Understanding Ischaemic Heart Disease (IHD): A Deep Dive into Pathophysiology

 Hey future doctors! 👋 Let’s talk about ischaemic heart disease (IHD)—one of the most common and clinically significant conditions you’ll encounter. 

So, grab a coffee ☕, and let’s break it down step by step!

What is Ischaemic Heart Disease?

Ischaemic heart disease, also called coronary artery disease (CAD), occurs when there’s a mismatch between myocardial oxygen demand and supply. In simple terms:

💔 The heart isn’t getting enough oxygen-rich blood!

This happens due to narrowing or blockage of the coronary arteries—the vessels that keep the heart pumping. 🚧🩸

🧐 The Big Picture: Why Does This Happen?

The root cause? Atherosclerosis—a progressive disease where fatty deposits (plaques) build up inside arteries. But this doesn’t happen overnight! It’s driven by:

⚠️ Risk Factors:

• Hypertension 🩸
• Smoking 🚬
• Diabetes 🍬
• Hyperlipidaemia 🍔
• Sedentary lifestyle 🛋️

Now, let’s dive deeper into the pathophysiology! ⬇️

🧬 Step 1: Endothelial Dysfunction – The Starting Point

The endothelium isn’t just a barrier—it regulates blood flow, inflammation, and clotting. When it's damaged (by smoking, high BP, or LDL cholesterol), it becomes dysfunctional. 🚨

🔬 Key Players:

• Oxidized LDL cholesterol 🟡 → Accumulates in vessel walls.
• Inflammatory cytokines 🔥 → Attract immune cells (e.g., macrophages).
• Nitric oxide (NO) ↓ ❌ → Less NO = Vasoconstriction & clot risk!

🩸 Step 2: Fatty Streak Formation

• 🔹 Damaged endothelium allows LDL cholesterol to sneak into the arterial wall.
• 🔹 Macrophages gobble up LDL, transforming into foam cells. 🤢
• 🔹 These foam cells accumulate, forming fatty streaks—the earliest sign of atherosclerosis!

🛑 Step 3: Plaque Formation & Growth

• 🔹 Smooth muscle cells migrate to the area.
• 🔹 A fibrous cap forms over the fatty core, creating a plaque.

But not all plaques are created equal:

• ✅ Stable plaques: Thick fibrous caps 🏰 → Less likely to rupture but cause angina.
• ⚠️ Vulnerable plaques: Thin fibrous caps 🪶 → Prone to rupture → Can trigger heart attacks!

🩺 Step 4: Reduced Blood Flow & Ischemia

As plaques narrow arteries, the heart struggles to get oxygen during exertion (exercise, stress). 🚴‍♂️💨

Symptoms:

• ⚡ Angina pectoris → Chest pain from temporary ischaemia.
• 💔 Myocardial infarction (heart attack) → Complete blockage = irreversible heart muscle damage!

🚨 Step 5: Plaque Rupture & Thrombosis – The Game Changer

When a vulnerable plaque ruptures, it triggers a clot (thrombus), blocking blood flow. 🛑

• 🔹 Platelets activate 🏃‍♂️ → Form a clot 🩸.
• 🔹 Thrombosis can completely block the artery, causing an acute myocardial infarction (AMI).
• 🔹 This is why aspirin & antiplatelets 🏥 are essential!

🩻 Clinical Consequences of IHD

The pathophysiology of IHD leads to several conditions:

• 🔸 Stable angina → Predictable chest pain on exertion, relieved by rest.
• 🔸 Unstable angina → Unpredictable pain, even at rest—warning sign of infarction! 🚨
• 🔸 Myocardial infarction (MI) → Prolonged ischemia causing heart muscle death.
• 🔸 Chronic ischaemic cardiomyopathy → Long-term ischemia leading to heart failure.

🏆 Key Takeaways

• ✅ Atherosclerosis is the cornerstone of IHD.
• ✅ Endothelial dysfunction starts the process.
• ✅ Plaque rupture is the critical event leading to heart attacks.
• ✅ Lifestyle changes & early intervention save lives!

🎯 Why Does This Matter?

Understanding IHD isn’t just for exams—it’s about saving lives. 🩺 By knowing how this disease develops, you’ll be better equipped to diagnose, treat, and prevent it in your future patients. 

🤔 Food for Thought

🔹 How do lifestyle changes impact atherosclerosis progression?

Let’s discuss in the comments! 👇

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