Myocardial hypertrophy and its clinical forms

1. Definition

• Hypertrophy = ↑ cell size → ↑ organ size; no new cells (vs hyperplasia). Acts on cells with limited division (cardiac, skeletal muscle).
• Triggers: mechanical (↑demand), trophic/hormonal, growth factors → ↑protein translation, gene expression, polyploidization, ECM remodeling.
• Physiological (exercise; pregnant uterus, lactating breast) vs pathological (cardiac, from HTN / valve disease). Normal ventricular thickness = 3–5 mm.

2. Left-Sided Hypertrophy

Type	Overload	Sarcomeres	Geometry	Causes
Concentric	Pressure	Parallel	↑wall, cavity not enlarged	HTN, aortic stenosis, coarctation
Eccentric	Volume	Series	↑cavity, wall not thicker	Aortic/mitral insufficiency

3. Right-Sided Hypertrophy

• From ↑pulmonary resistance → cor pulmonale (RV enlargement/failure).
• Causes: parenchymal lung disease (emphysema, bronchitis→bronchiectasis, pneumoconiosis, sarcoidosis, CF), vascular (thromboembolism, vasculitis — Wegener), chest deformity (kyphoscoliosis), pleural disease.

4. Consequences of Cardiac Hypertrophy

• Diastolic failure: stiff thick wall → poor filling → atrial dilation.
• CIHD: capillary supply can’t meet enlarged demand → relative ischemia → terminal dilation (Frank-Starling: stretch → forceful contraction, until exhaustion).
• Apoplexia: very high BP (>200 mmHg) → cerebral haemorrhage; Charcot-Bouchard aneurysms (basal ganglia, chronic HTN) → hemorrhagic stroke.
• Renal failure: pressure → hyaline arteriolosclerosis → luminal narrowing.
• RV failure → backward congestion (nutmeg liver, spleen, GI).

💡 High-yield: Concentric (pressure/parallel → thick wall) vs eccentric (volume/series → dilated cavity). Right-sided hypertrophy = cor pulmonale from lung disease. Distinguish adaptive LVH from HCM (myofiber disarray, outflow obstruction).