1.2 Coronary Artery Disease & Myocardial Infarction

Coronary Artery Disease & Myocardial Infarction

PANCE High-Yield Focus: Differentiating stable angina from the three forms of Acute Coronary Syndrome (ACS) - Unstable Angina, NSTEMI, and STEMI - is essential. Focus on ECG lead localization of infarction, troponin kinetics, immediate medical management using the MONA-BASH protocol, and the time-sensitive reperfusion thresholds for PCI versus fibrinolytic therapy.

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Ischemic Heart Disease Spectrum

Ischemic heart disease represents a mismatch between myocardial oxygen supply and demand, most commonly caused by atherosclerotic narrowing of the epicardial coronary arteries.

Angina Types

• Stable Angina: Predictable chest discomfort (typically retrosternal pressure radiating to the left arm or jaw, accompanied by dyspnea) precipitated by exertion or emotional stress. It lasts <10-15 minutes and is promptly relieved by rest or sublingual nitroglycerin.
• Unstable Angina (UA): Chest pain that is new-onset, occurs at rest or with minimal exertion, or represents a significant acceleration of previous stable symptoms (more frequent, longer duration, lower threshold). Characterized by subtotal coronary occlusion. Cardiac biomarkers (troponins) remain normal.
• Prinzmetal (Variant) Angina: Transient coronary vasospasm rather than atherosclerotic plaque rupture. Presents as episodic chest pain occurring at rest, often in the early morning, and is highly associated with tobacco and cocaine use. ECG shows transient ST-segment elevations during the spasm, which resolve completely when pain subsides or when treated with calcium channel blockers or nitrates. PANCE Warning: Beta-blockers are contraindicated in Prinzmetal angina as they cause unopposed alpha-1 receptor vasoconstriction, worsening the spasm.

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Acute Coronary Syndromes (ACS)

ACS includes Unstable Angina, Non-ST-Segment Elevation Myocardial Infarction (NSTEMI), and ST-Segment Elevation Myocardial Infarction (STEMI). These are triggered by plaque rupture or erosion, which exposes the thrombogenic lipid core, leading to platelet adhesion, activation, aggregation, and localized thrombus formation.

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ECG Interpretation and Myocardial Localization

For STEMI, prompt ECG interpretation is required to identify the culprit coronary artery and localize the infarcted ventricular wall. Contiguous leads are defined as two or more leads looking at the same anatomical area.

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Cardiac Biomarkers

Myocardial necrosis releases intracellular proteins into the systemic circulation.

• Cardiac Troponins (I and T): The gold standard biomarkers for myocardial infarction due to high sensitivity and cardiospecificity. Troponins rise within 3-4 hours of myocardial injury, peak at 18-24 hours, and can remain elevated for 10-14 days. Serial troponins should be checked at presentation and 3-6 hours later to rule out myocardial injury.
• CK-MB (Creatine Kinase-Myocardial Band): Rises within 4-6 hours, peaks at 24 hours, and returns to baseline within 48-72 hours. Because of its rapid clearance, CK-MB is clinically useful for diagnosing early reinfarction if a patient develops recurrent chest pain within a few days of the index MI (when troponins would still be elevated from the initial event).

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Management Guidelines

Acute Pharmacological Management: The MONA-BASH Protocol

Every patient with suspected ACS must be managed immediately with a combination of antiplatelet, anticoagulant, and anti-ischemic therapies:

1. M - Morphine: IV for severe chest pain refractory to nitroglycerin. Use cautiously as it may delay the absorption of oral antiplatelet agents.
2. O - Oxygen: Administered only if O2 saturation is <90% or the patient is in respiratory distress.
3. N - Nitroglycerin: Sublingual or IV. Induces venodilation to reduce preload and myocardial oxygen demand. Absolute Contraindications: Systolic BP <90 mmHg, Right Ventricular Infarction, or recent phosphodiesterase-5 inhibitor use (e.g., sildenafil within 24 hours).
4. A - Aspirin: Immediate non-enteric coated chewable aspirin (162-325 mg) to inhibit thromboxane A2.
5. B - Beta-blockers: Start oral beta-blockers (e.g., Metoprolol) within 24 hours if the patient is hemodynamically stable. Avoid in patients with signs of acute heart failure or cardiogenic shock.
6. A - ACE Inhibitors: Initiated within 24 hours (especially in anterior MI, HFrEF, or stable CKD) to prevent adverse ventricular remodeling.
7. S - Statins: Immediate initiation of high-intensity statin therapy (Atorvastatin 80 mg) for lipid-lowering and plaque-stabilizing (pleiotropic) effects.
8. H - Heparin: Anticoagulation (Unfractionated Heparin or LMWH like Enoxaparin) to prevent clot propagation.

Note on Dual Antiplatelet Therapy (DAPT): In addition to aspirin, all patients undergoing PCI or medical management require a P2Y12 inhibitor (Clopidogrel, Ticagrelor, or Prasugrel) for a minimum of 12 months.

Reperfusion Strategies in STEMI

STEMI requires immediate coronary reperfusion. The clinical choice depends on the availability of a cardiac catheterization laboratory:

• Primary Percutaneous Coronary Intervention (PCI): The preferred reperfusion strategy. The target door-to-balloon time is <=90 minutes at a PCI-capable hospital, or <=120 minutes if the patient requires transfer from a non-PCI-capable facility.
• Fibrinolytic Therapy (Alteplase, Tenecteplase): Indicated if PCI cannot be performed within the 120-minute window. The target door-to-needle time is <=30 minutes.
  • Absolute Contraindications to Fibrinolytics: History of intracranial hemorrhage, structural cerebrovascular lesions, malignant intracranial neoplasm, ischemic stroke within 3 months, active internal bleeding, suspected aortic dissection, or active bleeding diathesis.

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PANCE Clinical Traps

• Right Ventricular (RV) Infarction: Suspect this in a patient presenting with an inferior wall MI (ST elevations in II, III, aVF) accompanied by severe hypotension, clear lung fields, and jugular venous distention. These patients are highly preload-dependent. Avoid nitroglycerin, morphine, and diuretics, as reducing preload will cause profound cardiogenic shock. Treat immediately with intravenous fluid boluses (normal saline) to maintain right ventricular fill.
• Silent Myocardial Infarction: Diabetics, elderly patients, and females frequently present with atypical symptoms (epigastric pain, dyspnea, nausea, unexplained fatigue) rather than classic crushing substernal chest pain. Maintain a low threshold for obtaining an ECG in these populations.
• Post-MI Mechanical Complications (Timeline 3-5 days):
  • Papillary Muscle Rupture: Most common after inferior MI. Causes acute mitral regurgitation, presenting as sudden pulmonary edema and a new holosystolic murmur at the apex radiating to the left axilla.
  • Ventricular Septal Rupture: Presents as cardiogenic shock with a new, harsh holosystolic murmur heard best at the left lower sternal border, accompanied by a palpable thrill.