A systematic review and meta-analysis of the association between markers of hemostasis and abdominal aortic aneurysm presence and size

Sidloff, David; Stather, P.W.; Choke, Edward; Bown, Matthew J.; Sayers, Robert D.

doi:10.1016/j.jvs.2013.10.088

Cited by 60 publications

(67 citation statements)

References 43 publications

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“…Importantly, platelets and platelet-specific secretions (soluble P-selectin, soluble CD40L, soluble glycoprotein V, and platelet-derived microparticles) are present in plasma of AAA patients and are specifically released from the luminal thrombus of an aneurysm (25). Despite these results, several meta-analyses and retrospective clinical trials reported no significant benefit of platelet inhibitors on aneurysm growth and incidence of rupture (32-34). …”

Section: Introductionmentioning

confidence: 98%

Platelet Inhibitors Reduce Rupture in a Mouse Model of Established Abdominal Aortic Aneurysm

Owens

Edwards

Antoniak

et al. 2015

ATVB

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Objective Rupture of abdominal aortic aneurysms (AAAs) causes a high morbidity and mortality in the elderly population. Platelet-rich thrombi form on the surface of aneurysms and may contribute to disease progression. In this study, we used a pharmacologic approach to examine a role of platelets in established aneurysms induced by angiotensin II (AngII) infusion into hypercholesterolemic mice. Approach and Results Administration of the platelet inhibitors aspirin (ASA) or clopidogrel bisulfate to established AAAs dramatically reduced rupture. The mechanism of protection appears to be a reduction in abdominal aortic platelet and macrophage recruitment resulting in decreased active matrix metalloproteinases (MMPs) 2 and 9. Platelet inhibitors also resulted in reduced plasma concentrations of platelet factor 4, cytokines, and components of plasminogen activation system in mice. To determine the validity of these findings in human subjects, eligible aneurysm patients were retrospectively analyzed using developed and validated algorithms in the electronic medical record database at Vanderbilt University. Similar to mice, administration of ASA or P2Y12 inhibitors was associated with reduced death amongst AAA patients. Conclusions These results suggest that platelets contribute to AAA progression and rupture.

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Section: Introductionmentioning

confidence: 98%

Platelet Inhibitors Reduce Rupture in a Mouse Model of Established Abdominal Aortic Aneurysm

Owens

Edwards

Antoniak

et al. 2015

ATVB

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“…While contemporary imaging can readily determine the dimensions of AAAs, one of the hopes of biomarkers is their ability to discriminate propensity to rupture. Recently, two large meta-analysis studies assessed a wide array of molecular markers for application as AAA biomarkers [17,18]. Sidloff et al [17] demonstrated significant increase plasma concentrations of fibrinogen, D-dimer, and thrombin-antithrombin III complex in people with AAA; and also a significant correlation between aortic diameter and D-dimer In addition to these hemostasis markers.…”

Section: Introductionmentioning

confidence: 99%

“…Recently, two large meta-analysis studies assessed a wide array of molecular markers for application as AAA biomarkers [17,18]. Sidloff et al [17] demonstrated significant increase plasma concentrations of fibrinogen, D-dimer, and thrombin-antithrombin III complex in people with AAA; and also a significant correlation between aortic diameter and D-dimer In addition to these hemostasis markers. Stather et al [18*] demonstrated a significant difference in a number of biomakers in patients with AAAs including: matrix metalloproteinase (MMP) 9, tissue inhibitor of matrix metalloproteinase 1, interleukin (IL) 6, Creactive protein (CRP), α1-antitrypsin, apolipoprotein A and high-density lipoprotein.…”

Section: Introductionmentioning

confidence: 99%

Abdominal aortic aneurysm

Davis

Rateri

Daugherty

2015

Current Opinion in Cardiology

134

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Purpose of review Abdominal aortic aneurysm (AAA) is a pathological condition of permanent dilation that portends the potentially fatal consequence of aortic rupture. This review emphasizes recent advances in mechanistic insight into aneurysm pathogenesis and potential pharmacologic therapies that are on the horizon for AAAs. Recent Findings An increasing body of evidence demonstrates that genetic factors, including 3p12.3, DAB2IP, LDLr, LRP1, MMP3, TGFβR2 and SORT1 loci, are associated with AAA development. Current human studies and animal models have shown that many leukocytes and inflammatory mediators, such as IL-1, IL-17, TGF-β and angiotensin II, are involved in the pathogenesis of AAAs. Leukocytic infiltration into aortic media leads to smooth muscle cell depletion, generation of reactive oxygen species, and extracellular matrix fragmentation. Recent preclinical investigations into pharmacological therapies for AAAs have provided intriguing insight for roles of microRNAs to regulate many pathological pathways in AAA development. Several large clinical trials are ongoing seeking to translate preclinical findings into therapeutic options. Summary Recent studies have identified many potential mechanisms involved in AAA pathogenesis that provide insight for the development of a medical treatment for this disease.

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“…Perioperative assessment of changes in tissue factor and its inhibitor in patients with abdominal aortic aneurysm treated using classical and intravascular methods the bloodstream [7][8][9] and elevated TF in plasma is the evidence of the state of hyper coagulation. Previously Hobbs and co-workers showed the elevated level of TF in patients with ruptured AAA when compared to asymptomatic patients without concurrent differences in TFPI levels [10].…”

Section: Resultsmentioning

confidence: 99%

Perioperative assessment of changes in tissue factor and its inhibitor in patients with abdominal aortic aneurysm treated using classical and intravascular methods

Zapotoczny¹,

Kotschy²,

Grendziak³

et al. 2017

Interventional-Cardiology

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Objectives:We examined plasma concentrations of essential regulators of coagulation cascade, tissue factor (TF) and tissue factor inhibitor pathway (TFPI) in patients with abdominal aortic aneurysm (AAA) during two types of surgical repair , open (OAR) and endovascular repair (EVAR). Background:The interplay between TF and TFPI is important for the proper functioning of coagulation cascade. Although abnormal coagulation is known to contribute to the formation of AAA, little is known about the prognostic value of TF and TFPI levels in the perioperative stage of AAA repair. Methods:We have selected the reference group of 53 healthy, first-time blood donors and 66 patients scheduled for AAA repair using EVAR or OAR and measured TF and TFPI in their blood plasma using ELISA (enzyme-linked immunosorbent assay) before surgery, immediately after and 24 hours after surgery. Results:Patients with AAA had elevated levels of TF (219.242 pg/ml) compared to the reference group (149.170 pg/ml). TF levels were higher in AAA patients with limb ischemia (p=0.0026) and mural thrombi >30 mm (p=0.0015) but decreased in patient with BMI >25 (p=0.027). No differences were observed in TF and TFPI levels during EVAR and OAR or de-pending on the stent graft type. However, there was a correlation between the TF level and occurrence of post-surgical complications in OAR type of surgery Conclusions: Our results suggest that monitoring levels of TF and TFPI in perioperative period would be useful in risk assessment of surgery complications, especially in AAA patients with ischemic disorders undergoing OAR surgery.

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A systematic review and meta-analysis of the association between markers of hemostasis and abdominal aortic aneurysm presence and size

Cited by 60 publications

References 43 publications

Platelet Inhibitors Reduce Rupture in a Mouse Model of Established Abdominal Aortic Aneurysm

Platelet Inhibitors Reduce Rupture in a Mouse Model of Established Abdominal Aortic Aneurysm

Abdominal aortic aneurysm

Perioperative assessment of changes in tissue factor and its inhibitor in patients with abdominal aortic aneurysm treated using classical and intravascular methods

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