Mi with acute infarct
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"myocardial infarction"[MeSH Terms] AND "acute" AND management
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Myocardial Infarction (MI) with Acute Infarct
Definition and Diagnosis
Acute MI is defined as myocardial cell death with necrosis occurring in the setting of acute myocardial ischemia. Per the Fourth Universal Definition of Myocardial Infarction (ACC/ESC), a diagnosis requires:
- Elevated cardiac troponin above the 99th percentile upper reference limit (URL) with a rising or falling pattern (confirming acuity), PLUS at least one of:
- Symptoms of myocardial ischemia
- New ECG changes (ST-segment or T-wave changes, new pathologic Q waves)
- Imaging evidence of new loss of viable myocardium or regional wall motion abnormality
- Angiographic or autopsy evidence of coronary thrombus
- ROSEN's Emergency Medicine, block 10
Types of MI (Classification)
| Type | Description |
|---|---|
| Type 1 | Spontaneous MI from plaque rupture/erosion/fissuring with thrombus - the "true ACS" event |
| Type 2 | Ischemia from supply-demand mismatch (spasm, embolism, severe anemia, arrhythmia, hypotension) |
| Type 3 | Sudden cardiac death before biomarker sampling - fresh coronary thrombus on autopsy/angio |
| Type 4 | PCI-related MI (biomarkers >3x 99th percentile URL) |
| Type 5 | CABG-related MI (biomarkers >5x 99th percentile URL + new Q waves, graft occlusion, or imaging evidence) |
- ROSEN's Emergency Medicine, block 10
Pathophysiology
Type 1 AMI results from atherosclerotic plaque rupture or erosion, exposing thrombogenic material and triggering platelet aggregation and thrombus formation, abruptly occluding or severely narrowing a coronary artery. This leads to downstream ischemia, injury, and infarction following the sequence:
- Ischemia (reversible) → Injury (potentially reversible) → Infarction/necrosis (irreversible)
The infarct territory depends on the culprit vessel:
- LAD: anterior wall, anterior septum, apex
- RCA: inferior wall, posterior wall, RV
- LCx: lateral and posterior wall
ECG Evolution
| Phase | ECG Findings |
|---|---|
| Hyperacute (minutes) | Tall, peaked (hyperacute) T waves |
| Acute (hours) | ST elevation (STEMI) or ST depression/T-wave inversion (NSTEMI/UA) |
| Hours-days | ST elevation persists; Q waves begin to form; T-wave inversion |
| Days-weeks | Q waves established; ST returns to baseline; T-wave inversion deepens |
| Months-years | Persistent Q waves; T waves may normalize |
Acute Management
Immediate (First Hours) - "MONA + Antiplatelet + Anticoagulation"
| Drug | Indication/Dose | Notes |
|---|---|---|
| Aspirin | 162-325 mg loading, then 75-100 mg daily | Give immediately; chewed for faster absorption |
| P2Y12 inhibitor (ticagrelor, clopidogrel, prasugrel) | Loading dose | Dual antiplatelet therapy (DAPT) for all ACS |
| Anticoagulation (UFH, enoxaparin, or fondaparinux) | Immediately | Fondaparinux 2.5 mg SC daily (if no PCI) reduces bleeding vs. UFH |
| Nitrates | Sublingual/IV if ongoing pain and BP adequate | Avoid in RV infarct, hypotension, or PDE5 inhibitor use |
| Beta-blockers | Oral metoprolol 25-50 mg; IV if tachycardia/hypertension | Avoid in: decompensated HF, hypotension, bradycardia, advanced AV block |
| Oxygen | Only if SpO2 <90% | Routine O2 not recommended for normoxic patients |
| Morphine | For refractory pain | Use cautiously - may delay antiplatelet absorption |
- Goldman-Cecil Medicine, block 7
Reperfusion Strategy (Most Critical Intervention)
STEMI (ST-Elevation MI)
Primary PCI is the gold standard - target door-to-balloon time <90 minutes (or <120 min from first medical contact).
"Rapid revascularization of the infarct-related artery is the only evidence-based treatment strategy for mortality reduction." - Harrison's 22E
Fibrinolysis is indicated when:
- PCI will be delayed >120 minutes from first medical contact
- No contraindications
- Within 12 hours of symptom onset
- Door-to-needle time goal: <30 minutes
Preferred fibrinolytic agents:
| Agent | Dose |
|---|---|
| Tenecteplase (TNK-tPA) | 30-50 mg IV bolus over 5 seconds (weight-based; half-dose in >75 yrs) |
| Reteplase (r-PA) | 10 U + 10 U, 30 min apart |
| Alteplase (t-PA) | 100 mg over 90 min |
| Streptokinase | 1.5 MU over 30-60 min (antigenic, less preferred) |
Major risk of fibrinolysis: intracranial hemorrhage (0.5-1%) - risk increased by age >75, female sex, hypertension.
If fibrinolysis fails → rescue PCI (transfer immediately to PCI-capable center).
- Goldman-Cecil Medicine, block 7
NSTEMI/Unstable Angina
- Early invasive strategy (coronary angiography within 24 hrs for very high-risk; 36-80 hrs for high-risk patients)
- Optimal medical therapy (DAPT + anticoagulation + beta-blocker + statin) while awaiting
Multivessel Disease at PCI
- In stable STEMI patients: treat non-culprit vessels (either at index procedure or within ~1 month) - reduces recurrent MI and cardiovascular death
- In cardiogenic shock: culprit-only PCI preferred (CULPRIT-SHOCK trial) - immediate multivessel PCI increases 30-day mortality and renal replacement therapy
- Goldman-Cecil Medicine, block 7; Harrison's 22E, block 33
Cardiogenic Shock Complicating AMI
- Maintain mean arterial BP 60-65 mmHg (systolic ~90 mmHg)
- Correct hypoxemia and acidosis (up to 90% require ventilatory support)
- Glucose control: target ≤180 mg/dL, avoid hypoglycemia
- Vasopressors: norepinephrine first-line (fewer arrhythmias vs. dopamine per randomized trials)
- Inotropes: use lowest dose for shortest time; no single agent proven to change outcome
Complications of Acute MI
| Complication | Timing | Notes |
|---|---|---|
| Ventricular fibrillation/tachycardia | Minutes to hours | Prehospital VF causes most out-of-hospital SCD; incidence ~3-4% in STEMI reaching hospital |
| Accelerated idioventricular rhythm (AIVR) | Often reperfusion marker | Rate <120 bpm, usually benign |
| Atrial fibrillation | Up to 25% of ACS patients | Increases stroke risk; IV amiodarone or beta-blockers for rate control; cardioversion if hemodynamically compromised |
| Cardiogenic shock | Hours | Early revascularization saves 132 lives/1000 treated (SHOCK trial) |
| Mechanical complications | Days 3-7 | Ventricular septal defect, free wall rupture, acute mitral regurgitation (papillary muscle rupture) - require urgent surgery |
| Pericarditis (Dressler's syndrome) | Weeks-months | Autoimmune post-infarction |
Secondary Prevention (Discharge)
| Drug | Target/Dose | Duration |
|---|---|---|
| Aspirin | 75-100 mg/day | Lifelong |
| P2Y12 inhibitor | Per agent | 12 months (DAPT), then reconsider |
| High-intensity statin | LDL-C reduction >50% | Lifelong |
| ACE inhibitor/ARB | EF <40%, hypertension, diabetes, CKD | Lifelong (or long-term) |
| Beta-blocker | Titrate to HR 50-60 bpm | Especially if EF reduced or ongoing ischemia |
| Eplerenone/spironolactone | EF ≤40% + HF or diabetes | Long-term |
Note (2025 meta-analysis, PMID 39298680): A recent updated meta-analysis (Chi KY et al., Eur J Prev Cardiol 2025) questions the benefit of beta-blockers for secondary prevention in post-MI patients without reduced ejection fraction or heart failure. Current guidelines still recommend them for reduced EF, but evidence is evolving for preserved EF patients.
Sources: ROSEN's Emergency Medicine (Concepts and Clinical Practice); Goldman-Cecil Medicine International Edition; Harrison's Principles of Internal Medicine 22E (2025); Braunwald's Heart Disease
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