Hypertensive Heart Disease

Overview

Cardiac disease from prolonged systemic HTN, manifests as LVH. Even mild HTN (>140/90) of sufficient duration causes it. 2nd commonest heart disease after IHD — overlaps heavily (HTN→atherosclerosis too). Death causes: CHF decompensation (~1/3), IHD, stroke, renal failure (arteriolar nephrosclerosis), aortic dissection, sudden death.

Pathophysiology

Stimulus = pressure overload. Genetic+haemodynamic factors. Wall stress → ↑myofilaments/myofibrils/organelles, nuclear enlargement. Adult fibres can’t divide → HYPERTROPHY not proliferation (sarcomere division → ↑cell width).

Two phases:

Concentric hypertrophy (early/compensated) — wall thickens, NO dilatation
Eccentric hypertrophy (late/decompensated) — wall dilates+thins, ± right heart involvement

LVH diagnosed by ECG. BP control can regress LV mass (specific agent mechanism unclear beyond BP-lowering). Diastolic dysfunction common — present in ~1/3 with normal systolic function (diastolic impairment precedes systolic decline).

Morphology

Gross: marked LV hypertrophy. Heart weight ≥500g (normal ~300g). LV wall 13-15mm→20mm+. Rounded prominent papillary muscles/trabeculae. Concentric (compensated) → eccentric (decompensated, dilated+thinned, ±RV).

Micro: less striking than gross. Fibre enlargement+degeneration, focal fibrosis; advanced — oedema, necrosis foci.

Clinical relevance

Concentric→eccentric transition = key structural concept — anatomic signature of compensated→decompensated transition; echo geometry directly shows trajectory stage, not just “big heart.” HTN as shared upstream driver of both hypertensive heart disease (via LVH) and IHD (via atherosclerosis) explains why they coexist so often — rarely “pure” hypertensive heart disease alone. Diastolic dysfunction preceding systolic dysfunction in 1/3 of patients = easy-to-miss point — HF symptoms can appear before EF drops, so normal systolic function doesn’t rule out significant cardiac impairment.

Overview

Hypertensive heart disease (hypertensive cardiomyopathy) is cardiac disease resulting from prolonged systemic hypertension, manifesting as left ventricular hypertrophy (LVH). Even mild hypertension (>140/90 mmHg) of sufficient duration can induce it. It is the second most common heart disease after IHD — and the two overlap substantially, since hypertension itself predisposes to atherosclerosis, so most hypertensive heart disease patients also carry advanced coronary atherosclerosis and progressive IHD risk. Among causes of death in hypertensive patients: cardiac decompensation to CHF (~one-third), plus IHD, cerebrovascular stroke, renal failure (arteriolar nephrosclerosis), aortic dissection, and sudden cardiac death.

Pathophysiology

The stimulus to LVH is pressure overload from systemic hypertension. Both genetic and haemodynamic factors contribute. Mechanically: wall stress from pressure overload increases production of myofilaments, myofibrils, other organelles, and causes nuclear enlargement. Since adult myocardial fibres cannot divide, the existing fibres hypertrophy rather than proliferate — though individual sarcomeres can divide, increasing cell width.

Two sequential structural phases:

Concentric hypertrophy (early, compensated) — wall thickens without chamber dilatation.
Eccentric hypertrophy (late, decompensated) — once cardiac failure supervenes, the wall dilates and thins, sometimes with right heart hypertrophy/dilatation too as the failure becomes biventricular.

LVH is diagnosable by ECG. Aggressive blood pressure control can regress left ventricular mass, though which specific antihypertensive agents achieve this beyond their blood-pressure-lowering effect isn’t clearly established. Diastolic dysfunction is common in hypertension — present in about one-third of patients who still have normal systolic function, i.e. diastolic impairment can precede any detectable systolic decline.

Morphology

Gross: the defining finding is marked cardiac hypertrophy, chiefly left ventricular. Heart weight rises to 500 g or more (normal ~300 g); LV wall thickness increases from a normal 13–15 mm to 20 mm or more. Papillary muscles and trabeculae carneae become rounded and prominent. Concentric hypertrophy (no dilatation) in the compensated phase; eccentric hypertrophy (with dilatation, thinned wall, ± right heart involvement) once decompensation sets in.

Microscopy: less striking than the gross picture. Enlargement and degeneration of myocardial fibres, focal myocardial fibrosis; in advanced disease, myocardial oedema and foci of necrosis.

Clinical Relevance

The concentric-to-eccentric transition is the single most important structural concept here — it is the anatomic signature of the compensated-to-decompensated transition, meaning a hypertensive patient’s ventricular geometry on echo directly indicates where they sit on that trajectory, not just a static description of “big heart.”
Hypertensive heart disease and IHD sharing hypertension as a common upstream driver (hypertension → atherosclerosis → IHD, and separately hypertension → pressure overload → LVH) explains why these two conditions coexist so often clinically — a patient rarely has “pure” hypertensive heart disease in isolation from coronary disease.
Diastolic dysfunction preceding systolic dysfunction in a third of hypertensive patients with otherwise normal function is a clinically important, easy-to-miss point — heart failure symptoms in a hypertensive patient can appear before any drop in ejection fraction, so normal systolic function does not rule out clinically significant cardiac impairment from hypertension.