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Atherosclerosis, Ischemic & Rheumatic Heart Disease

Atherosclerosis is the slow buildup of fatty, cholesterol-rich plaques inside the walls of large and medium-sized arteries. Over years, the plaque thickens and stiffens the artery wall and narrows the channel through which blood flows, reducing the supply of oxygen downstream.

It matters because when a coronary artery narrows or a plaque suddenly ruptures, the heart muscle is starved of oxygen — that is ischemic heart disease, the world's leading cause of death. Rheumatic heart disease is a different story: it begins as an untreated strep throat in childhood and ends, years later, as scarred, leaking heart valves. It still strikes young people in India and is almost entirely preventable.

Key Concepts

  • Endothelium: the single-cell inner lining of arteries; injury to it is where atherosclerosis begins.
  • LDL cholesterol: the "bad cholesterol" that deposits in artery walls; ideally below 100 mg/dL.
  • Plaque (atheroma): a mix of LDL, dead macrophages (foam cells), smooth muscle cells and a fibrous cap.
  • Ischemia: tissue starved of blood; angina — chest pain on exertion — is cardiac ischemia.
  • Myocardial infarction (heart attack): plaque rupture triggers a clot that blocks the artery completely, killing heart muscle.
  • Rheumatic fever: an autoimmune reaction to a Group A Streptococcus throat infection, striking 2–4 weeks after the sore throat.
  • Rheumatic heart disease (RHD): chronic scarring of the heart valves, classically causing mitral stenosis.
  • Jones criteria: clinical rules for diagnosing rheumatic fever — major signs include carditis and migratory polyarthritis.

How It Works

  1. LDL cholesterol slips into an injured patch of endothelium and becomes oxidized.
  2. Monocytes from the blood follow it in, turn into macrophages, and gorge on the oxidized LDL until they become foam cells — the yellow "fatty streak" seen in young arteries.
  3. Smooth muscle cells migrate over the deposit and lay down a fibrous cap, forming a plaque that bulges into the lumen.
  4. As the plaque grows, the lumen narrows: flow suffices at rest but not on exertion — stable angina.
  5. If the fibrous cap ruptures, a clot forms within minutes — complete blockage means a heart attack or stroke.
  6. In rheumatic disease the mechanism differs: streptococcal M protein resembles valve proteins (molecular mimicry), so the body's own antibodies scar the valves over years; symptoms appear 10–20 years after the childhood infection.

Worked Example

A 55-year-old man: total cholesterol 240, HDL 38, LDL 165 mg/dL, BP 150/95 mmHg.

  1. Non-HDL cholesterol = total − HDL = 240 − 38 = 202 mg/dL. The target is below 130 mg/dL, so he is 202 − 130 = 72 mg/dL above target.
  2. His blood pressure (150/95) is Grade 1 hypertension — a second major modifiable risk factor.
  3. Statins typically cut LDL by 30–50%. With a 40% reduction: 165 × 0.60 = 99 mg/dL, which hits the under-100 target.

Common Misconceptions

  • "Chest pain always means a heart attack." Stable angina eases with rest and comes from fixed narrowing, not a clot — but it still needs urgent evaluation.
  • "Rheumatic heart disease is an infection of the heart." The valves are damaged by the patient's own immune response, not by bacteria living on them.
  • "Cholesterol comes only from food." The liver makes most of the body's cholesterol; diet, exercise, genes and medicines all move the number.

Real-World Applications

  • Lipid-profile screening from age 30, with statins as first-line therapy for high LDL.
  • ECG and troponin diagnose a heart attack; clot-busting drugs or angioplasty in the "golden hour" save heart muscle.
  • A full penicillin course for strep throat prevents rheumatic fever; survivors take monthly benzathine penicillin for years.
  • Severely scarred valves are repaired or replaced surgically.

Atherosclerosis is decades of plaque building in artery walls, ending in angina or heart attack when flow fails; rheumatic heart disease is immune-mediated valve scarring after strep throat. Both are managed by measuring risk factors — lipids, blood pressure, strep treatment — and acting on the numbers early.