Which of the following is the primary mechanism by which cardiac myocytes undergo hypertrophy in response to chronic hypertension?

Explanation

## Cardiac Hypertrophy Mechanism **Key Point:** Hypertrophy is defined as an increase in cell size due to increased protein synthesis and accumulation of cellular components, WITHOUT an increase in cell number (no mitosis). ### Pathophysiology of Cardiac Hypertrophy In response to chronic hypertension, cardiac myocytes experience sustained mechanical stress. This triggers: 1. **Activation of growth signaling pathways** — mechanical stretch activates receptor tyrosine kinases (RTKs) and G-protein coupled receptors (GPCRs) 2. **Increased protein synthesis** — upregulation of mRNA translation and ribosomal activity 3. **Accumulation of contractile proteins** — sarcomeric proteins (actin, myosin, tropomyosin) increase in quantity 4. **Cell enlargement** — the myocyte increases in volume and mass 5. **NO cell division** — cardiac myocytes are terminally differentiated and do not undergo mitosis ### Key Distinction: Hypertrophy vs. Hyperplasia | Feature | Hypertrophy | Hyperplasia | |---------|-------------|------------| | **Cell size** | Increased | Normal or decreased | | **Cell number** | Normal | Increased | | **Mechanism** | Protein synthesis ↑ | Cell division ↑ | | **Reversibility** | Partially reversible | Reversible | | **Example** | Cardiac hypertrophy in HTN | Endometrial hyperplasia in estrogen excess | **High-Yield:** Cardiac myocytes are post-mitotic cells — they cannot divide. Therefore, the ONLY adaptive response to increased workload is hypertrophy. **Clinical Pearl:** Eccentric hypertrophy (chamber dilation + wall thickening) occurs in volume overload; concentric hypertrophy (wall thickening without dilation) occurs in pressure overload like hypertension.