scholarly journals Aortic Stiffness, Central Blood Pressure, and Pulsatile Arterial Load Predict Future Thoracic Aortic Aneurysm Expansion

Hypertension ◽  
2021 ◽  
Vol 77 (1) ◽  
pp. 126-134
Author(s):  
Kevin E. Boczar ◽  
Munir Boodhwani ◽  
Luc Beauchesne ◽  
Carole Dennie ◽  
Kwan Leung Chan ◽  
...  

Thoracic aortic aneurysm is a disease associated with high morbidity and mortality. Clinically useful strategies for medical management of thoracic aortic aneurysm are critically needed. To address this need, we sought to determine the role of aortic stiffness and pulsatile arterial load on future aneurysm expansion. One hundred five consecutive, unoperated subjects with thoracic aortic aneurysm were recruited and prospectively followed. By combining arterial tonometry with echocardiography, we estimated measures of aortic stiffness, central blood pressure, steady, and pulsatile arterial load at baseline. Aneurysm size was measured at baseline and follow-up with imaging; growth was calculated in mm/y. Stepwise multivariable linear regression assessed associations of arterial stiffness and load measures with aneurysm growth after adjusting for potential confounders. Mean±SD age, baseline aneurysm size, and follow-up time were 62.6±11.4 years, 46.24±3.84 mm, and 2.92±1.01 years, respectively. Aneurysm growth rate was 0.43±0.37 mm/y. After correcting for multiple comparisons, higher central systolic (β±SE: 0.026±0.009, P =0.007), and pulse pressures (β±SE: 0.032±0.009, P =0.0002), carotid-femoral pulse wave velocity (β±SE: 0.032±0.011, P =0.005), amplitudes of the forward (β±SE: 0.044±0.012, P =0.0003) and reflected (β±SE: 0.060±0.020, P =0.003) pressure waves, and lower total arterial compliance (β±SE: −0.086±0.032, P =0.009) were independently associated with future aneurysm growth. Measures of aortic stiffness and pulsatile hemodynamics are independently associated with future thoracic aortic aneurysm growth and provide novel insights into disease activity. Our findings highlight the role of central hemodynamic assessment to tailor novel risk assessment and therapeutic strategies to patients with thoracic aortic aneurysm.

2017 ◽  
Vol 69 (11) ◽  
pp. 2041
Author(s):  
Thais Coutinho ◽  
Katie Y. Cheung ◽  
Munir Boodhwani ◽  
Luc Beauchesne ◽  
Carole Dennie ◽  
...  

2018 ◽  
Vol 34 (10) ◽  
pp. S73-S74
Author(s):  
K. Boczar ◽  
M. Boodwhani ◽  
L. Beauchesne ◽  
K. Chan ◽  
C. Dennie ◽  
...  

Circulation ◽  
2019 ◽  
Vol 139 (8) ◽  
pp. 1124-1126
Author(s):  
Jennifer Jue ◽  
Munir Boodhwani ◽  
Luc Beauchesne ◽  
Carole Dennie ◽  
Sudhir Nagpal ◽  
...  

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
T Zhu ◽  
M Boodhwani ◽  
L Beauchesne ◽  
K Chan ◽  
C Dennie ◽  
...  

Abstract Introduction Thoracic aortic aneurysm (TAA) is a clinically silent disease which can lead to significant morbidity when complicated by an acute aortic syndrome. Although TAA size is the only variable used in decision-making, it is an imperfect predictor of risk. Conversely, hemodynamic measures that reflect the aorta's function, such as aortic stiffness and pulsatile hemodynamics, may provide additional insights into risk of TAA expansion. Purpose We hypothesized that combining aortic size with measures of arterial function (stiffness and pulsatile hemodynamics) would improve prediction of TAA expansion, as compared to aortic size alone. Methods 105 unoperated participants with TAA were recruited between 2014 and 2017 and followed prospectively for ≥1 yr. TAA size was measured at enrolment and at the latest imaging study according to published consensus; TAA expansion was calculated as mm/year. Arterial function was non-invasively assessed at baseline with validated methods that integrate arterial tonometry with echocardiography. Multivariable linear regression assessed independent associations of baseline TAA size and each arterial function measure, initially separately and then in combination (by multiplying them when direction of association was the same, and dividing them when direction of association was opposite), with future TAA expansion. Standardized beta coefficients were calculated to allow direct comparisons. Models were adjusted for age, sex, body size, aneurysm location and etiology, type of imaging modality, follow-up time, mean arterial pressure, and history of hypertension, diabetes and smoking. Results Seventy-seven percent of participants were men, and the ratio of degenerative to heritable TAAs was 62/43. Mean ± SD age, baseline TAA size, and follow-up time were 62.8±11.3yrs, 46.3±3.9cm, and 2.2±0.7 years, respectively. Results of the multivariable linear regression models are summarized in the Table. While baseline TAA size and each arterial function measure were independently associated with TAA expansion, some of the arterial function measures were superior in predicting TAA growth (Table, left). In addition, combining aortic size and function further improved the prediction of TAA growth beyond each variable alone (Table, right). Conclusion(s) Combining aortic size with arterial function improved prediction of TAA expansion over any individual variable alone, independently of confounders. Assessing arterial function may confer a clinical advantage, when compared to current practice, in determining TAA disease activity and estimating one's TAA-related risk. Acknowledgement/Funding Canadian Institute of Health Research, Canadian Vascular Network, and Heart and Stroke Foundation of Canada


Author(s):  
Katie Cheung ◽  
Munir Boodhwani ◽  
Kwan‐Leung Chan ◽  
Luc Beauchesne ◽  
Alexander Dick ◽  
...  

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
K Boczar ◽  
M Boodhwani ◽  
L Beauchesne ◽  
C Dennie ◽  
K.L Chan ◽  
...  

Abstract Background Thoracic aortic aneurysm (TAA) is a deadly disease in critical need of novel strategies for risk assessment and medical management. To address this need, we have previously shown that directly measured carotid-femoral pulse wave velocity (cfPWV), a marker of aortic stiffness and health, independently predicts future TAA expansion. Since aortic pulse wave velocity can be estimated from age and mean arterial pressure (MAP), in the present study we sought to determine whether estimated aortic pulse wave velocity (e-aPWV) also predicts TAA expansion. Methods One hundred and five consecutive, unoperated subjects with TAA were recruited. e-aPWV was estimated from validated equations based on age and MAP. cfPWV was measured with arterial tonometry according to guidelines. TAA size was measured at baseline and at the latest follow-up using available imaging modalities according to guidelines. Stepwise multivariable linear regression (P≤0.25 to enter, P≤0.10 to stay in the model) assessed independent associations of e-aPWV and cfPWV with future TAA growth. Variables considered in the models were: age, sex, BSA, MAP, TAA etiology and location, baseline TAA size, follow-up time, imaging modality, history of hypertension, diabetes and smoking. Results Seventy eight percent of subjects were men. Mean±SD age, baseline aneurysm size and follow-up time were 62.6±11.4 years, 46.2±3.8 mm and 3.0±1.0 years, respectively. e-aPWV and cfPWV were moderately correlated (Pearson's correlation coefficient = 0.61). Results of the linear regression analyses showed that both measured (cfPWV) and estimated (e-aPWV) independently predicted future TAA expansion (β±SE: 0.032±0.011, P=0.048 and 0.240±0.085, P=0.006, respectively). The base model's R-squared value of 0.39 was increased to 0.44 with addition of either cfPWV or e-aPWV to the model, confirming that each parameter of aortic stiffness enhances prediction of TAA growth. Conclusion Aortic stiffness is relevant for assessment of TAA disease activity. Similar to cfPWV, e-aPWV is also independently associated with future TAA expansion. Thus, e-aPWV represents a tool to improve TAA risk stratification that is simple, free of cost, and obviates the need for specialized equipment or dedicating training, which leads to excellent potential for widespread incorporation into clinical practice. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): Canadian Institutes of Health Research


2019 ◽  
Vol 35 (10) ◽  
pp. S76
Author(s):  
K. Boczar ◽  
M. Boodhwani ◽  
K. Chan ◽  
C. Dennie ◽  
G. Wells ◽  
...  

2021 ◽  
Vol 39 (Supplement 1) ◽  
pp. e312
Author(s):  
Alexandra Gurevich ◽  
Nicolay Zherdev ◽  
Igor Emelyanov ◽  
Mikhail Chernyavskiy ◽  
Vladimir Uspenskiy ◽  
...  

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