ACS and STEMI

In depth

The one-page summary above is what the PDF prints. These sections go further.

Mechanisms: plaque, thrombus and the MI types

Type 1 MI starts at a plaque. Rupture tears a thin fibrous cap (under 65 µm) over a lipid-rich, inflamed core; erosion strips the endothelium from an intact, smooth-muscle-rich plaque; a calcified nodule breaks through the cap in older patients. Optical coherence tomography of ACS culprits found rupture in 44%, erosion in 31% and calcified nodules in 8% (Jia 2013), with erosion more common in younger patients and NSTE-ACS. Treating erosion with antithrombotics and no stent (EROSION 2017) is still investigational.

Exposed collagen activates platelets, amplified by thromboxane A₂ and ADP at the P2Y12 receptor, and they aggregate through GP IIb/IIIa; tissue factor drives thrombin, which makes fibrin. A partly occlusive, platelet-rich thrombus classically gives NSTE-ACS and an occlusive, fibrin-rich one STEMI. Necrosis spreads from subendocardium to epicardium, starting 20–40 min after occlusion and largely transmural by 3–6 h (Reimer and Jennings 1977, in dogs), so salvage is greatest in the first 2–3 h.

Supply depends on coronary perfusion pressure (aortic diastolic minus LVEDP) and diastolic time; demand depends on heart rate, contractility and wall stress. Tachycardia, hypotension and a rising LVEDP worsen both sides. Losing about 40% of the LV causes cardiogenic shock (Page 1971).

Myocardial injury is a troponin above the URL, acute when values rise or fall and chronic when stable (CKD, heart failure). MI needs acute injury plus at least one of: ischemic symptoms, new ischemic ECG changes or Q waves, new wall-motion loss, or thrombus at angiography; sepsis, PE, myocarditis and Takotsubo cause injury without MI. Type 2 MI is treated by correcting the trigger. MINOCA (AHA 2019) is MI with no stenosis of 50% or more; cardiac MRI often finds the cause.

SCAD (AHA 2018): most dissections with preserved flow heal, so stable patients are managed medically, but extension or new SCAD threatens 5% to 10% early, which justifies 3 to 5 days of in-hospital monitoring. Chest pain alone may come from the dissection itself and is not a reason for emergency revascularization; repeat angiography needs worsening symptoms with ECG ischemia or significant arrhythmia. Preferred contraception is partner vasectomy, tubal ligation (once dual antiplatelet therapy stops) or a levonorgestrel IUD, which also cuts menstrual blood loss by 71% to 95%.

Takotsubo is a form of acquired long QT syndrome (Ghadri 2018): most malignant arrhythmias come with a QTc over 500 ms, as pause-dependent torsades degenerating into VF. Beta-blockers are used cautiously with bradycardia and a QTc over 500 ms, QT-prolonging drugs cautiously in the acute phase, and the ECG is monitored continuously.

High-sensitivity troponin pathways

High-sensitivity assays measure troponin in at least half of healthy adults, report in ng/L, and use assay- and sex-specific URLs: about 16 ng/L in women and 34 in men for Abbott hs-cTnI, 14 and 22 for Roche hs-cTnT in the US. Troponin rises within 1–3 h of injury, peaks at about 12–24 h and stays high for 7–14 days, so reinfarction is a new rise of more than 20% from a stable or falling value (4th UDMI).

The 0/1-h algorithm rules out about 60% of patients with a negative predictive value above 99% and rules in about 15%; the observe zone gets a 3-h sample and echo (ESC 2020). US guidance (2021 AHA/ACC chest pain guideline) repeats hs-cTn at 1–3 h, or conventional troponin at 3–6 h, within a validated pathway. The deltas assume the stated interval, so record symptom onset and exact draw times.

The ECG: culprit artery, reciprocal change and equivalents

ST elevation over the injured wall is mirrored by depression in leads facing it from the other side. Reciprocal change favors occlusion over pericarditis (diffuse concave elevation, PR depression, reciprocal change only in aVR and V1), early repolarization and LV aneurysm.

A quarter of NSTEMIs have a totally occluded culprit at angiography and higher mortality (Khan 2017), so read the whole ECG for occlusion, not only the millimeters. STEMI equivalents:

In LBBB and RV pacing the ST segment normally points away from the main QRS deflection. Sgarbossa (1996) scores concordant ST elevation ≥1 mm (5 points), concordant depression ≥1 mm in V1–V3 (3) and discordant elevation ≥5 mm (2); 3 or more is specific but insensitive. Smith's modification replaces the 5-mm rule with discordant elevation ≥1 mm and at least 25% of the preceding S-wave depth: sensitivity 80% and specificity 99%, versus 49% and 100% for the weighted original (Meyers 2015).

Elevation in aVR with widespread depression usually means diffuse subendocardial ischemia (left main, 3-vessel disease or demand), not an occluded left main (LITFL): urgent angiography if pain persists, and no lytic, since 2025 ACC/AHA makes fibrinolysis for ST depression alone Class 3 unless it is posterior MI.

Reperfusion: timelines and strategy

Each 30 min of delay to primary PCI raised the relative risk of death at 1 year by 7.5% (De Luca 2004). Goals run from first medical contact: device ≤90 min at a PCI center, ≤120 min with transfer, and door-in-door-out ≤30 min (AHA Mission: Lifeline). Primary PCI restores TIMI 3 flow in over 90%, against 54% with accelerated alteplase in GUSTO-I, with less intracranial bleeding.

If PCI within 120 min is impossible and symptoms began under 12 h ago, lyse within 30 min and transfer: emergently for failed reperfusion or shock, otherwise for angiography at 2–24 h. In STREAM (2013), in patients seen within 3 h, this pharmacoinvasive approach matched primary PCI (30-day composite 12.4% vs 14.3%), but intracranial hemorrhage ran 1.0% vs 0.2% until the tenecteplase dose was halved at 75 or older.

Tenecteplase is one weight-based bolus of 30–50 mg (label). Adjuncts (2013 ACCF/AHA): aspirin, clopidogrel and enoxaparin (under 75: 30 mg IV, then 1 mg/kg SC every 12 h; 75 or older: no bolus, 0.75 mg/kg) or UFH to an aPTT 1.5–2 times control.

PCI from 12 to 24 h is reasonable (2025, 2a) and is indicated at any time for ongoing ischemia, heart failure, shock or arrhythmic instability; opening an occluded artery days later in a stable patient does not help (OAT 2006). NSTE-ACS (2025): immediate angiography for refractory angina or instability; within 24 h is reasonable at high risk (ESC marker: GRACE >140); invasive care during the admission is recommended at intermediate or high risk.

At PCI: radial access (2021 ACC/AHA/SCAI, Class 1), drug-eluting stents, intracoronary imaging for complex lesions (2025, Class 1) and no routine aspiration thrombectomy (TOTAL 2015). In stable multivessel disease, non-culprit lesions are treated at the index procedure or staged (2025, Class 1); in shock only the culprit is opened (CULPRIT-SHOCK).

Antiplatelet and anticoagulant choices

Ticagrelor or prasugrel is preferred over clopidogrel (2025, Class 1). In NSTE-ACS prasugrel waits for the anatomy: pretreatment nearly doubled major bleeding without reducing events (ACCOAST 2013). Ticagrelor can be loaded during a cangrelor infusion; prasugrel and clopidogrel only after it stops (Kengreal label).

DAPT runs 12 months by default (2025, Class 1); from 1 month after PCI, patients tolerating ticagrelor can drop aspirin and continue ticagrelor alone (2025, Class 1; TWILIGHT, ULTIMATE-DAPT). With atrial fibrillation, aspirin stops after 1–4 weeks, leaving a DOAC plus clopidogrel (ACC/AHA; AUGUSTUS). Usual holds before CABG: clopidogrel 5 days, prasugrel 7, ticagrelor 3–5 (sources differ).

Anticoagulants: UFH 70–100 units/kg at PCI to an ACT of 250–300 s; enoxaparin 1 mg/kg SC every 12 h (daily if CrCl <30) for medically treated NSTE-ACS, without switching to or from UFH (SYNERGY: more bleeding); bivalirudin in heparin-induced thrombocytopenia; fondaparinux 2.5 mg SC daily bled least (OASIS-5) but needs UFH at PCI because of catheter thrombosis. Stop after uncomplicated PCI.

Mechanical complications, RV infarction and shock

Mechanical complications now follow well under 1% of MIs (septal rupture 0.2% in GUSTO-I), mostly large first infarcts with late or no reperfusion (AHA 2021). They present as sudden deterioration, classically at day 3–5 but sooner after lytics (septal rupture median day 1 in GUSTO-I). Echo makes the diagnosis, and mechanical support bridges to surgery (2025, 2a).

The posteromedial papillary muscle ruptures far more often than the anterolateral because it depends on the posterior descending artery alone. Septal rupture repair carried 54% operative mortality within 7 days of MI versus 18% later (STS database, Arnaoutakis 2012), partly because only stable patients reach late surgery.

RV infarction accompanies up to 40% of inferior STEMIs (LITFL). V4R elevation marked 31% vs 6% in-hospital mortality (Zehender 1993) and fades within 10 h in half of patients. Expect hypotension, clear lungs and raised JVP, with RAP ≥10 mm Hg close to the wedge (RAP:PCWP ≥0.8). Reperfuse; no nitrates or diuretics; fluid in 250–500 mL steps while output rises, stopping near a CVP of 15; keep AV synchrony (atropine, AV sequential pacing, cardioversion of AF); then dobutamine or norepinephrine, and Impella RP or VA-ECMO.

Cardiogenic shock complicates 5–10% of MIs. Revascularize the culprit emergently whatever the delay (SHOCK, CULPRIT-SHOCK), transfer to a shock center (2025, Class 1), start norepinephrine and add dobutamine or milrinone, and track lactate, urine output and cardiac power output (<0.6 W is high risk). A microaxial pump is 2a in selected STEMI shock (DanGer Shock); routine IABP and VA-ECMO are Class 3, though an IABP still bridges mechanical complications.

Arrhythmias and conduction block after MI

Polymorphic VT with a normal QT means ongoing ischemia: beta-blocker, amiodarone and urgent angiography. Many units keep potassium ≥4.0 mmol/L and magnesium ≥2.0 mg/dL, although in-hospital mortality was lowest at potassium 3.5–4.5 and higher above 4.5 (Goyal 2012).

Inferior MI blocks at the AV node, supplied by the RCA in about 90% of hearts: a narrow junctional escape at 40–60/min, often vagal (Bezold–Jarisch reflex at reperfusion) and usually gone within days. Anterior MI blocks below the node, with a wide, slow, unreliable escape that marks a large infarct; atropine does not help, so pace. Permanent pacing is for block that persists, not block that resolves (2018 ACC/AHA/HRS).

Primary-prevention ICD: wait 40 days after MI and 90 days after revascularization, then implant for EF ≤35% with NYHA II–III or ≤30% with class I. Earlier ICDs did not improve survival (DINAMIT, IRIS), and a wearable defibrillator did not reduce arrhythmic death (VEST 2018).

After the cath lab: access sites, bleeding and discharge

Radial: the compression band uses patent hemostasis, stopping bleeding while radial flow continues (checked with a pulse oximeter on the thumb), which more than halved radial artery occlusion in PROPHET (2008). Deflate in steps per protocol, checking the site, hand color, capillary refill and sensation. Forearm swelling or pain signals a hematoma that can progress to compartment syndrome: re-compress, elevate, call the operator.

Femoral: sheaths come out when the ACT is below about 150–180 s (protocols vary), with 15–20 min of firm pressure just above the skin nick, then 2–6 h of bed rest with the leg straight, less after a closure device. Watch for a vasovagal response during removal (bradycardia, hypotension, nausea, yawning): atropine, fluid, legs up. Check the site and distal pulses every 15 min for the first hour.

A puncture above the inguinal ligament can bleed into the retroperitoneum, often without a groin hematoma. Clues are back, flank or lower abdominal pain, unexplained hypotension or tachycardia, a falling hemoglobin, or thigh numbness from femoral nerve compression; Grey Turner flank bruising is late. Call the operator, give fluid and blood and reverse heparin (protamine); noncontrast CT, then a covered stent or embolization if needed.

Check creatinine at 48–72 h for contrast-associated AKI; after intra-arterial contrast, hold metformin for 48 h if eGFR is 30–60 (FDA label). New chest pain with ST elevation in the stented territory is stent thrombosis until proven otherwise.

• DAPT is never stopped without the cardiologist; PPI with GI risk, but not omeprazole or esomeprazole with clopidogrel.
• High-intensity statin; add ezetimibe, a PCSK9 inhibitor, inclisiran or bempedoic acid if LDL-C stays ≥70 mg/dL (2025, Class 1), reasonable at 55–69 (2a).
• ACE inhibitor or ARB with EF ≤40%, hypertension, diabetes or CKD; eplerenone if EF ≤40% with heart failure or diabetes (EPHESUS).
• Cardiac rehab referral (Class 1), smoking cessation, BP below 130/80, yearly influenza vaccine (IAMI 2021: death 2.9% vs 4.9%).
• Teach: one sublingual nitroglycerin, then call 911 if pain is not better in 5 min.

Evidence: the 2025 guideline and key trials

The 2025 ACC/AHA/ACEP/NAEMSP/SCAI guideline replaced the 2013 STEMI and 2014 NSTE-ACS guidelines. Main changes: ticagrelor monotherapy from 1 month; complete revascularization Class 1 except in shock; intracoronary imaging for complex PCI; microaxial pump 2a, routine IABP and VA-ECMO Class 3; nonstatin therapy at LDL-C ≥70 mg/dL.

PLATO also lowered all-cause death (4.5% vs 5.9%). COMPLETE's gain came mainly from fewer MIs and held whether non-culprit PCI was done during or after the admission. ISCHEMIA excluded recent ACS, left main disease and EF <35%, so it is no argument for conservative ACS care. DanGer Shock excluded comatose arrest survivors and RV shock, and dialysis rose from 26.7% to 41.9%.

Unsettled: long-term beta-blockers with preserved EF (REDUCE-AMI 2024 and REBOOT 2025 neutral; BETAMI-DANBLOCK 2025 14.2% vs 16.3%, mostly reinfarction), colchicine after MI (COLCOT 5.5% vs 7.1%; CLEAR SYNERGY 9.1% vs 9.3%) and occlusion-MI criteria.

Exam pearls

• Killip I–IV (no failure, rales or S3, pulmonary edema, shock): 6%, 17%, 38% and 81% mortality in 1967.
• Type 1 MI is atherothrombosis, type 2 supply–demand mismatch; both need a troponin rise or fall plus ischemia.
• III > II with depression in I and aVL means RCA; V4R for RV infarct; V7–V9 for ST depression in V1–V3.
• de Winter and Wellens both mean proximal LAD; never stress-test Wellens.
• Times: ECG 10 min, first contact to device 90 (120 with transfer), lytic 30, door-in-door-out 30.
• Papillary muscle rupture: inferior MI, flash edema, soft murmur, giant v waves; septal rupture: harsh murmur, O₂ step-up.
• RV infarct: hypotension, clear lungs, JVD; fluids, no nitrates.
• Back or flank pain and hypotension after femoral access: retroperitoneal bleed.
• Culprit-only PCI in shock (CULPRIT-SHOCK); complete revascularization in stable STEMI (COMPLETE).