A 58-year-old man with a 20-year history of hypertension (BP 160/100 mmHg on current therapy) presents with dyspnoea on exertion and orthopnoea. Echocardiography reveals a thickened left ventricular wall (14 mm; normal

Question

A 58-year-old man with a 20-year history of hypertension (BP 160/100 mmHg on current therapy) presents with dyspnoea on exertion and orthopnoea. Echocardiography reveals a thickened left ventricular wall (14 mm; normal <11 mm), reduced chamber volume, and preserved ejection fraction (EF 55%). Cardiac catheterization shows elevated left ventricular end-diastolic pressure. Histological examination of a myocardial biopsy would most likely show which cellular adaptation?

Accepted Answer

C. Hypertrophy of individual cardiomyocytes with increased cell size but normal cell number. ## Diagnosis: Left Ventricular Hypertrophy (LVH) Secondary to Chronic Hypertension

### Pathological Mechanism

**Key Point:** Chronic hypertension causes **hypertrophy** of cardiomyocytes — an increase in the SIZE of individual myocardial cells — NOT an increase in their NUMBER. The left ventricle thickens but the chamber volume decreases (concentric hypertrophy).

### Hypertrophy vs. Hyperplasia in Cardiac Tissue

| Feature | Hypertrophy (LVH) | Hyperplasia |
|---------|------------------|----------|
| **Cell number** | Normal/unchanged | Increased |
| **Individual cell size** | **Markedly increased** | Normal |
| **Mechanism** | ↑ Protein synthesis; ↑ sarcomeres in parallel | Increased mitotic activity |
| **Stimulus** | Pressure/volume overload | Growth factors, hormones |
| **Reversibility** | Partially reversible if load removed | Reversible if stimulus removed |
| **Cardiomyocyte nuclei** | Enlarged, polyploid | Normal |
| **Histology** | Large cells, normal architecture | More cells, normal size |

**High-Yield:** Adult cardiomyocytes are **terminally differentiated and non-proliferative**. They cannot undergo hyperplasia in response to chronic load. Instead, they enlarge (hypertrophy) by increasing sarcomeric protein content.

### Clinical Pearl

The echocardiographic findings are diagnostic:
- **Thickened LV wall** (14 mm) = hypertrophy
- **Reduced chamber volume** = concentric pattern
- **Preserved EF initially** = compensation is still adequate
- **Elevated LVEDP** = diastolic dysfunction (stiff, hypertrophied ventricle)

This is **concentric LVH** — the classic response of the heart to sustained systemic hypertension.

### Histological Features of LVH

1. **Enlarged cardiomyocytes** with increased cytoplasmic volume
2. **Enlarged, often polyploid nuclei** (nuclear enlargement parallels cell enlargement)
3. **Increased sarcomeric proteins** (actin, myosin, Z-disc proteins)
4. **Interstitial fibrosis** (secondary; due to impaired perfusion and neurohumoral activation)
5. **Normal myocyte number** (no hyperplasia)

**Mnemonic: HyPERtrophy = PERsonal growth (cell gets bigger); HyPERplasia = PERcentage increases (more cells)**

### Why NOT Hyperplasia?

Adult cardiomyocytes lack significant regenerative capacity. They respond to chronic overload by:
- Increasing protein synthesis (hypertrophy) ✓
- NOT by dividing (hyperplasia) ✗

Hyperplasia of cardiomyocytes occurs only during fetal development and early infancy, not in adult chronic hypertension.

![Cellular Adaptations — Hyperplasia, Hypertrophy diagram](https://mmcphlazjonnzmdysowq.supabase.co/storage/v1/object/public/blog-images/explanation/2792.webp)

Answer

A. Metaplasia of cardiomyocytes to fibroblasts causing fibrosis

Answer

B. Atrophy of cardiomyocytes due to chronic pressure overload

Answer

D. Hyperplasia of cardiomyocytes with increased cell number and normal cell size

Explanation

Diagnosis: Left Ventricular Hypertrophy (LVH) Secondary to Chronic Hypertension

Pathological Mechanism

Hypertrophy vs. Hyperplasia in Cardiac Tissue

Clinical Pearl

Histological Features of LVH

Why NOT Hyperplasia?

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Feature	Hypertrophy (LVH)	Hyperplasia
Cell number	Normal/unchanged	Increased
Individual cell size	Markedly increased	Normal
Mechanism	↑ Protein synthesis; ↑ sarcomeres in parallel	Increased mitotic activity
Stimulus	Pressure/volume overload	Growth factors, hormones
Reversibility	Partially reversible if load removed	Reversible if stimulus removed
Cardiomyocyte nuclei	Enlarged, polyploid	Normal
Histology	Large cells, normal architecture	More cells, normal size