Coronary Artery Disease (CAD) / Ischemic Heart Disease (IHD) Revision Sheet

1. 📌 Essentials

• CAD/IHD results from an imbalance of myocardial oxygen supply and demand.
• Stable angina is exertional chest pain relieved by rest/nitroglycerin.
• Unstable angina and MI are forms of acute coronary syndrome with prolonged, unrelieved pain.
• Atherosclerosis (95%) is the main cause of coronary stenosis.
• Vasospasm (5%) causes functional restenosis; embolism can occlude arteries.
• Typical angina: retrosternal, radiates to arm, jaw, shoulder; constrictive or heavy sensation.
• ECG changes: T wave inversion (ischemia), ST elevation (injury), Q waves (necrosis).
• Cardiac enzymes (Troponin, CPK) rise during MI but not in stable angina.
• Coronary angiography confirms stenosis location and severity.
• Revascularization: PTCA, stents, CABG; pharmacotherapy includes nitrates, antiplatelets, anticoagulants.
• Rest: myocardial oxygen demand and supply are balanced at 3 Oxygen/sec; exercise raises demand to 9 Oxygen/sec, demand-supply mismatch causes ischemia.

2. 🧩 Key Structures & Components

• Coronary arteries — supply oxygenated blood to myocardium.
• Left coronary artery (LCA) — includes LAD and LCX, supplies left heart.
• Right coronary artery (RCA) — supplies right heart tissues.
• Atherosclerotic plaque — narrows lumen, causes stenosis.
• Vasospasm — functional constriction of coronary vessels.
• Myocardium — tissue affected by ischemia or infarction.
• ECG leads — detect electrical changes due to ischemia/injury.
• Cardiac enzymes — biomarkers for myocardial necrosis.

3. 🔬 Functions, Mechanisms & Relationships

• Normal Heart Physiology:
  • Contraction depends on adequate oxygen supply.
  • Supply relies on coronary lumen patency and flow.
  • Demand increases with exercise; supply adjusts via coronary vasodilation.
• Pathophysiology of Ischemia:
  • Organic stenosis (atherosclerosis) reduces flow; causes ischemia during increased demand.
  • Vasospasm constricts arteries temporarily; causes spasm-induced ischemia.
  • Embolism blocks flow acutely, leading to sudden ischemia.
• Clinical Manifestation:
  • Imbalance during exertion → angina.
  • Plaque rupture → thrombus formation → ACS.
• ECG & Biomarkers:
  • Ischemia: T wave inversion.
  • Injury: ST elevation.
  • Infarction: Q waves, enzyme elevation.
• Revascularization:
  • Restores flow in stenosed arteries.
  • Pharmacotherapy alleviates symptoms and prevents progression.

4. Comparative Table for Angina and MI

5. 🗂️ Hierarchical Diagram

Coronary Artery Disease (CAD / IHD)
 ├─ Normal Myocardial Oxygen Physiology
 │    ├─ Rest: demand = supply = 3 oxygen/sec
 │    └─ Exercise: demand = supply = 9 oxygen/sec
 ├─ Pathological Causes of Imbalance
 │    ├─ Organic stenosis (atherosclerosis) - 95%
 │    ├─ Functional spasm - 5%
 │    └─ Embolism
 ├─ Clinical Manifestations
 │    ├─ Stable angina
 │    ├─ Unstable angina (ACS)
 │    ├─ Myocardial infarction
 │    └─ Sudden arrhythmic death
 ├─ Symptoms
 │    ├─ Chest pain: retrosternal, radiates
 │    └─ Quality: constrictive, like pressure
 └─ Diagnostic & Treatment Strategies
      ├─ ECG & enzyme tests
      ├─ Imaging and catheterization
      └─ Pharmacological and surgical revascularization

6. ⚠️ High-Yield Pitfalls & Confusions

• Confusing stable vs. unstable angina—duration and relief differ.
• Mistaking ST depression for infarction (which shows ST elevation).
• Assuming all chest pain is cardiac—exclude GI or musculoskeletal causes.
• Not recognizing that enzyme elevation (Troponin) confirms infarction specifically.
• Believing vasospasm always causes pain during exertion—sometimes occurs at rest.
• Confusing angina location with other causes of chest pain.
• Overlooking that stable angina does not cause enzyme elevation.
• Mistaking Q waves development as total infarction; early MI may have no Q waves.
• Assuming angiography is always required for diagnosis—initial assessment may be clinical/ECG.

7. ✅ Final Exam Checklist

• Understand the concept of myocardial oxygen demand and supply.
• Know the common causes of coronary artery stenosis and spasm.
• Distinguish between stable angina, unstable angina, and MI.
• Recognize typical chest pain features and radiation.
• Correlate ECG changes with ischemic/infarctive stages.
• Know key cardiac enzymes and their significance.
• Be familiar with diagnosis tools: ECG, enzymes, angiography, imaging.
• Know pharmacological treatments: nitrates, antiplatelets, anticoagulants.
• Understand revascularization options: PTCA, stents, CABG.
• Remember the pathophysiological basis of sudden death in arrhythmias.
• Be aware that exercise testing helps detect ischemia.
• Know the role of vasospasm and embolism in CAD.
• Recognize the importance of lifestyle modification and risk factor control.
• Know the typical presentation and location of anginal pain.
• Familiarize with the hierarchy of coronary arteries and common sites of disease.
• Recognize that enzyme elevation confirms myocardial necrosis.