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Related Concept Videos

Coronary Artery Disease I: Introduction01:30

Coronary Artery Disease I: Introduction

Coronary Artery Disease (CAD): An Overview with Scientific InsightsCoronary Artery Disease (CAD), often referred to as C-A-D, is a prevalent blood vessel disorder classified under the broader category of atherosclerosis. Atherosclerosis is a pathological process characterized by the hardening and narrowing of arteries due to the accumulation of atherosclerotic plaques. These plaques are composed of cholesterol, fatty substances, inflammatory cells, calcium, and fibrin, reducing blood flow to...
Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
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Regulation of Angiogenesis and Blood Supply

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Aging01:26

Aging

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Cellular Clock Theory
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Several body functions deteriorate with age. The external signs of aging are easily identifiable. For example, the skin becomes dry, less elastic, and thins out, forming wrinkles. The skin of the face begins to appear looser due to a decrease in the levels of elastic and collagen fibers in the connective tissue. Additionally, melanin production in the hair follicle decreases with age, resulting in gray hair. Moreover, the senses of sight and hearing decline, so glasses and hearing aids may...
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Age-related pharmacokinetic changes are extensively documented, but understanding age-related pharmacodynamic alterations is relatively limited. This knowledge gap can be partly attributed to the complexity of developing appropriate measures of drug responses compared to bioanalytical methods for determining drug concentrations.Most information regarding age-related differences in human pharmacodynamics originates from cross-sectional studies. However, these studies assume that observed mean...

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Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
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Accelerated Vascular Ageing: An Early Prognostic Signal for Risk Stratification and Prevention.

Catherine Liao1, Carmel M McEniery2, Ian B Wilkinson2

  • 1Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom.

European Journal of Preventive Cardiology
|June 3, 2026
PubMed
Summary
This summary is machine-generated.

Vascular ageing, a key factor in many diseases, can be measured using biomarkers of arterial stiffness. Early detection is crucial as interventions to reverse structural stiffening are limited, highlighting the need for improved diagnostic and management strategies.

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Area of Science:

  • Cardiovascular Science
  • Vascular Biology
  • Clinical Epidemiology

Background:

  • Vascular ageing contributes to cardiovascular, renal, cognitive, and pregnancy-related diseases.
  • It stems from cumulative hemodynamic stress and arterial stiffening.
  • Understanding vascular ageing is vital for disease prevention.

Purpose of the Study:

  • To review methods for measuring and interpreting vascular ageing.
  • To explore the translation of vascular ageing assessment into clinical prevention strategies.
  • To identify barriers and opportunities for clinical adoption of vascular ageing biomarkers.

Main Methods:

  • Integration of evidence from arterial mechanics, vascular biology, clinical epidemiology, diagnostic science, and health economics.
  • Analysis of biomarkers reflecting arterial stiffness, central pressures, and wave reflection indices.
  • Review of current guidelines and clinical decision-making pathways.

Main Results:

  • Biomarkers of arterial stiffness predict adverse outcomes independently of brachial blood pressure.
  • Lifestyle and pharmacologic interventions primarily modify vascular tone, not structural stiffening.
  • Clinical adoption is hindered by fragmented biomarkers and lack of outcome-based pathways.

Conclusions:

  • Early detection of accelerated vascular ageing is critical due to limited options for reversing structural stiffening.
  • Harmonized measurement, outcome-anchored thresholds, and integrated evidence are needed for effective prevention.
  • Targeted assessment in intermediate-risk populations can inform treatment intensification and monitoring.