A systematic review and meta-analysis of the association between markers of hemostasis and abdominal aortic aneurysm presence and size.
OBJECTIVE
The purpose of this study was to summarize the current evidence of the association between markers of hemostasis and both the presence and size of abdominal aortic aneurysms (AAAs).


METHODS
A systematic review and meta-analysis was performed according to Preferred Reporting Items for Systematic reviews and Meta-Analyses guidelines by use of the search terms "aneurysm AND abdominal AND aortic AND coagulation" NOT "thoracic." Outcome data including concentration of hemostatic marker, number of patients, and significance level were recorded.


RESULTS
A total of 22 nonrandomized studies were included in the analysis, with a total of 9862 patients. Fibrinogen mean difference (MD) (0.43 g/L; 95% confidence interval [CI], 0.28-0.58 g/L; P ≤ .00001), D-dimer MD (325.82 ng/mL; 95% CI, 199.74-451.89 ng/mL; P ≤ .00001), and thrombin-antithrombin III complex MD (5.58 g/L; 95% CI, 3.34-7.83 g/L; P ≤ .0001) were significantly elevated in the presence of AAAs. Tissue plasminogen activator, prothrombin fragments F1+F2, and platelet count were not shown to be significantly different between patients with and those without AAAs. Meta-regression of studies reporting plasma D-dimer concentration and aneurysm diameter suggests a strong and significant association (r(2) = 0.94; P ≤ .0001).


CONCLUSIONS
This study suggests that the presence of AAAs is associated with increased fibrin turnover, fibrinolysis, and thrombin generation, as shown by increased levels of fibrinogen, D-dimer, and thrombin-antithrombin III complex. This is clinically relevant because markers of hemostasis are independent risk factors for cardiovascular events, highlighting the necessity of addressing all modifiable cardiovascular risk factors in patients with AAAs. Furthermore, the finding that plasma D-dimer concentration appears to have a linear relationship with aneurysm diameter may be useful as a future biomarker of AAAs.
Vascular Surgery Group, Department of Cardiovascular Sciences, University of Leicester, Leicester, United Kingdom. Electronic address: ds343@le.ac.uk.
David A
DA
Sidloff
Vascular Surgery Group, Department of Cardiovascular Sciences, University of Leicester, Leicester, United Kingdom.
Philip W
PW
Stather
Vascular Surgery Group, Department of Cardiovascular Sciences, University of Leicester, Leicester, United Kingdom.
Edward
E
Choke
Vascular Surgery Group, Department of Cardiovascular Sciences, University of Leicester, Leicester, United Kingdom; NIHR Leicester Biomedical Research Unit, University of Leicester, Leicester, United Kingdom.
Matthew J
MJ
Bown
Vascular Surgery Group, Department of Cardiovascular Sciences, University of Leicester, Leicester, United Kingdom.
Robert D
RD
Sayers
D000990:Antithrombin III; D001012:Aorta, Abdominal / Q000473:pathology*; D017544:Aortic Aneurysm, Abdominal / Q000097:blood* / Q000473:pathology*; D015415:Biomarkers / Q000097:blood; D004108:Dilatation, Pathologic; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D005340:Fibrinogen / Q000032:analysis; D006487:Hemostasis; D006801:Humans; D010447:Peptide Hydrolases / Q000097:blood; D011379:Prognosis; D012307:Risk Factors
D015415:Biomarkers; D005338:Fibrin Fibrinogen Degradation Products; C046193:antithrombin III-protease complex; C036309:fibrin fragment D; D000990:Antithrombin III; D005340:Fibrinogen; D010447:Peptide Hydrolases