Acute Coronary Syndromes

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]

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.

• 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).

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]

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.

• 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.

• 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.

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.

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.

1. Recurrent or ongoing ischemia: optimize antianginal therapy and consider urgent angiography/revascularization if not already performed.
2. New heart failure: treat aggressively per standard heart failure management; consider angiography/revascularization if LVEF <40% post-MI.
3. 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.
4. 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.
5. 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.

• 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.

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

Anticoagulants

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

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).

ACE inhibitors / ARB

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

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.

Lipid-lowering therapy

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

Antianginal agents

Post-MI pericarditis