scholarly journals Hemodynamic variables in aneurysms are associated with thrombotic risk in children with Kawasaki disease

2019 ◽  
Vol 281 ◽  
pp. 15-21 ◽  
Author(s):  
Noelia Grande Gutierrez ◽  
Mathew Mathew ◽  
Brian W. McCrindle ◽  
Justin S. Tran ◽  
Andrew M. Kahn ◽  
...  
2022 ◽  
Author(s):  
Qiong Yao ◽  
Chen Peng ◽  
Sheng-zhang Wang ◽  
Xi-hong Hu

Abstract Objectives Thrombosis is a major adverse outcome for coronary artery aneurysms (CAA) in Kawasaki disease (KD). We investigated the geometric and hemodynamic abnormalities in patients with CAA and identified the risk factors for thrombosis by computational fluid dynamics (CFD) simulation. Methods We retrospectively studied 27 KD patients with 77 CAAs, including 20 CAAs with thrombosis in 12 patients. Patient-specific anatomic models obtained from cardiac magnetic resonance imaging (CMRI) were constructed to perform a CFD simulation. From the simulation results, we produced local hemodynamic parameters comprising of time-averaged wall shear stress (TAWSS), oscillatory shear index (OSI) and relative resident time (RRT). The CAA’s maximum diameter (Dmax) and Z-score were measured on CMRI. Results Giant CAAs tended to present with more severe hemodynamic abnormalities. Thrombosed CAAs exhibited lower TAWSS (1.551 ± 1.535 vs. 4.235 ± 4.640dynes/cm2, p = 0.002), higher Dmax (10.905 ± 4.125 vs. 5.791 ± 2.826mm, p = 0.008), Z-score (28.301 ± 13.558 vs. 13.045 ± 8.394, p = 0.002), OSI (0.129 ± 0.132 vs. 0.046 ± 0.080, p = 0.01), and RRT (16.780 ± 11.982s vs. 9.123 ± 11.770s, p = 0.399) than the non-thrombosed group. An ROC analysis for thrombotic risk proved that all of the five parameters had area under the ROC curves (AUC) above 0.7, with Dmax delineating the highest AUC (AUCDmax = 0.871) and a 90% sensitivity, followed by Z-score (AUCZ−score = 0.849). Conclusions It is reasonable to combine the geometric index with hemodynamic information to establish a severity classification for KD cases.


2018 ◽  
Vol 2017 (3) ◽  
Author(s):  
Noelia Grande Gutierrez ◽  
Andrew Kahn ◽  
Jane C Burns ◽  
Alison L Marsden

[first paragraph of article]Coronary artery aneurysms (CAA) as a result of Kawasaki disease (KD) create abnormal flow conditions that can ultimately lead to thrombosis, with associated risks of myocardial infarction and sudden death. The primary long-term clinical decision required for KD patients with aneurysms is whether to treat with anticoagulation therapy. Current clinical guidelines recommend CAA diameter 8 mm or Z-score >10 as the criterion for initiating systemic anticoagulation therapy. In general, these aneurysms cause regions of flow stagnation, but the complexity of their geometry including changes in diameter, tortuosity and even proximal and distal stenoses make it difficult to evaluate thrombotic risk and predict patient outcomes based solely on a single anatomical measurement taken from image data, usually the maximum aneurysm diameter. 


2014 ◽  
Vol 13 (6) ◽  
pp. 1261-1276 ◽  
Author(s):  
Dibyendu Sengupta ◽  
Andrew M. Kahn ◽  
Ethan Kung ◽  
Mahdi Esmaily Moghadam ◽  
Olga Shirinsky ◽  
...  

2021 ◽  
Vol 17 (9) ◽  
pp. e1009331
Author(s):  
Noelia Grande Gutiérrez ◽  
Mark Alber ◽  
Andrew M. Kahn ◽  
Jane C. Burns ◽  
Mathew Mathew ◽  
...  

Coronary artery thrombosis is the major risk associated with Kawasaki disease (KD). Long-term management of KD patients with persistent aneurysms requires a thrombotic risk assessment and clinical decisions regarding the administration of anticoagulation therapy. Computational fluid dynamics has demonstrated that abnormal KD coronary artery hemodynamics can be associated with thrombosis. However, the underlying mechanisms of clot formation are not yet fully understood. Here we present a new model incorporating data from patient-specific simulated velocity fields to track platelet activation and accumulation. We use a system of Reaction-Advection-Diffusion equations solved with a stabilized finite element method to describe the evolution of non-activated platelets and activated platelet concentrations [AP], local concentrations of adenosine diphosphate (ADP) and poly-phosphate (PolyP). The activation of platelets is modeled as a function of shear-rate exposure and local concentration of agonists. We compared the distribution of activated platelets in a healthy coronary case and six cases with coronary artery aneurysms caused by KD, including three with confirmed thrombosis. Results show spatial correlation between regions of higher concentration of activated platelets and the reported location of the clot, suggesting predictive capabilities of this model towards identifying regions at high risk for thrombosis. Also, the concentration levels of ADP and PolyP in cases with confirmed thrombosis are higher than the reported critical values associated with platelet aggregation (ADP) and activation of the intrinsic coagulation pathway (PolyP). These findings suggest the potential initiation of a coagulation pathway even in the absence of an extrinsic factor. Finally, computational simulations show that in regions of flow stagnation, biochemical activation, as a result of local agonist concentration, is dominant. Identifying the leading factors to a pro-coagulant environment in each case—mechanical or biochemical—could help define improved strategies for thrombosis prevention tailored for each patient.


2001 ◽  
Vol 120 (5) ◽  
pp. A282-A282
Author(s):  
I KOUTROUBAKIS ◽  
A SFIRIDAKI ◽  
A THEODOROPOULOU ◽  
A LIVADIOTAKI ◽  
P DIMOULIOS ◽  
...  

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