Study Notes: Ischemic Heart Disease (IHD)

Definition & Overview

Ischemic Heart Disease (IHD) — also called Coronary Artery Disease (CAD) -occurs when blood flow to the myocardium (heart muscle) is reduced, causing a drop in oxygen (hypoxia), nutrient delivery, and waste removal.

• The underlying cause is usually atherosclerosis (plaque buildup in the coronary arteries).

• IHD is the leading cause of death worldwide (~30% of Americans over 35 die from it).

Key Pathophysiology

• Ischemia = decreased blood flow → ↓ O₂, ↓ nutrients, ↓ waste removal.

• Hypoxia alone is not ischemia — ischemia implies impaired blood flow.

• Affected tissue: The myocardium, supplied by coronary arteries.

Coronary Artery Anatomy & Territories

Artery	Major Supply Area
Left Anterior Descending (LAD)	Anterior wall of LV + anterior 2/3 of interventricular septum
Left Circumflex (LCx)	Lateral wall of LV
Right Coronary Artery (RCA)	Right ventricle + posterior 1/3 of septum
Posterior Descending Artery (PDA)	Inferior/posterior LV wall (branch of RCA in most cases)

Coronary arteries are epicardial (on the outer surface) and then penetrate inward.

Causes of Ischemic Heart Disease

1. Atherosclerosis (>90% of cases)

   • Fatty/cholesterol plaques form under the endothelium.

   • Two main types:

     • Stable Plaque → Thick fibrous cap, fixed narrowing.

     • Unstable Plaque → Thin cap prone to rupture → thrombosis.

2. Vasospasm

   • Transient → causes Prinzmetal’s angina (reversible with nitrates).

   • Sustained → can lead to myocardial infarction (MI).

3. Microvascular Dysfunction

   • Damage to small vessels → contributes to ACS.

   • Severe cases → Takotsubo (Stress) Cardiomyopathy (“Broken Heart Syndrome”).

Angina Types

Type	Mechanism	Trigger	Duration	Relief	Troponin
Stable Angina	Fixed atherosclerotic narrowing	Exercise/stress	<20 min	Rest, nitrates	Normal
Unstable Angina	Plaque rupture + partial thrombus	May occur at rest	>20 min	Not relieved easily	Normal
Prinzmetal (Variant) Angina	Coronary vasospasm	Often at rest	Variable	Nitrates	Normal

Acute Coronary Syndrome (ACS)

ACS includes:

1. Unstable Angina (no necrosis)

2. NSTEMI – Non-ST Elevation MI (partial thickness necrosis)

3. STEMI – ST Elevation MI (full thickness necrosis)

Myocardial Infarction (MI)

Types:

• NSTEMI: Subendocardial infarct (inner layer only) → ST depression on ECG.

• STEMI: Transmural infarct (full wall thickness) → ST elevation on ECG.

Troponin:

• Elevated in both NSTEMI and STEMI (marker of myocardial necrosis).

• Normal in angina.

ECG Changes & Infarct Localization

ECG Leads	Affected Area	Likely Artery
V1–V4	Anterior wall / septum	LAD
V5, V6, I, aVL	Lateral wall	LCx
II, III, aVF	Inferior wall	RCA / PDA

Mechanism of ST Elevation vs. Depression

• ST Elevation (STEMI):
  Transmural infarction → depolarization away from the lead → baseline lowered → ST appears elevated.

• ST Depression (NSTEMI):
  Subendocardial infarction → depolarization toward the lead → baseline elevated → ST appears depressed.

Summary Table

Condition	Vessel Flow	Tissue Damage	ECG	Troponin	Key Features
Stable Angina	↓ Flow during stress	None	Normal	Normal	Predictable, relieved by rest/nitrates
Unstable Angina	↓ Flow due to unstable plaque	None	ST/T changes possible	Normal	Pain at rest, precursor to MI
NSTEMI	Partial occlusion	Subendocardial necrosis	ST depression	Elevated	Partial-thickness infarct
STEMI	Complete occlusion	Transmural necrosis	ST elevation	Elevated	Full-thickness infarct

 Special Condition: Takotsubo (Stress) Cardiomyopathy

• Triggered by severe emotional/physical stress.

• Temporary LV dysfunction (“apical ballooning”).

• ECG mimics MI but normal coronaries on angiography.

Management Overview

1. Immediate:

   • Oxygen (if hypoxic), Nitrates, Aspirin, Morphine, Beta-blockers.

   • Antiplatelets (clopidogrel), Heparin (anticoagulant).

2. Definitive:

   • Reperfusion therapy: PCI (angioplasty/stent) or CABG.

3. Long-term:

   • Lifestyle modification, Statins, ACE inhibitors, β-blockers.