End Organ Damage in Hypertension - Cardiovascular System and Eye

Hypertension causes a pressure overload on the left ventricle, leading to concentric hypertrophy, where the left ventricular wall thickens uniformly.
This thickening is due to an increase in the size of cardiac myocytes.
A normal heart weighs approximately 250 grams in women and 300 grams in men; in cases of left ventricular hypertrophy, the heart weight can nearly double to around 500 grams.
The thickness of the left ventricular wall in adults should be less than 1 cm, but in hypertrophy, it can increase to 2 cm or more.

Increased demand for blood due to the enlarged muscle mass increases the risk of coronary atherosclerosis.
Reduced left ventricular filling volume due to the decreased size of the ventricular chamber. This is known as diastolic dysfunction.
The thickened wall becomes more rigid, further impeding diastolic filling.
Outflow tract obstruction below the aortic valve may occur, adding to the pressure overload on the left ventricle.

Microscopically, the myocytes are hypertrophied (increased in size).
The nuclei also increase in size, becoming large, irregular, and hyperchromatic (darker) due to increased activity in producing contractile proteins.

A heart cut horizontally shows a massively thickened left ventricular wall, with the wall thickening being uniform, or concentric.
The lumen of the left ventricle is reduced in size, leading to a reduction in left ventricular end-diastolic filling volume.
Pale fibrous material may be visible within the wall of the left ventricle, indicating an increase in fibrotic tissue.

Cardiac myocytes are significantly larger, potentially three to four times the thickness of normal cardiac myocytes.
The nuclei of the cardiac myocytes are more prominent, hyperchromatic, and irregular in shape.

In a normal heart, myocytes closest to blood vessels receive ample oxygen.
During cardiac hypertrophy, the diffusion distance for oxygen increases, leading to ischemia in myocytes furthest from blood vessels.
Ischemia causes necrosis of these myocytes, which are then replaced by fibrotic tissue.

Transversely cut cardiac myocytes show tracts of dense fibrotic tissue between them, known as interstitial fibrosis.

The left ventricular wall becomes stiffer, worsening diastolic dysfunction.
Fibrotic tissue acts as an insulator, disrupting the transmission of electrical activity, predisposing to arrhythmias.

Pulmonary hypertension strains the right ventricle, often caused by lung diseases.
Common causes: cystic fibrosis and pulmonary interstitial fibrosis (e.g., silicosis from silica dust inhalation).
Silicosis causes inflammation and fibrotic tissue formation in the lungs.

Right ventricular hypertrophy is dominated by right ventricular dilatation due to the thinner-walled chamber.

A silicotic lung paired with a heart shows a massively dilated, thinned right ventricle.
Fibrotic scarring in the lungs obstructs blood flow through capillary beds, causing pulmonary hypertension.

Hypertension increases stress on the walls of arterioles.
Vascular smooth muscle cells die off and are replaced by amorphous proteinaceous material.
Extravasation of plasma proteins (mostly albumin) into the vessel wall due to endothelial damage.
Fibrotic tissue forms, thickening the wall and narrowing the lumen.
Increased leakiness can lead to proteinuria.

Small arterioles exhibit a very small lumen and a thick wall.
Absence of most vascular smooth muscle cells, replaced by hyaline material (extravasated plasma proteins).

Hypertension damages arteries due to constant pulsatile stress. The primary damage is hypertensive arteriosclerosis (fibrosis of the arteriolar wall).
Characterized by loss of elastin and accumulation of extracellular matrix from vascular smooth muscle cells.
Can be considered an accelerated aging of the arterial system.

Hypertension mechanically activates the endothelium, making the arterial wall leaky.
Lipid leaks out, driving an inflammatory response within the vessel wall, leading to atherosclerosis.
Atherosclerosis involves atherosclerotic plaques with a fibrous cap and a lipid-rich necrotic core.
The lumen of the vessel is dramatically reduced.

Artery shows relatively uniform thickening of the vessel wall (concentric thickening).
Characterized by loss of elastin, vascular smooth muscle cells, and replacement by accumulated extracellular matrix.

Provides direct examination of the arterial system by observing blood vessels in the retina.

Fovea centralis: area for visual acuity with smaller blood vessels.
Optic cup: blood vessels enter and leave through the base; clear edge is visible in a normal retina.
Veins are generally thicker than arteries.

Features: AV nipping and silver wiring.
Arteries develop arteriosclerosis, thickening the wall and making it more rigid.
Silver wiring: reflection of light along the surface of the artery due to thickening.
AV nipping: arteries impinge on veins due to increased rigidity.

Key feature: papilledema (blurred edge of the optic cup).
Blood vessels become blurred due to increased edema fluid within the retina.
Causes of papilledema: malignant hypertension, raised intracranial pressure (bleeds, tumors).
Other features: cotton wool exudates (pale retina due to edema fluid) and flame hemorrhages (ruptured blood vessels forming flame shapes).