Hypertension, Shear Stress & Aortic Dissection

Site-Specific Mechanisms and Clinical Implications

Professor Atef Allam • Pathophysiology • Hemodynamics

Key Concepts & Definitions

Hypertension

Chronic high blood pressure → Increases wall stress on aorta

Low Shear Stress (LSS)

Disturbed/oscillatory flow (near branches/curves)

High Shear Stress (HSS)

Elevated flow velocity (in narrowed segments)

Site-Specific Mechanisms

🔴 Ascending Aorta

Hypertension + High Pulse Pressure

↑ Cyclic wall stress → Fatigue of elastic fibers

LSS at Sinotubular Junction

Flow turbulence → Endothelial dysfunction → Medial degeneration

Anatomic Vulnerabilities

Less vasa vasorum perfusion → Medial ischemia
Highest pressure load in aorta

🔵 Distal to Left Subclavian

Hypertension + Flow Acceleration

Sudden aortic tapering → Increased HSS → Wall strain

LSS at Attachment Points

Ligamentum arteriosum fixes aorta → Flow turbulence

Structural Weakness

Transition: elastic (ascending) to muscular (descending) aorta

Shear Stress Comparison

Factor Ascending Aorta Distal to Subclavian
Shear Pattern LSS (turbulence near valve) HSS (acceleration) + LSS (attachment)
Hypertension Effect ↑ Radial stress → Tear initiation ↑ Longitudinal stress → Propagation
Histologic Changes Cystic medial necrosis Elastic fiber fragmentation

Clinical Evidence

Therapeutic Implications

Blood Pressure Control

Target SBP <120 mmHg in high-risk patients (Marfan syndrome)

Surgical Strategy

  • Ascending: Graft replacement (high rupture risk)
  • Descending: TEVAR if feasible

Medical Therapy

  • Beta-blockers: Reduce dP/dt (↓ shear stress)
  • ARBs (losartan): Protect ECM in Marfan patients

Key Clinical Principles