Error Analysis in Patient-Specific Blood Flow Modeling of Coronary Artery Disease

Author(s):  
Dan Rafiroiu ◽  
Izabella Molnar ◽  
Angela Lungu
Author(s):  
Lazaros Papamanolis ◽  
Hyun Jin Kim ◽  
Clara Jaquet ◽  
Matthew Sinclair ◽  
Michiel Schaap ◽  
...  

AbstractPatient-specific models of blood flow are being used clinically to diagnose and plan treatment for coronary artery disease. A remaining challenge is bridging scales from flow in arteries to the micro-circulation supplying the myocardium. Previously proposed models are descriptive rather than predictive and have not been applied to human data. The goal here is to develop a multiscale patient-specific model enabling blood flow simulation from large coronary arteries to myocardial tissue. Patient vasculatures are segmented from coronary computed tomography angiography data and extended from the image-based model down to the arteriole level using a space-filling forest of synthetic trees. Blood flow is modeled by coupling a 1D model of the coronary arteries to a single-compartment Darcy myocardium model. Simulated results on five patients with non-obstructive coronary artery disease compare overall well to [$$^{15}$$ 15 O]$$\text {H}_{{2}}$$ H 2 O PET exam data for both resting and hyperemic conditions. Results on a patient with severe obstructive disease link coronary artery narrowing with impaired myocardial blood flow, demonstrating the model’s ability to predict myocardial regions with perfusion deficit. This is the first report of a computational model for simulating blood flow from the epicardial coronary arteries to the left ventricle myocardium applied to and validated on human data.


Circulation ◽  
1995 ◽  
Vol 91 (5) ◽  
pp. 1381-1388 ◽  
Author(s):  
Ernest L. Fallen ◽  
Claude Nahmias ◽  
Anita Scheffel ◽  
Geoff Coates ◽  
Rob Beanlands ◽  
...  

Author(s):  
Jenifer M Brown ◽  
Wunan Zhou ◽  
Brittany Weber ◽  
Sanjay Divakaran ◽  
Leanne Barrett ◽  
...  

Abstract Aims The transition from hypertension to heart failure (HF) remains poorly understood. We hypothesized that insufficient perfusion to match global metabolic demand, reflected by a low ratio of myocardial blood flow to global myocardial mass, may be a HF risk marker. Methods and results A retrospective cohort (n = 346) of patients with hypertension who underwent clinical positron emission tomography (PET) myocardial perfusion imaging for chest pain and/or dyspnoea at Brigham and Women’s Hospital (Boston, MA, USA) were studied. Patients without obstructive coronary artery disease by history or PET perfusion (summed stress score <3), HF, cardiomyopathy, or ejection fraction (EF) <40% were followed for HF hospitalization (primary outcome), all-cause death, and their composite. Myocardial blood flow, left ventricular (LV) mass, volumes, and EF were obtained from PET, and a ‘flow/mass ratio’ was determined as hyperaemic myocardial blood flow over LV mass indexed to body surface area. A lower flow/mass ratio was independently associated with larger end-diastolic (β = −0.44, P < 0.001) and end-systolic volume (β = −0.48, P < 0.001) and lower EF (β = 0.33, P < 0.001). A flow/mass ratio below the median was associated with an adjusted hazard ratio of 2.47 [95% confidence interval (CI) 1.24–4.93; P = 0.01] for HF hospitalization, 1.95 (95% CI 1.12–3.41; P = 0.02) for death, and 2.20 (95% CI 1.39–3.49; P < 0.001) for the composite. Conclusion An integrated physiological measure of insufficient myocardial perfusion to match global metabolic demand identifies subclinical hypertensive heart disease and elevated risk of HF and death in symptomatic patients with hypertension but without flow-limiting coronary artery disease.


2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
VI Maslovskyi ◽  
IA Mezhiievska ◽  
YV Maslovskyi

Abstract Funding Acknowledgements Type of funding sources: None. High phospholipase A2 activity is associated with atherosclerotic disorders of the arteries, while paraoxonase activity decreases with increasing atherogenic plasma activity. The purpose is to study the relationship between the combined effect of phospholipase A2 and paraoxonase activity on vascular endothelial dysfunction in various forms of coronary artery disease. We examined 152 men 52.5 ± 0.8 years, including 53 - STEMI, 32 - NSTEMI, 67 - chronic chronic coronary syndromes (CCS). Methods. All patients were examined for endothelial function of the brachial artery with a test for reactive hyperemia and vasodilation with exogenous NO, as well as determination of phospholipase A2 activity and plasma paraoxonase activity. All studiies conform to the principles of the Declaration of Helsinki of the World Medical Association. Results. Dynamics evaluation of endothelial function indicates a significant increase in blood flow in the brachial artery after compression in the NSTEMI group, but a decrease in the STEMI group after vasodilation of exogenous NO. Analysis of phospholipase A2 activity and paraoxonase showed an increasing the first in STEMI group compared to NSTEMI one and CCS while decreasing the second in the corresponding groups (Tab. 1). The results of the study confirm the association of increased activity of phospholipase A2 with vascular disorders severity, the correction of which should be considered a priority in prospective studies. The fact of reducing the activity of paraoxonase should be considered in the correction treatment of vascular disorders. Tab. 1 CCS NSTEMI STEMI LSD criteria D% 7,48 ± 0,39 6,65 ± 0,54 6,77 ± 0,62 {1-2} V% 54,71 ± 1,01 51,13 ± 1,92 42,16 ± 3,29 p1 < 0,0001 p2 = 0,010 {3} / {1, 2} D% (NO) 10,35 ± 0,47 8,24 ± 0,96 10,28 ± 0,98 {1, 2} V% (NO) 55,60 ± 1,12 37,71 ± 3,72 p1 < 0,0001 28,12 ± 3,94 p1 < 0,0001 {1} / {2, 3} sPA2 1,12 ± 0,03 1,25 ± 0,04 p1 < 0,0001 1,34 ± 0,04 p1 < 0,0001 {1} / {2, 3} PAO 0,54 ± 0,01 0,50 ± 0,01 0,44 ± 0,01 p1 < 0,0001 p2 < 0,0001 {1} / {2,3} D% - diameter of brachial artery after compression. V% - blood flow velocity after compression. sPA2 -phospholipase A2. PAO - paraoxanase. p - reliability on Sheffe"s criteria.


Author(s):  
Soroush Nobari ◽  
Rosaire Mongrain ◽  
Richard Leask ◽  
Raymond Cartier

Coronary artery disease (CAD) is considered to be a major cause of mortality and morbidity in the developing world. It has recently been shown that aortic root pathologies such as aortic stiffening and calcific aortic stenosis can contribute to the initiation and progression of this disease by affecting coronary blood flow [1,2]. Such pathologies influence the distensibility of the aortic root and therefore the hemodynamics of the entire region. As a consequence the coronary blood flow and velocity profiles will be altered [3,4,5] which could accelerate the development of an existing coronary artery disease. However, it would be very interesting to see if an occluded coronary artery would have a mutual impact on valvular dynamics and aortic root pathologies. This bi-directionality could aggravate and contribute to the progression of both the coronary and aortic root pathology.


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