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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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Management of atherosclerosis involves an integrated strategy encompassing pharmacological treatment, surgical interventions, lifestyle changes, and nutrition therapy to address the multifactorial nature of the disease.Pharmacological TherapyA cornerstone of atherosclerosis management is the use of pharmacological agents. Statins, such as atorvastatin, are pivotal in inhibiting HMG-CoA reductase, an enzyme that catalyzes an initial step in cholesterol synthesis in the liver. This reduction in...
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Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
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Peripheral artery disease (PAD) predominantly results from atherosclerosis, which involves the accumulation of fatty deposits, or plaques, within the walls of arteries. This causes them to narrow and harden, significantly reducing blood flow. PAD predominantly affects the legs but also impacts other areas, such as the arms, thereby impairing overall circulation and organ function.Etiology of PAD:The principal cause of PAD is atherosclerosis, which results from fatty deposits inside the arterial...
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Related Experiment Video

Updated: Aug 3, 2025

Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein
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Lipoprotein (a), Inflammation, and Atherosclerosis.

Stefania Angela Di Fusco1, Aldo Pietro Maggioni2, Pietro Scicchitano3

  • 1Clinical and Rehabilitation Unit, San Filippo Neri Hospital, ASL Rome 1, 00135 Rome, Italy.

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High levels of lipoprotein (a) and chronic inflammation contribute to residual cardiovascular risk. Targeting these factors may reduce future cardiovascular events in patients.

Keywords:
cardiovascular preventioncolchicineinflammationlipoprotein (a)personalized medicine

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Area of Science:

  • Cardiovascular Medicine
  • Biochemistry
  • Inflammation Research

Background:

  • Residual cardiovascular risk persists despite optimal evidence-based management.
  • Elevated lipoprotein (a) (Lp(a)) and chronic inflammation are implicated in this residual risk.
  • Lp(a) >125 nmol/L and high-sensitivity C-reactive protein >2 mg/dL are associated with increased cardiovascular events.

Purpose of the Study:

  • To review the role of lipoprotein (a) and chronic inflammation in residual cardiovascular risk.
  • To discuss current therapeutic limitations and emerging strategies for these risk factors.
  • To highlight the importance of improved risk stratification for atherosclerotic cardiovascular disease.

Main Methods:

  • Review of clinical studies and evidence linking Lp(a) and inflammation to cardiovascular disease.
  • Analysis of current lipid-lowering drug efficacy on Lp(a) levels.
  • Examination of anti-inflammatory drugs (e.g., canakinumab, colchicine) in cardiovascular risk reduction.

Main Results:

  • High Lp(a) levels correlate with ischemic heart disease, stroke, and aortic stenosis.
  • Standard lipid-lowering drugs have minimal effect on Lp(a).
  • Canakinumab and colchicine show potential for cardiovascular risk reduction by targeting inflammation.

Conclusions:

  • Lipoprotein (a) and chronic inflammation are key contributors to residual cardiovascular risk.
  • Novel diagnostic and therapeutic strategies targeting Lp(a) and inflammation are crucial.
  • Refined patient management through risk stratification may reduce atherosclerotic cardiovascular disease burden.