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Ischemic heart disease

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IHD Fundamentals - The Clogged Pipes

  • Pathophysiology: Myocardial O₂ supply-demand mismatch, typically from ↓ supply.
  • Etiology: Atherosclerosis is the primary cause, leading to coronary artery stenosis.
    • Stable Plaque: Thick fibrous cap, small lipid core → predictable, exertional angina.
    • Unstable Plaque: Thin cap, large lipid core, high inflammation → prone to rupture.
  • Acute Coronary Syndrome (ACS): Plaque rupture exposes thrombogenic core → thrombus formation → acute occlusion.

Stable vs. Unstable Atherosclerotic Plaque Comparison

⭐ The Left Anterior Descending (LAD) artery is the most common site of thrombotic occlusion.

Angina Pectoris - The Warning Pains

  • Chest pain due to transient, reversible myocardial ischemia. No myocyte necrosis.
TypePathophysiologyPresentation & ECGTreatment
StableAtherosclerosis (>70% stenosis)Exertional; relieved by rest/NTG. ST depression.Nitrates, β-blockers
UnstablePlaque rupture, thrombosisRest/crescendo pain. ST depression.Hospitalize, antiplatelets
PrinzmetalCoronary vasospasmEpisodic, often at rest/night. ST elevation.Ca²⁺ channel blockers, Nitrates
ECG showing transient ST elevation in Prinzmetal angina

Prinzmetal Angina Treatment Pearl: Avoid non-selective β-blockers as they can worsen vasospasm by blocking β₂-mediated vasodilation, leading to unopposed α₁-receptor vasoconstriction.

Myocardial Infarction - The Big One

  • Irreversible necrosis of cardiac muscle from prolonged ischemia, typically due to acute thrombotic occlusion of a coronary artery (LAD > RCA > LCX).
  • Key diagnostic markers include elevated cardiac troponins (most sensitive and specific), characteristic ECG changes, and clinical presentation.

Myocardial stunning and troponin I levels after ischemia

⭐ The period of greatest risk for ventricular free wall rupture is 3-14 days post-MI. This is when macrophages have removed necrotic debris, but the collagenous scar is not yet fully formed, leaving the wall at its weakest.

Post-MI Complications - The Domino Effect

  • Timeline of Events: Complications are predictable based on the post-infarct timeline.
  • Mechanical Complications (Days 3-14): Result from macrophage-mediated degradation.
    • Free Wall Rupture: Leads to cardiac tamponade, sudden death. Most common cause of death from rupture.
    • Septal Rupture: New holosystolic murmur, ↑O₂ sat in RV.
    • Papillary Muscle Rupture: Severe mitral regurgitation.

Post-MI Cardiac Rupture Locations and Clinical Features

Posteromedial papillary muscle is more prone to rupture due to its singular blood supply from the posterior descending artery (PDA).

  • Atherosclerosis of the coronary arteries is the overwhelming cause of IHD, typically in the left anterior descending (LAD) artery.
  • Stable angina presents as exertional chest pain from >70% stenosis; unstable angina is pain at rest due to plaque rupture and thrombosis.
  • Myocardial infarction means irreversible necrosis; troponins are the most sensitive and specific biomarkers.
  • STEMI reflects a transmural infarct with ST elevation, while NSTEMI indicates a subendocardial infarct.
  • Key MI complications include arrhythmias, mural thrombus, and ventricular aneurysm.

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