial triage: STEMI vs NSTE-ACS

Suspected ACS: ischemic symptoms, ECG and troponin obtained immediately

ST elevation or new LBBB on ECG

STEMI — activate cath lab / reperfusion protocol immediately, proceed to Algorithm B

No ST elevation

NSTE-ACS (unstable angina or NSTEMI) — calculate TIMI/GRACE score, proceed to Algorithm C

Algorithm B — STEMI reperfusion

STEMI confirmed

Give ASA, P2Y12 inhibitor (ticagrelor/prasugrel preferred), anticoagulant, and assess reperfusion access

Primary PCI achievable, first-medical-contact-to-device ≤90 min

Primary PCI — preferred strategy, especially if age >75 or thrombolytic contraindication

Primary PCI not achievable within 2 hours

Pharmacoinvasive strategy: fibrinolysis (door-to-needle ≤30 min) then transfer for angiography

Start beta-blocker, ACE inhibitor (within 24h), high-intensity statin before discharge

Assess LVEF post-stabilization — guides mineralocorticoid receptor antagonist use and ICD referral timing

Algorithm C — NSTE-ACS risk-stratified management

NSTE-ACS confirmed; TIMI/GRACE score calculated

High risk: TIMI ≥3, positive markers, ST changes, recurrent ischemia, HF, instability, sustained VT, or prior revascularization

Urgent invasive strategy — angiography under 24h

Lower risk

Invasive strategy on a more routine timeline within the same admission

ASA + P2Y12 inhibitor (ticagrelor/prasugrel preferred) + anticoagulant (enoxaparin or UFH) + beta-blocker + high-intensity statin

Refractory angina, hemodynamic/electrical instability, or mechanical complication at any point: escalate to urgent angiography regardless of initial risk category

Drug Tables

How to use this table: Doses are adult doses and require patient-specific confirmation (renal/hepatic function, weight, allergy history). Pediatric dosing is weight-based per the current product monograph unless stated. Drug pricing is intentionally omitted. Select any drug name to open its complete Pharmasist Drug Database page.

Antiplatelet agents

Drug	Dosage	Adverse effects	Drug interactions	Comments
ASA	Loading dose: 160-325 mg PO chewed Maintenance: 81 mg PO daily, indefinitely	Gastritis, GI ulceration/hemorrhage, rare bronchospasm, tinnitus/vertigo at high dose	Increased bleeding with heparin, warfarin, other NSAIDs	Give immediately on presentation if not already taking it; chew the loading dose for faster absorption.
Ticagrelor	Loading dose: 180 mg PO Maintenance: 90 mg PO BID	Bleeding, dyspnea (may require agent switch), bradyarrhythmias	Avoid strong CYP3A4 inhibitors/inducers; caution with other agents affecting hemostasis	Co-equal 1st-line P2Y12 inhibitor with prasugrel for both STEMI and NSTE-ACS. Hold 5 days before non-urgent CABG.
Prasugrel	Loading dose: 60 mg PO Maintenance: 10 mg PO daily	Increased bleeding, especially age >75, weight under 60 kg, prior stroke/TIA	Caution with other agents affecting hemostasis	Do not start until coronary anatomy is defined by angiography. Contraindicated with prior stroke/TIA. Hold 7 days before non-urgent CABG.
Clopidogrel	Loading dose (PCI or STEMI): 300-600 mg PO Loading dose (UA/NSTEMI, high bleed risk): 300 mg PO (or omit) Maintenance: 75 mg PO daily	Bleeding, rash, purpura	PPI use may reduce efficacy; caution with NSAIDs	Reserve for when ticagrelor/prasugrel are contraindicated, not tolerated, or unavailable. Hold 5 days before non-urgent CABG.

Anticoagulants

Drug	Dosage	Adverse effects	Drug interactions	Comments
Enoxaparin	UA/NSTEMI: 1 mg/kg SC Q12H STEMI (age ≤75): 30 mg IV bolus, then 1 mg/kg SC Q12H STEMI (age >75): No bolus; 0.75 mg/kg SC Q12H, first 2 doses max 75 mg each	Bleeding, injection-site hematoma, rare heparin-induced thrombocytopenia	Additive bleeding risk with other antiplatelet/anticoagulant agents	Preferred over UFH if ClCr >30 mL/min. Never give IM.
Unfractionated heparin	Dosing: Weight-based bolus and infusion per institutional protocol, titrated to aPTT	Bleeding, heparin-induced thrombocytopenia	Additive bleeding risk with other antiplatelet/anticoagulant agents	Preferred when ClCr ≤30 mL/min, or per institutional protocol post-PCI.
Fondaparinux	NSTE-ACS: 2.5 mg SC once daily	Bleeding	Additive bleeding risk with other antiplatelet/anticoagulant agents	As effective as enoxaparin in NSTEMI with a lower major bleeding rate in trial data — a reasonable alternative anticoagulant.

Fibrinolytics (STEMI only, when primary PCI is not timely accessible)

Drug	Dosage	Adverse effects	Drug interactions	Comments
Tenecteplase	Adults: Single weight-based IV bolus per institutional protocol	Bleeding, intracranial hemorrhage	Give with an anticoagulant (UFH or enoxaparin)	Greatest benefit within 6 hours of symptom onset; reduced benefit 6-12 hours; unclear benefit beyond 12 hours.
Alteplase	Adults: Weight-based accelerated infusion per institutional protocol	Bleeding, intracranial hemorrhage	Give with an anticoagulant (UFH or enoxaparin)	Alternative fibrinolytic; requires an infusion rather than a single bolus.

Beta-blockers

Start within 24 hours in all patients without contraindication (reactive airway disease, HR ≤50, 2nd-/3rd-degree heart block without pacemaker, SBP under 100 mmHg).

Drug	Dosage	Adverse effects	Drug interactions	Comments
Metoprolol	Oral: Start low, titrate every 12-24h as tolerated	Bradycardia, hypotension, bronchospasm, fatigue	Additive bradycardia with diltiazem/verapamil/digoxin	IV formulation for ongoing pain/tachycardia without contraindication; otherwise start oral. Titrate to resting HR 50-60 bpm.
Bisoprolol	Oral: Start low, titrate as tolerated	Bradycardia, hypotension, fatigue	Additive bradycardia with diltiazem/verapamil/digoxin	Alternative beta-1-selective agent, once-daily dosing.
Carvedilol	Oral: 3.125 mg BID initial, double no sooner than every 2 weeks to max 25 mg BID	Bradycardia, hypotension, fatigue, bronchospasm (non-selective)	Additive bradycardia with diltiazem/verapamil/digoxin; caution with CYP2D6 inhibitors	Preferred when concomitant heart failure with reduced ejection fraction is present — requires slow titration (see Drug Database entry).

ACE inhibitors / ARB

Start within 24 hours unless SBP under 100 mmHg; continue indefinitely, even with preserved LV function.

Drug	Dosage	Adverse effects	Drug interactions	Comments
Ramipril	Initial: 1.25-2.5 mg PO BID Target: 5 mg BID or 10 mg once daily	Cough, hyperkalemia, hypotension, rare angioedema	Hyperkalemia risk with potassium-sparing diuretics/spironolactone; avoid with lithium
Lisinopril	Initial: 2.5 mg PO daily Target: 20-40 mg daily	Cough, hyperkalemia, hypotension, rare angioedema	Hyperkalemia risk with potassium-sparing diuretics/spironolactone; avoid with lithium
Perindopril	Initial: 2 mg PO daily Target: 8 mg daily	Cough, hyperkalemia, hypotension, rare angioedema	Hyperkalemia risk with potassium-sparing diuretics/spironolactone; avoid with lithium
Candesartan (ARB alternative)	Dosing: Per current heart failure dosing guidance	Hyperkalemia, hypotension	Hyperkalemia risk with potassium-sparing diuretics/spironolactone	Use if ACE inhibitor not tolerated (e.g., cough) and clinical/radiological heart failure or documented LV dysfunction is present.

Mineralocorticoid receptor antagonists

For patients on an ACE inhibitor/ARB and beta-blocker who still have clinical heart failure, LVEF under 40%, or both. Use with caution in renal insufficiency given hyperkalemia risk.

Drug	Dosage	Adverse effects	Drug interactions	Comments
Spironolactone	Dosing: Per current heart failure dosing guidance	Hyperkalemia, gynecomastia	Hyperkalemia risk with ACE inhibitor/ARB and potassium supplements
Eplerenone	Dosing: Per current heart failure dosing guidance	Hyperkalemia	Hyperkalemia risk with ACE inhibitor/ARB and potassium supplements; avoid strong CYP3A4 inhibitors	More selective for the mineralocorticoid receptor than spironolactone — less gynecomastia.

Lipid-lowering therapy

High-intensity statin for every ACS patient regardless of baseline LDL, started before discharge.

Drug	Dosage	Adverse effects	Drug interactions	Comments
Atorvastatin (high-intensity)	Dosing: 40-80 mg PO daily	Myalgia, transaminase elevation	Diltiazem and other CYP3A4 inhibitors increase levels
Rosuvastatin (high-intensity)	Dosing: 20-40 mg PO daily	Myalgia, transaminase elevation	Fewer CYP3A4 interactions than atorvastatin
Ezetimibe	Dosing: 10 mg PO daily	Myalgia (mild), GI upset	None significant	Add if LDL remains ≥1.8 mmol/L (70 mg/dL) on maximally tolerated statin.
Evolocumab or alirocumab (PCSK9 inhibitor)	Dosing: Per current lipid-management dosing guidance	Injection-site reaction	None significant	Add if LDL remains ≥1.8 mmol/L (70 mg/dL) despite maximally tolerated statin plus ezetimibe.

Antianginal agents

Drug	Dosage	Adverse effects	Drug interactions	Comments
Nitroglycerin	Sublingual: 0.3-0.6 mg PRN, may repeat IV: Titrated per institutional protocol	Headache, hypotension, reflex tachycardia	Contraindicated with PDE5 inhibitors (sildenafil/vardenafil under 24h, tadalafil under 48h)	IV if pain not relieved within 15-20 minutes of sublingual dosing. Avoid in right ventricular infarct (preload-dependent) and significant hypotension.
Diltiazem	Low-dose example: 90-120 mg/day in divided doses, with close heart-rate monitoring	Bradycardia, hypotension, worsening heart failure	Additive bradycardia/AV block with beta-blockers; CYP3A4 interactions	For ongoing ischemia despite maximal beta-blocker/nitrate therapy, or when beta-blockers are contraindicated. Avoid in STEMI with LV dysfunction/pulmonary congestion.

Post-MI pericarditis

Drug	Dosage	Adverse effects	Drug interactions	Comments
ASA (high-dose, pericarditis)	Dosing: 650 mg PO QID for 1-2 weeks	GI upset, GI bleeding at this higher dose	Increased bleeding with anticoagulants	For symptomatic post-MI pericarditis, usually within 72 hours of MI.
Colchicine	Dosing: Per current pericarditis dosing guidance	GI upset (diarrhea, nausea) — usually dose-limiting	CYP3A4/P-glycoprotein interactions (e.g., clarithromycin, cyclosporine) can raise levels significantly	Add if pericarditis symptoms persist despite increased ASA dose.

References

2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes — Circulation, American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines (Rao SV, O'Donoghue ML, Ruel M, et al.). Circulation 2025;151(13):e771-e862
2023 ESC Guidelines for the management of acute coronary syndromes — European Heart Journal, European Society of Cardiology. Eur Heart J 2023;44(38):3720-3826
The TIMI risk score for unstable angina/non-ST elevation MI: a method for prognostication and therapeutic decision making — JAMA (Antman EM, Cohen M, Bernink PJ, et al.). JAMA 2000;284(7):835-842
Predictors of hospital mortality in the global registry of acute coronary events — Archives of Internal Medicine (Granger CB, Goldberg RJ, Dabbous O, et al.). Arch Intern Med 2003;163(19):2345-2353
Ticagrelor versus clopidogrel in patients with acute coronary syndromes — New England Journal of Medicine (Wallentin L, Becker RC, Budaj A, et al.). N Engl J Med 2009;361(11):1045-1057
Oxygen therapy in suspected acute myocardial infarction — New England Journal of Medicine (Hofmann R, James SK, Jernberg T, et al., DETO2X-AMI investigators). N Engl J Med 2017;377(13):1240-1249

Professional reference only. Apply clinical judgment and verify patient-specific decisions against current authoritative guidance and product information.