2.1 Coronary Artery Disease & Acute Myocardial Infarction

Coronary Artery Disease & Acute Myocardial Infarction

1. Pathophysiology & Atherosclerotic Cascade

Coronary Artery Disease (CAD) arises from the progressive deposition of lipids, inflammatory cells, and fibrous tissue within the intima of epicardial coronary arteries, forming atherosclerotic plaques.

• Stable Plaque: Thick fibrous cap with a dense lipid core, causing predictable exertional ischemia when luminal obstruction exceeds 70% (Stable Angina).
• Vulnerable Plaque: Thin cap fibroatheroma (TCFA) rich in macrophages and lipids. Plaque fissure, erosion, or rupture exposes subendothelial collagen and tissue factor to circulation, triggering rapid platelet activation, aggregation, and thrombosis.
• Partial/Transient Occlusion: Manifests clinically as Unstable Angina (UA) or Non-ST-Elevation Myocardial Infarction (NSTEMI) depending on the presence of myocardial necrosis biomarkers.
• Complete Transmural Occlusion: Leads to ST-Elevation Myocardial Infarction (STEMI), resulting in ischemic necrosis propagating from endocardium to epicardium over 6 hours.

2. Clinical Classification & Diagnostic Spectrum

Clinical Gem (UPSC CMS Focus): Prinzmetal (Variant) Angina is caused by focal coronary artery vasospasm (often at sites of minor plaque). It presents with rest chest pain occurring predominantly at night or early morning, accompanied by transmural transient ST elevation on ECG, but with normal cardiac biomarkers. It responds promptly to sublingual nitrates and Calcium Channel Blockers (Diltiazem/Amlodipine); Beta-blockers are contraindicated as they worsen un-opposed alpha-adrenergic vasospasm.

3. ECG Localization & Coronary Anatomy Correlation

Localization of the culprit vessel is paramount for predicting hemodynamic complications and guiding invasive coronary angiography:

Critical Guideline: In any patient presenting with an Inferior MI (ST elevation in II, III, aVF), right-sided ECG leads (V3R–V6R) MUST be obtained immediately. If RV infarction is confirmed:

1. AVOID Nitrates, Morphine, and Diuretics (these reduce preload and precipitate severe, fatal hypotension).
2. Primary treatment consists of aggressive IV isotonic saline (0.9% NaCl) boluses to maintain right ventricular preload and cardiac output.

4. Cardiac Biomarkers Dynamics

Understanding the temporal profile of cardiac enzymes is crucial for both initial diagnosis and detecting early re-infarction:

• Cardiac Troponin I & T (cTnI / cTnT):
  • Initial Rise: 3–4 hours after myocardial injury.
  • Peak: 18–24 hours.
  • Duration of Elevation: 7–14 days.
  • Clinical Significance: Gold standard for diagnosing MI. High sensitivity assays detect minor myocardial necrosis.
• Creatine Kinase-MB (CK-MB):
  • Initial Rise: 4–6 hours.
  • Peak: 12–24 hours.
  • Duration of Elevation: Normalizes within 48–72 hours.
  • Clinical Significance: Because troponin remains elevated for up to two weeks, CK-MB is the diagnostic biomarker of choice for detecting recurrent re-infarction occurring within 3 to 10 days after the index event.
• Myoglobin:
  • Initial Rise: 1–2 hours (earliest marker).
  • Duration: Normalizes within 24 hours. Lack of specificity limits its utility.

5. Emergency Management Protocols & Reperfusion Strategies

Immediate Medical Therapy (MONAH Protocol)

1. Aspirin: 300 mg chewed immediately (non-enteric coated) to achieve rapid antiplatelet inhibition.
2. P2Y12 Inhibitor: Loading dose of Ticagrelor (180 mg) or Prasugrel (60 mg); Clopidogrel (300–600 mg) is used if thrombolysis is planned or contraindications exist.
3. Nitrates: Sublingual Nitroglycerin (0.4 mg every 5 min up to 3 doses) for chest pain, unless SBP <90 mmHg, HR <50 or >100 bpm, or RV infarction is present.
4. Analgesia: IV Morphine (2–4 mg) for severe refractory chest pain (used judiciously due to potential delay in oral antiplatelet absorption).
5. Oxygen: Indicated ONLY if arterial oxygen saturation ($SpO_2$) is <90% or patient is in respiratory distress (routine oxygen in normoxic patients causes coronary vasoconstriction via reactive oxygen species).
6. Anticoagulation: Unfractionated Heparin (UFH) IV bolus or Enoxaparin SC.

Reperfusion Windows in STEMI

Reperfusion must be initiated rapidly for all patients presenting within 12 hours of symptom onset with persistent ST elevation:

• Primary Percutaneous Coronary Intervention (PCI): Preferred reperfusion strategy.
  • Target Door-to-Balloon Time: ≤90 minutes (if presenting to a PCI-capable facility).
  • Target Transfer Time: ≤120 minutes from first medical contact (FMC) to balloon inflation if transferred from a non-PCI facility.
• Fibrinolytic / Thrombolytic Therapy: Indicated when Primary PCI cannot be performed within 120 minutes of FMC.
  • Target Door-to-Needle Time: ≤30 minutes.
  • Preferred Agents: Fibrin-specific agents (Tenecteplase weight-adjusted single IV bolus, Reteplase, or Alteplase) are superior to Streptokinase (1.5 million units IV over 60 min).

Thrombolytic Contraindications (High-Yield UPSC CMS Checklist)

6. Post-MI Complications & Long-Term Management

Complications follow a distinct chronological sequence post-MI:

1. Arrhythmias (Hours 0–24): Ventricular Fibrillation (VF) and Ventricular Tachycardia (VT) are the leading cause of pre-hospital sudden cardiac death. Managed with unsynchronized defibrillation (VF/pulseless VT) or IV Amiodarone.
2. Acute Pericarditis (Days 1–3): Sharp pleuritic chest pain radiating to the trapezius ridge, relieved by leaning forward. Shows diffuse concave ST elevation and PR depression on ECG. Treated with High-dose Aspirin (650 mg tid); NSAIDs/corticosteroids should be avoided as they impair myocardial scar formation.
3. Myocardial Rupture Syndromes (Days 3–14):
   • Free Wall Rupture: Sudden electromechanical dissociation, cardiac tamponade, death.
   • Ventricular Septal Rupture (VSD): New loud holosystolic murmur at left lower sternal border with thrill, acute biventricular failure.
   • Papillary Muscle Rupture (Posteromedial papillary muscle supplied solely by RCA): Sudden onset severe dyspnea, flash pulmonary edema, new apical pansystolic murmur radiating to axilla (Acute Severe Mitral Regurgitation).
4. Dressler Syndrome (Weeks 2–10): Autoimmune pleuropericarditis presenting with fever, pericardial friction rub, pleuritic pain, and elevated ESR/CRP. Managed with Aspirin + Colchicine.

Secondary Prevention (The 5 Essential Drug Classes)

• Dual Antiplatelet Therapy (DAPT): Aspirin (75–100 mg daily) + P2Y12 inhibitor for at least 12 months.
• High-Intensity Statin: Atorvastatin 80 mg or Rosuvastatin 40 mg daily (target LDL-C <55 mg/dL).
• Beta-Blockers: (e.g., Metoprolol succinate, Bisoprolol, Carvedilol) initiated within 24 hours if hemodynamically stable; reduces myocardial oxygen demand and sudden cardiac death risk.
• ACE Inhibitors / ARBs: Initiated within 24 hours, especially in anterior MI, LVEF ≤40%, or hypertension; prevents adverse ventricular remodeling.
• Mineralocorticoid Receptor Antagonists (MRA): (Spironolactone or Eplerenone) indicated if LVEF ≤40% and patient has clinical heart failure or diabetes.