Vascular Complications

In hypertensive patients, blood vessels are subjected to chronic hemodynamic stress, leading to a series of structural and functional changes that progressively impair their ability to adapt to blood pressure fluctuations.

The main histological alterations observed in the vessels of hypertensive patients include:

• Hypertrophy of the tunica media: Increased blood pressure stimulates the proliferation of smooth muscle cells, resulting in thickening of the vascular wall. This adaptation aims to contain wall tension but leads to a progressive narrowing of the vascular lumen and increased peripheral resistance.
• Fibrosis and extracellular matrix deposition: Hypertension induces excessive deposition of collagen and proteoglycans in the vascular wall, reducing arterial elasticity and increasing vessel stiffness.
• Arteriolar remodeling: Small arteries and arterioles undergo concentric narrowing due to lumen reduction and wall thickening, which worsens blood flow to peripheral tissues.
• Loss of elasticity: The accumulation of fibrotic material and degeneration of elastic fibers impair the ability of blood vessels to respond to normal blood pressure fluctuations, increasing cardiac afterload.

Hypertension affects not only the structure of blood vessels but also their function. The main pathophysiological consequences include:

• Impaired autoregulation of blood flow: Chronic hypertension shifts the autoregulatory threshold upward, making vessels less able to respond to sudden pressure changes. This increases the risk of hypoperfusion in case of blood pressure reduction.
• Reduced endothelium-dependent vasodilation: Endothelial dysfunction leads to decreased nitric oxide (NO) production, impairing the vessels' ability to dilate properly.
• Increased arterial stiffness: Reduced vascular elasticity leads to an increase in systolic pressure wave reflection, contributing to elevated systolic blood pressure and increased cardiac workload.

The vascular alterations associated with hypertension directly contribute to ischemic and hemorrhagic events. Specifically:

• Formation of microaneurysms: Weakening of the small vessel walls, due to chronic pressure elevation and elastic fiber degeneration, can lead to the formation of **microaneurysms** (Charcot-Bouchard), which are at risk of rupture and bleeding.
• Increased susceptibility to trauma: In hypertensive patients, stiffened blood vessels are less capable of absorbing mechanical forces, increasing the risk of hemorrhages following even minor trauma, especially in the elderly.
• Fibrinoid necrosis: In severe forms of hypertension, particularly **malignant hypertension**, fibrinoid necrosis of the arteriolar wall can occur, leading to loss of vascular integrity and increased risk of organ damage.
• Accelerated atherosclerosis: Hypertension promotes endothelial damage and accelerates the progression of atherosclerotic plaques, increasing the risk of thrombotic and ischemic events.

The most severe vascular complications occur in the following regions:

• Brain: ischemic stroke (thrombosis, embolism) and hemorrhagic stroke (rupture of microaneurysms).
• Heart: ischemic heart disease, myocardial infarction, unstable angina.
• Kidneys: hypertensive nephrosclerosis, chronic kidney failure.
• Eyes: hypertensive retinopathy, macular edema, retinal hemorrhages.

The vascular complications of hypertension require close blood pressure monitoring and targeted management of risk factors to prevent irreversible organ damage.

References
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