Myocardial Adaptations to Increased Workload: Hypertrophy, Hyperplasia & More

Cellular Responses to Chronic Pressure/Volume Overload

1. Hypertrophy – Myocyte enlargement (↑ protein synthesis, sarcomere addition). Concentric (pressure overload) vs. eccentric (volume overload). Maintains stroke volume initially.
2. Hyperplasia – Rare in adult humans; mainly seen in extreme athletic conditioning or developmental stages. Increases myocyte number.
3. Angiogenesis – New capillary growth matches myocyte hypertrophy to preserve oxygen diffusion distance.
4. Metabolic shift – ↑ Glucose uptake, ↓ fatty‑acid oxidation (fetal gene program re‑expression). Less efficient ATP generation per O₂.
5. Electrical remodeling – Altered ion‑channel expression (↓ I_to, ↓ I_K1, ↑ late I_Na) prolongs action potential, predisposes to arrhythmias.
6. Fibrosis – Excess collagen deposition stiffens ventricle, impairs diastolic filling, disrupts conduction.

Compensation → Decompensation

Adaptive hypertrophy preserves function temporarily. Sustained overload → maladaptive remodeling → heart failure (HFpEF or HFrEF). Early intervention (afterload reduction, neurohormonal blockade) can reverse remodeling.