1.1 Acute Coronary Syndromes & Myocardial Infarction Management

1.1 Acute Coronary Syndromes & Myocardial Infarction Management

Clinical Scenario: A 62-year-old male presents with two hours of crushing retrosternal chest pressure radiating to the left jaw, diaphoresis, and nausea. Vital signs: BP 88/54 mmHg, HR 52 bpm, SpO2 96% on room air. The 12-lead ECG demonstrates 2.5 mm ST elevation in leads II, III, and aVF with reciprocal ST depression in leads I and aVL. Breath sounds are clear bilaterally, but physical examination reveals marked jugular venous distention.

Spectrum of Acute Coronary Syndromes & Diagnostic Criteria

Acute coronary syndromes (ACS) represent myocardial ischemia triggered by atherosclerotic plaque disruption and thrombosis:

• Unstable Angina (UA): Rest angina (>20 min), new-onset severe angina, or crescendo angina without myocardial necrosis. High-sensitivity cardiac troponin (hs-cTn) remains below the 99th percentile upper reference limit (URL).
• NSTEMI: Acute myocardial ischemia with a rise and/or fall in hs-cTn and at least one value above the sex-specific 99th percentile URL, without persistent diagnostic ST elevation.
• STEMI: Transmural ischemia from acute coronary occlusion. Diagnostic criteria require new J-point ST elevation in $\ge 2$ contiguous leads: $\ge 1$ mm in all leads except V2–V3 (where thresholds are $\ge 2.5$ mm in men <40, $\ge 2.0$ mm in men $\ge 40$, and $\ge 1.5$ mm in women).

The 2026 definition distinguishes primary MI from acute coronary pathology and secondary MI from supply–demand imbalance due to another acute condition. Older references call plaque-related MI Type 1 and supply–demand MI Type 2. Treat the precipitating illness, but do not assume that a supply–demand trigger excludes acute coronary occlusion. Troponin elevation without evidence of ischemia is myocardial injury, not MI.

12-Lead ECG Localization & Coronary Anatomy

High-Risk STEMI Equivalents & Conduction Abnormalities

Acute coronary occlusion can occur without classic ST elevation:

• de Winter Pattern: Indicates acute proximal LAD occlusion. Characterized by 1–3 mm upsloping ST depression at the J-point in V1–V4, continuing into tall, symmetrical T-waves, with 0.5–1 mm ST elevation in aVR.
• Wellens Syndrome: Critical proximal LAD stenosis presenting pain-free after angina. Type A (25%) shows biphasic T-waves in V2–V3; Type B (75%) shows deeply inverted, symmetric T-waves in V2–V4. Provocative stress testing is strictly contraindicated; urgent coronary angiography is required.
• Modified Sgarbossa Criteria: Positive in LBBB or ventricular pacing when any one of these is present:
  1. Concordant ST elevation $\ge 1$ mm in a lead with a positive QRS.
  2. Concordant ST depression $\ge 1$ mm in V1–V3.
  3. Discordant ST elevation $\ge 1$ mm with amplitude at least 25% of the preceding S-wave depth (ST/S ratio $\le -0.25$). Do not add weighted points to the modified rule. In a compatible ischemic presentation, a positive criterion warrants emergent coronary angiography.

Reperfusion Timelines & Initial Pharmacotherapy

• Reperfusion Benchmarks: For STEMI within 12 hours, target first-medical-contact-to-device time $\le 90$ min at PCI-capable centers or $\le 120$ min with transfer. If the anticipated delay exceeds 120 min, give fibrinolysis within 30 min of arrival only when eligible and without contraindications (including prior intracranial hemorrhage, active bleeding, or suspected aortic dissection), then transfer immediately to a PCI center.
• Aspirin: 162–325 mg non-enteric chewable PO immediately, then 81 mg daily indefinitely.
• P2Y12 Inhibitors: For PCI, ticagrelor (180 mg load, then 90 mg BID) or prasugrel (60 mg load, then 10 mg daily) is preferred when appropriate. Avoid prasugrel after stroke/TIA; use 5 mg daily maintenance with caution if age $\ge75$ or weight <60 kg. With fibrinolysis, use clopidogrel 300 mg loading then 75 mg daily if age $\le75$; at age >75, start 75 mg daily without loading.
• Anticoagulation: Unfractionated heparin bolus (60 units/kg, max 4,000 units) and infusion (12 units/kg/hr, max 1,000 units/hr; target aPTT 60–80 sec), or Enoxaparin 1 mg/kg SC q12h.
• High-Intensity Statin: Atorvastatin 80 mg or Rosuvastatin 40 mg initiated prior to PCI.
• Beta-Blockers: Oral metoprolol tartrate started within 24 hours only if free of heart failure, low output, or shock risk factors (age >70, SBP <120 mmHg, HR >110 or <60 bpm, PR >0.24 sec). Avoid IV beta-blockers acutely.
• Nitrates: Sublingual nitroglycerin (0.4 mg q5min up to 3 doses) followed by IV infusion (5–200 mcg/min). Avoid in RV infarction, SBP <90 mmHg, or PDE-5 inhibitor use within 24–48 hours.

Mechanical Complications of Acute MI

Mechanical complications typically develop 3 to 7 days post-MI due to tissue necrosis:

1. Papillary Muscle Rupture: Most commonly posteromedial muscle following inferior MI (solitary PDA supply). Presents with sudden pulmonary edema, cardiogenic shock, and a new harsh holosystolic apical murmur radiating to the axilla. Echocardiography confirms severe mitral regurgitation. Requires emergency surgery and mechanical support.
2. Ventricular Septal Defect (VSD): Presents with biventricular failure, a harsh holosystolic murmur at the left lower sternal border with a palpable thrill, and an oxygen saturation step-up from RA to RV due to left-to-right shunting.
3. Free Wall Rupture: Transmural rupture causes sudden hemopericardium, cardiac tamponade, electromechanical dissociation (PEA), and rapid death.
4. Post-MI Pericarditis: Early pericarditis (days 1–3) presents with pleuritic chest pain relieved by sitting forward and diffuse PR depression. Treat with high-dose aspirin (650 mg PO q6–8h); avoid NSAIDs and corticosteroids. Dressler syndrome is an autoimmune pericarditis presenting 2–10 weeks post-MI, managed with aspirin and colchicine.