Hypertensive heart disease

1. Concept

Hypertensive heart disease results from chronic pressure overload → ventricular hypertrophy. Because myocytes cannot proliferate (no hyperplasia), they respond to increased workload by hypertrophy (↑cell size) → ↑heart size and weight. Persistent hypertension → dysfunction, dilation, chronic HF, even sudden cardiac death.

2. Hypertrophy patterns

• Concentric — pressure overload (HTN, aortic stenosis): ↑wall thickness, ↓cavity.
• Eccentric — volume overload (valve insufficiency): hypertrophy + dilation.

3. Systemic (left-sided) hypertensive heart disease

• Morphology: concentric LV hypertrophy → wall stiffness → impaired diastolic filling → LA dilation.
• Histology: ↑myocyte diameter, nuclear enlargement + hyperchromasia, interstitial fibrosis.
• Clinical: often asymptomatic (compensated) — ECG shows LVH. Consequences: progressive ischemic heart disease (HTN-related coronary AS), renal failure / cerebral hemorrhage (stroke), progressive HF.
• Diagnosis: LVH (usually concentric) + history of hypertension, without other cardiovascular cause.

4. Pulmonary (right-sided) hypertensive heart disease = cor pulmonale

• RV hypertrophy + dilation (± right HF) from pulmonary hypertension due to primary lung disease.
• Acute — massive PE (>50%) → RV dilation only.
• Chronic — COPD, interstitial fibrosis, pneumoconiosis, cystic fibrosis, recurrent PE → RV hypertrophy.

💡 High-yield: Hypertensive heart disease = pressure overload → concentric LVH (myocytes hypertrophy, can’t divide). LVH → diastolic dysfunction → LA dilation; complications = IHD, stroke, renal failure, HF. Right-sided = cor pulmonale (RV hypertrophy from pulmonary HTN/lung disease). Concentric = pressure, eccentric = volume.