Mechanisms and consequences of large artery rigidity

Area of Science:

• Cardiovascular Science
• Pathophysiology
• Vascular Biology

Background:

• Large artery rigidity is a common characteristic across various diseases including hypertension, diabetes mellitus, dyslipidemia, congestive heart failure, chronic uremia, and senescence.
• These arterial changes are often nonspecific to the primary disease etiology, suggesting common underlying mechanisms.

Purpose of the Study:

• To review the mechanisms of large artery structural and functional changes.
• To explore the potential for targeting these common abnormalities for therapeutic benefit.
• To discuss clinical evaluation methods and therapeutic strategies.

Main Methods:

• Review of classical and recent literature on large artery rigidity.
• Analysis of structural and functional abnormalities in vasculopathy.
• Discussion of clinical evaluation techniques, including pulse-wave velocity.
• Overview of non-pharmacological and pharmacological interventions.

Main Results:

• Common structural abnormalities include smooth muscle cell hypertrophy, increased matrix collagen, and proteoglycan metabolism dysfunction.
• Functional issues involve bradykinin-dependent smooth muscle hyper-reactivity and vasa vasorum disturbances.
• Endothelial dysfunction contributes to target organ damage via altered permeability and matrix disorganization.

Conclusions:

• Shared vasculopathy mechanisms in diverse diseases offer therapeutic targets for reducing morbidity and mortality.
• Noninvasive methods like pulse-wave velocity are valuable for clinical assessment.
• Interventions such as exercise and renin-angiotensin-aldosterone system modulators show promise.