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Acute Coronary Syndromes

Name: Acute Coronary Syndromes
Creator: Veli Bakalov, MD

Read the ECG, open the artery, and start the drugs that save lives

Cardiology·Ischemic Heart Disease·5 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

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Unstable angina = rest ischemia with normal troponin; NSTEMI = troponin rise without ST elevation; STEMI = ST elevation from transmural occlusion.
Localize: V1–V4 = LAD; I, aVL, V5–V6 = circumflex; II, III, aVF = RCA; ST depression with tall R in V1–V3 = posterior MI.
Inferior MI with hypotension after nitroglycerin = RV infarction: check V4R, give IV fluids, avoid nitrates and diuretics.
Troponin rises in 3–4 h, peaks at about 24 h, and stays up 7–10 days; re-infarction is a further troponin rise of more than 20% (CK-MB no longer recommended).
Give chewed aspirin 162–325 mg first, then a P2Y12 inhibitor, heparin, beta-blocker, and atorvastatin 80; oxygen only if SpO2 is below 90%.
STEMI: primary PCI with door-to-balloon under 90 min; if PCI cannot happen within 120 min, fibrinolysis within 30 min of arrival (within 12 h of onset).
Any prior intracranial hemorrhage, ischemic stroke or head trauma within 3 months, brain tumor/AVM, active bleeding, or suspected dissection rules out fibrinolysis.
Never give fibrinolytics for NSTEMI/unstable angina; prasugrel is contraindicated after stroke or TIA; continue DAPT about 12 months.
Post-MI: VF in the first 48 h; papillary muscle or septal rupture days 3–5; free wall rupture days 5–14; LV aneurysm and Dressler syndrome weeks later.

The spectrum and the ECG

Three syndromes, one plaque. ACS begins with rupture or erosion of a coronary plaque and superimposed thrombus. Troponin and the ST segment sort patients into three groups that share early antithrombotic therapy but differ in reperfusion.

Unstable angina, NSTEMI, and STEMI

Feature	Unstable angina	NSTEMI	STEMI
Troponin	Not elevated	Elevated	Elevated
ECG	Normal, ST depression, or T inversion	Often ST depression or T-wave inversion	ST elevation (or equivalent)
Injury	Ischemia without necrosis	Subendocardial infarction	Transmural infarction from full occlusion
Reperfusion	No fibrinolytics; early invasive if high risk	No fibrinolytics; early invasive if high risk	Immediate: primary PCI or fibrinolysis

STEMI criteria. New ST elevation of at least 1 mm in two or more contiguous limb leads, or about 2 mm in V2–V3 (the precordial threshold is slightly lower in women), in the right clinical setting. Reciprocal ST depression supports a true infarct. A new left bundle branch block with ischemic symptoms has traditionally been treated as a STEMI equivalent; because LBBB is often old, current practice looks for Sgarbossa-type concordant ST changes rather than the block alone.

Localizing the infarct

Territory	Leads	Usual artery
Anterior / anteroseptal	V1–V4 (septal V1–V2)	LAD
Lateral	I, aVL, V5–V6	Left circumflex
Inferior	II, III, aVF	RCA in most people
Posterior	Tall R waves with ST depression in V1–V3 (mirror image); ST elevation in V7–V9	Posterior descending (RCA or LCx)
Right ventricle	ST elevation in right-sided lead V4R	Proximal RCA

Inferior MI: think RV and conduction. An inferior STEMI can extend to the right ventricle, so record V4R. RV infarction presents with hypotension, JVD, and clear lungs; it is preload-dependent, so avoid nitrates and diuretics and give IV fluids for hypotension. Because the RCA usually feeds the AV node, inferior MI also causes bradycardia and AV block.

Hypotension right after nitroglycerin in an inferior MI suggests RV infarction: bolus fluids and hold further nitrates.

Biomarkers and first-hour therapy

Troponin. Cardiac troponin I or T is the most sensitive and specific marker: it rises 3–4 hours after injury, peaks around 24 hours, and stays elevated 7–10 days. Trend serial values; high-sensitivity assays allow a repeat at 1–3 hours. CK-MB normalizes within 48 to 72 hours but is no longer recommended; re-infarction is diagnosed by a further troponin rise of more than 20% (Fourth Universal Definition of MI).

Immediate drugs.

Aspirin 162–325 mg, chewed, at once: the highest-yield early drug.
A P2Y12 inhibitor plus anticoagulation (heparin).
Nitroglycerin for pain; morphine for pain that persists. Avoid nitrates with hypotension, RV infarction, or a recent PDE-5 inhibitor.
Early beta-blocker, unless there is heart failure, shock risk, bradycardia, heart block, or cocaine use.
High-intensity statin (atorvastatin 80 mg).
Oxygen only if SpO2 is below 90%; routine oxygen gives no benefit and may harm.

Dual antiplatelet therapy (DAPT). Aspirin plus a P2Y12 inhibitor: ticagrelor or prasugrel (preferred with PCI) or clopidogrel, continued for about 12 months after MI or stenting. Prasugrel is contraindicated with prior stroke or TIA because of intracranial bleeding. Clopidogrel is the P2Y12 inhibitor paired with fibrinolysis, and it is a prodrug that CYP2C19 poor metabolizers activate poorly.

Reperfusion in STEMI

<90 mindoor-to-balloon for primary PCI

<120 minacceptable delay when transferring for PCI

<30 mindoor-to-needle if fibrinolysis is chosen

12 hwindow from symptom onset for fibrinolysis

Diagnose STEMIST elevation or an equivalent with ischemic symptoms.
Can PCI happen within 120 minutes?Yes: primary PCI, door-to-balloon under 90 minutes. Cardiogenic shock goes to PCI regardless of delay.
If not: fibrinolysisTenecteplase or alteplase within 30 minutes of arrival, ideally within 12 hours of onset.
After lysis: transferRescue PCI if reperfusion fails (ongoing pain, under 50% ST resolution at 60–90 minutes); otherwise angiography within 3–24 hours.

Absolute contraindications to fibrinolysis. Any prior intracranial hemorrhage; ischemic stroke within 3 months; known brain tumor or AVM; active bleeding; suspected aortic dissection; significant closed-head trauma within 3 months. When lysis is contraindicated, transfer for PCI. Severe uncontrolled hypertension, recent major surgery, and oral anticoagulation are relative contraindications.

NSTEMI and unstable angina; secondary prevention

No lytics. Fibrinolytics give no benefit in NSTEMI or unstable angina and only add bleeding. Treat with aspirin, a P2Y12 inhibitor, anticoagulation, beta-blocker, statin, and nitrates. Risk-stratify with TIMI or GRACE: high-risk patients (rising troponin, dynamic ST depression, high score) go to early invasive angiography, generally within 24–48 hours, and those with refractory angina, instability, or heart failure go immediately.

The discharge cocktail (ABCS). Antiplatelets and ACE inhibitor, Beta-blocker, Cholesterol lowering, Smoking cessation:

Aspirin lifelong plus a P2Y12 inhibitor for about 12 months
High-intensity statin and beta-blocker
ACE inhibitor, especially with EF under 40%, heart failure, diabetes, or hypertension
Aldosterone antagonist if EF is under 40% with symptoms
Cardiac rehabilitation; avoid NSAIDs
Recheck EF: an ICD is indicated if it stays at or below 35% at least 40 days after MI

Post-MI complications

Complications by timing

Timing	Complication	Clues and action
Minutes to 48 h	VF or VT; bradycardia and AV block (inferior MI)	VF is the leading cause of early death: defibrillate
Days 1–3	Fibrinous pericarditis	Pleuritic pain, friction rub
Days 3–5	Papillary muscle rupture (often inferior MI)	Acute severe MR: new holosystolic murmur, flash pulmonary edema
Days 3–5	Interventricular septal rupture	New holosystolic murmur with an oxygen step-up from RA to RV
Days 5–14	Free wall rupture	Tamponade, PEA, sudden death
Weeks	LV aneurysm; Dressler (autoimmune) pericarditis	Aneurysm: persistent ST elevation, HF, arrhythmia, mural thrombus

All three mechanical ruptures need emergent echocardiography and surgery.

The posteromedial papillary muscle has a single blood supply from the posterior descending artery, which is why papillary rupture follows inferior MI more often than anterior MI.