Effect of Antiplatelet Agents on Abdominal Aortic Aneurysm Process: A Systematic Review and Meta-Analysis

Yang Yang1,2, Chang Li1, Zhi-Yuan Wu1,2

  • 1Department of Vascular Surgery, Beijing Hospital, National Center of Gerontology; Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, 100010 Beijing, China.

Insights

Antiplatelet agents do not impact abdominal aortic aneurysm (AAA) growth or rupture. This review found no evidence that these medications slow AAA diameter expansion in patients.

Area of Science:

  • Cardiovascular Research
  • Vascular Surgery
  • Pharmacology

Background:

  • Abdominal aortic aneurysm (AAA) is a life-threatening condition characterized by the dilation of the aorta.
  • Antiplatelet agents are commonly prescribed, but their role in AAA management is unclear.

Purpose of the Study:

  • To systematically review and meta-analyze the association between antiplatelet agents and AAA progression (reduction, expansion, rupture).

Main Methods:

  • Systematic review of EMBASE, Ovid, PubMed, and Scopus databases up to March 2023.
  • Meta-analysis of 13 studies involving 5392 patients.
  • Statistical analysis performed using R software v.4.1.

Main Results:

  • No significant difference in the annual growth rate of AAA diameter between antiplatelet and control groups (MD = -0.04, 95% CI = [-0.37, 0.30]).
  • No significant difference in aneurysm diameter expansion between groups (OR = 0.96, 95% CI = [0.41, 2.25]).
  • High heterogeneity observed in both analyses.

Conclusions:

  • Antiplatelet agents do not influence AAA reduction, expansion, or rupture.
  • Current evidence suggests no benefit of antiplatelet therapy for slowing AAA sac diameter growth.
Abstract

Related Concept Videos

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
505
Formation of the Platelet Plug01:22

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
5.5K
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
659
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
5.2K
Antianginal Drugs: Nitrates and β-Blockers01:16

Antianginal Drugs: Nitrates and β-Blockers

In cardiovascular health, antianginal drugs combat angina pectoris — a condition marked by chest pain owing to diminished blood flow to the heart.
Organic nitrates,  such as nitroglycerin, play a pivotal role. Once metabolized, they liberate nitric oxide, a molecular marvel. Nitric oxide triggers guanylyl cyclase and augments cGMP production. This biochemical cascade orchestrates the relaxation of vascular smooth muscles, ushering in vasodilation and enhancing coronary blood flow....
564
Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

Antihypertensive Drugs: Angiotensin II Receptor Blockers

In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
674