Stiffness matters: Improved failure risk assessment of ascending thoracic aortic aneurysms.

Objectives: Rupture and dissection are feared complications of ascending thoracic aortic aneurysms caused by mechanical failure of the wall. The current method of using the aortic diameter to predict the risk of wall failure and to determine the need for surgical resection lacks accuracy. Therefore, this study aims to identify reliable and clinically measurable predictors for aneurysm rupture or dissection by performing a personalized failure risk analysis, including clinical, geometrical, histologic, and mechanical data. Methods: The study cohort consisted of 33 patients diagnosed with ascending aortic aneurysms without genetic syndromes. Uniaxial tensile tests until failure were performed to determine the wall strength. Material parameters were fitted against ex vivo planar biaxial data and in vivo pressure-diameter relationships at diastole and systole, which were derived from multiphasic computed tomography (CT) scans. Using the resulting material properties and in vivo data, the maximal in vivo stress at systole was calculated, assuming a thin-walled axisymmetric geometry. The retrospective failure risk was calculated by comparing the peak wall stress at suprasystolic pressure with the wall strength. Results: The distensibility coefficient, reflecting aortic compliance and derived from blood pressure measurements and multiphasic CT scans, outperformed predictors solely based on geometrical features in assessing the risk of aneurysm failure. Conclusions: In a clinical setting, multiphasic CT scans followed by the calculation of the distensibility coefficient are of added benefit in patient-specific, clinical decision-making. The distensibility derived from the aneurysm volume change has the best predictive power, as it also takes the axial stretch into account.

Mechanical properties and cellular content of leukocyte- and platelet-rich fibrin membranes of patients on antithrombotic drugs.

INTRODUCTION: The aim of this study was to examine the potential influence of antithrombotics on leukocyte- and platelet-rich fibrin (L-PRF) membranes. METHODS: Tensile tests and cell counts were performed with L-PRF membranes originating from patients on anticoagulants and antiplatelets versus patients not taking antithrombotics. RESULTS: For the tensile tests, 13 control patients, 12 on anticoagulants, and 10 on antiplatelets donated blood. Compared to controls, membranes from anticoagulated donors were weaker (strength 0.57 ± 0.24 MPa vs. 0.80 ± 0.27 MPa, p = .03) and could not be stretched as far (1.8 ± 0.3 vs. 2.1 ± 0.3 times the initial length, p = .01). For the cell counting, 23 control patients, 16 on anticoagulants, and 16 on antiplatelets donated blood. The percentage of platelets was ±50% in the three groups. The percentage of leukocytes was lower in the anticoagulant group compared with controls (69 ± 10% vs. 78 ± 8%, p = .04). However, because of the unknown error of method, it is questionable whether the statistical significance is meaningful. There was no difference between membranes from the control group and the group on antiplatelets. CONCLUSION: Our results indicate that L-PRF membranes originating from patients on anticoagulants are weaker, stretch less far, and contain less leukocytes than L-PRF membranes of patients not taking these drugs.