Ischemic Heart Disease

IHD Basics - Heart's SOS Call

• Definition: Myocardial O₂ supply/demand mismatch → ischemia.
• Etiology: >90% due to coronary atherosclerosis (CAD).
• Epidemiology: Top global killer; high in India.
• Pathogenesis: Atheroma → progressive stenosis / acute plaque disruption → thrombosis → ↓coronary flow → ischemia.
• Risk Factors (Major):
  • Non-Modifiable: Advancing age, male gender, family history (1st degree, M<55y, F<65y).
  • Modifiable: Cigarette smoking, Hypertension (BP ≥140/90 mmHg), Diabetes Mellitus, Dyslipidemia (↑LDL, ↓HDL), Obesity (BMI ≥30), Physical inactivity.

⭐ Symptomatic ischemia (e.g., stable angina) often with >70-75% coronary stenosis.

Atherosclerosis - Plaque Attack

Chronic inflammation from endothelial injury.

• Pathogenesis:

• Plaque Components:
  • Fibrous cap: SMCs, collagen.
  • Necrotic core: Lipids, cholesterol crystals, foam cells.
  • Shoulder: Inflammatory cells; rupture site.
• Plaque Types:
  • Stable: Thick cap, small core, ↓inflammation → stenosis.
  • Vulnerable: Thin cap, large core, ↑inflammation (MMPs) → rupture.

    ⭐ Most common sites: Abdominal aorta > Coronaries > Popliteal > Carotids > Circle of Willis. (📌 A CoPoCaCi)

IHD Syndromes - Clinical Crisis

• Angina Pectoris: Chest pain due to transient myocardial ischemia.
  • Stable Angina: Predictable, on exertion; relieved by rest/nitrates.
  • Unstable Angina: Crescendo, at rest, or new-onset severe; high risk of MI.
  • Prinzmetal (Variant) Angina: Coronary artery spasm; occurs at rest, often at night; ST elevation during pain.
• Myocardial Infarction (MI): Myocardial necrosis due to prolonged ischemia.
• Chronic IHD: Progressive heart failure due to ischemic myocardial damage.
• Sudden Cardiac Death (SCD): Unexpected death from cardiac causes, often due to lethal arrhythmia (e.g., VFib) in IHD.

MI Deep Dive - Infarct Insights

• Pathophysiology: Coronary occlusion → necrosis. Irreversible injury: 20-40 mins. Wavefront: subendocardium → epicardium.
• Morphological Changes:

  Time	Gross	Microscopic
  0-4h	None/Mottling (late)	Wavy fibers, edema, early coag. necrosis
  4-24h	Dark Mottling	Coagulative necrosis, neutrophils
  1-7d	Yellow-tan center	Neutrophils (peak), Macrophages, phagocytosis
  1-2w	Max yellow, soft	Granulation tissue (capillaries, fibroblasts)
  2-8w	Gray-white scar	Increasing collagen, ↓cells
  >2m	Dense fibrous scar	Dense collagen

• Complications: Arrhythmias (early death), LV failure/shock, mural thrombus (emboli), ventricular aneurysm, rupture (free wall, septum, papillary), pericarditis (fibrinous; Dressler's).
• Markers: Troponin I/T (specific; ↑2-4h, peak 24-48h). CK-MB (↑3-6h, peak 12-24h; reinfarction).

⭐ Ventricular free wall rupture typically occurs 3-7 days post-MI, coinciding with peak macrophage lysis.

High‑Yield Points - ⚡ Biggest Takeaways

• Atherosclerosis of coronary arteries is the primary cause of IHD.
• Stable angina: Fixed stenosis (>70%), exertional pain. Unstable angina: Plaque rupture, rest pain.
• MI: Coagulative necrosis. Troponins (most sensitive/specific). CK-MB for reinfarction.
• MI morphology: Coagulative necrosis visible 4-12 hrs; neutrophils 1-3 days; granulation tissue 1-2 wks.
• Most common MI complications: Arrhythmias (early), Dressler's syndrome (late pericarditis).
• Sudden Cardiac Death (SCD): Often due to IHD-induced lethal ventricular arrhythmias.