Thoracic Aortic Aneurysms Expansion Research Articles

Combining Aortic Size With Arterial Hemodynamics Enhances Assessment of Future Thoracic Aortic Aneurysm Expansion.

Thoracic aortic aneurysm (TAA) is a deadly disease whose current method for risk stratification (aneurysm size) is imperfect. We sought to evaluate whether combining aortic size with hemodynamic measures that reflect the aorta's function was superior to aortic size alone in the assessment of TAA expansion. One hundred thirty-seven nonoperated participants with TAA were followed prospectively. Aortic stiffness and pulsatile hemodynamics were noninvasively assessed at baseline with a combination of arterial tonometry with echocardiography using validated methodology. Aneurysm growth was calculated from standard imaging modalities. Multivariable linear regression models adjusted for potential confounders evaluated the association of aneurysm size and arterial hemodynamics, alone and in combination, with TAA growth. Sixty-nine percent of participants were male. Mean ± SD age, baseline aneurysm size, follow-up, and aneurysm expansion were, respectively, 62.2 ± 11.4 years, 45.9 ± 4.0 mm, 4.5 ± 1.9 years, and 0.41 ± 0.46 mm/year. In the linear regression models, the standardised β (β∗) for the association of aneurysm size with aneurysm expansion was 0.178 (P= 0.044). This was improved by combining aortic size with most measures of aortic function, with β∗ ranging from 0.192 (for aneurysm size combined with central diastolic blood pressure) to 0.484 (for aneurysm size combined with carotid-femoral pulse-wave velocity) (P ≤ 0.05 for each). Combining aneurysm size with measures of arterial function improves assessment of aneurysm growth over TAA size alone, which is the standard for clinical decisions in TAA. Thus, combining aneurysm size with measures of aortic function provides a clinical advantage in the assessment of TAA disease activity.

Estimated Aortic Pulse Wave Velocity Is Associated With Faster Thoracic Aortic Aneurysm Growth: A Prospective Cohort Study With Sex-Specific Analyses.

Thoracic aortic aneurysm (TAA) is associated with high morbidity and mortality, and there is a critical need for improved tools for risk assessment and prognostication. We have previously shown that aortic stiffness, measured from arterial tonometry (carotid-femoral pulse wave velocity [cfPWV]), is independently associated with TAA expansion. To increase clinical applicability, we sought to determine the association of mathematically estimated aortic pulse wave velocity (e-PWV) with TAA expansion. One-hundred and five consecutive unoperated subjects with TAA were recruited. We used arterial tonometry to measure cfPWV and used mean arterial pressure and age to calculate e-PWV according to validated equations. Multivariable linear regression assessed associations of baseline e-PWV with future aneurysm growth. Given sex differences in TAA outcomes, sex-stratified analyses were performed. Seventy-eight percent of subjects were men. Mean ± standard deviation (SD) age, baseline aneurysm size, and follow-up time were 62.6 ± 11.4 years, 46.2 ± 3.8 mm, and 2.9 ± 1.0 years, respectively. Aneurysm growth was 0.43 ± 0.37 mm per year; e-PWV was independently associated with future aneurysm expansion (β ± SE: 0.240 ± 0.085, P= 0.006). In sex-specific analyses, e-PWV was associated with aneurysm growth in both men (β ± standard error (SE) : 0.076 ± 0.022, P= 0.001) and women (β ± SE : 0.145 ± 0.050, P= 0.012), but the strength of association nearly twice as strong in women as in men. Greater aortic stiffness reflects worse aortic health and provides novel insights into disease activity; e-PWV is independently associated with TAA growth. This finding increases clinical applicability, as e-PWV can be estimated simply, quickly, and free of cost without the need for specialized equipment.

Differential expansion and outcomes of ascending and descending degenerative thoracic aortic aneurysms

ObjectiveTo evaluate expansion of degenerative thoracic aortic aneurysms (TAAs) and compare results between ascending and descending TAAs. MethodsAmong patients with diagnosis of degenerative TAA (1995-2015) in Olmsted County, we studied those having at least 2 computed tomography scans of TAA throughout the follow-up. Patients were classified as ascending or descending groups according to the segment where the maximal aortic diameter was measured. Primary end points were expansion rates and factors associated with TAA growth. ResultsWe investigated 137 patients, 70 (51.1%) of whom were women; 78 (56.9%) were in the ascending and 59 (43.1%) were in the descending group. Median baseline maximal aortic diameter was 48.5 mm (interquartile range, 47.0-49.9 mm) for ascending and 42.4 mm (interquartile range, 40.0-45.4 mm) for descending group (P < .001). Median expansion rate was higher in the descending than the ascending group (2.0 mm/year [interquartile range, 0.9-3.2 mm/year] vs 0.2 mm/year [IQR, 0.1-0.6 mm/year]; P < .001). Aneurysm in the descending aorta and larger baseline maximal aortic diameter were independently associated with TAA expansion. Advanced age and chronic obstructive pulmonary disease but not aneurysm size or location were independently associated with overall mortality (P < .05). Aneurysm in the descending aorta was associated with aortic-related events (P < .05). ConclusionsDegenerative TAAs under surveillance expand slowly. Descending TAA and larger baseline maximal aortic diameter were independently associated with more rapid TAA expansion, but these factors did not influence all-cause mortality.

Single vs Serial Assessments of Arterial Hemodynamics to Predict Thoracic Aortic Aneurysm Expansion

BackgroundThoracic aortic aneurysm (TAA) is a highly morbid disease. We have previously shown that baseline hemodynamic measures reflecting aortic function are associated with future TAA expansion. However, whether serial arterial hemodynamic assessment further improves TAA growth assessment remains unknown. Therefore, we aimed to compare single vs serial arterial hemodynamic assessments in the evaluation of future TAA growth. MethodsEighty-six unoperated participants with TAA underwent noninvasive arterial hemodynamic assessment using arterial tonometry and echocardiography at baseline and after 1 year. Aortic diameter was measured serially with the use of standard imaging modalities. Stepwise multivariable linear regression was used to assess associations of baseline and 1-year change (Δ) in arterial hemodynamic measures with TAA growth. ResultsMean age was 62.7 ± 11.0 years; 79% were male. Mean aneurysm growth was 0.48 ± 0.54 mm/year after a follow-up of 2.96 ± 1.03 years. Yearly changes in arterial hemodynamic measures ranged from −3.2% to +4.2%. Linear regression results showed that while baseline arterial hemodynamic measures were independently associated with aneurysm growth (carotid-femoral pulse wave velocity: β ± SE = 0.038 ± 0.013; aortic characteristic impedance: β ± SE = 0.002 ± 0.001; proximal aortic compliance: β ± SE = −0.011 ± 0.006; forward pressure wave amplitude: β ± SE 0.009 ± 0.002; reflected pressure wave amplitude: β ± SE = 0.017 ± 0.006; P < 0.05 for each), the 1-year Δ in these measures did not incrementally add to aneurysm growth assessment (P > 0.05 for each Δ). ConclusionsAlthough baseline measures of aortic function independently predict TAA expansion, 1-year changes in these measures do not improve this prediction. Thus, for TAA risk assessment purposes, a baseline assessment of aortic function may suffice, which simplifies its use for potential predictive algorithms.

Sex-specific role of estimated aortic pulse wave velocity in the prediction of future thoracic aortic aneurysm expansion

Thoracic aortic aneurysm (TAA) is a deadly disease mostly affecting men, but with worse outcomes in women. Further, we have shown that TAA expansion is faster in women than men, and that aortic stiffness (measured by carotid-femoral pulse wave velocity with arterial tonometry) better predicts TAA growth in women. Since aortic pulse wave velocity can be mathematically estimated (e-aPWV), we examined sex-specific effects of e-aPWV on TAA expansion.

Obstructive sleep apnoea and the progression of thoracic aortic aneurysm: a prospective cohort study

BackgroundObstructive sleep apnoea (OSA) is associated with an increased prevalence of aortic aneurysms and it has also been suggested that severe OSA furthers aneurysm expansion in the abdomen. We evaluated whether OSA is a risk factor for the progression of ascending thoracic aortic aneurysm (TAA).MethodsPatients with TAA underwent yearly standardised echocardiographic measurements of the ascending aorta over 3 years and two level III sleep studies. The primary outcome was the expansion rate of TAA in relation to the apnoea–hypopnoea index (AHI). Secondary outcomes included surveillance for aortic events (composite end-points of rupture/dissection, elective surgery or death).ResultsBetween July 2014 and March 2020, 230 patients (median age 70 years, 83.5% male) participated in the cohort. At baseline, 34.8% of patients had AHI ≥15 events·h−1. There was no association between TAA diameter and AHI at baseline. After 3 years, mean±sdexpansion rates were 0.55±1.25 mm at the aortic sinus and 0.60±1.12 mm at the ascending aorta. In the regression analysis, after controlling for baseline diameter and cardiovascular risk factors, there was strong evidence for a positive association of TAA expansion with AHI (aortic sinus estimate 0.025 mm, 95% CI 0.009–0.040 mm; p&lt;0.001 and ascending aorta estimate 0.026 mm, 95% CI 0.011–0.041 mm; p=0.001). 20 participants (8%) experienced an aortic event; however, there was no association with OSA severity.ConclusionOSA may be a modest but independent risk factor for faster TAA expansion and thus potentially contributes to life-threatening complications in aortic disease.

Role of estimated aortic pulse wave velocity in the prediction of future thoracic aortic aneurysm expansion

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

ESTIMATED AORTIC PULSE WAVE VELOCITY PREDICTS FUTURE THORACIC AORTIC ANEURYSM EXPANSION: RESULTS FROM A PROSPECTIVE COHORT STUDY WITH SEX-SPECIFIC ANALYSES

Thoracic aortic aneurysm (TAA) is a disease of increasing prevalence and associated with high morbidity and mortality. As such, novel, clinically useful strategies for risk assessment and medical management of TAA are critically needed. We have previously shown that aortic stiffness (measured by carotid-femoral pulse wave velocity, cfPWV) independently predicts future TAA growth. Since aortic pulse wave velocity can be mathematically estimated based on age and blood pressure (e-PWV), obviating the need for equipment and increasing clinical applicability, we sought to determine the predictive role of e-PWV on future TAA expansion.

SINGLE VS. SERIAL ASSESSMENTS OF ARTERIAL HEMODYNAMICS TO PREDICT THORACIC AORTIC ANEURYSM EXPANSION

Thoracic aortic aneurysm (TAA) is a disease with high morbidity and mortality. We have previously shown that hemodynamic measures reflecting aortic function (AFx) predict future TAA expansion. However, whether serial assessment of AFx further improves TAA growth prediction remains unknown. Thus, we

MEASURES OF AORTIC STIFFNESS, CENTRAL BLOOD PRESSURE AND PULSATILE ARTERIAL LOAD PREDICT FUTURE ANEURYSM EXPANSION

Thoracic aortic aneurysm (TAA) is a disease of increasing prevalence and associated with high morbidity and mortality. As such, novel, clinically useful stcArategies for risk assessment and medical management of TAA are critically needed. To address this need, we sought to determine the predictive role of aortic stiffness and pulsatile arterial load (which reflect the aorta’s health and function) on future TAA expansion. One hundred and six consecutive, unoperated subjects with TAA were recruited. By combining arterial tonometry with echocardiography using validated methods, we estimated measures of aortic stiffness, central blood pressure (BP), steady and pulsatile arterial load at baseline. Measures of aortic stiffness, central BP and pulsatile arterial load correlate directly with aortic health and function, while measures of steady arterial load reflect resistive load from peripheral arteries instead. Aneurysm size was measured at baseline and follow-up with imaging and indexed to height. TAA growth was calculated in (mm/m)/year. Stepwise multivariable linear regression assessed associations of baseline arterial stiffness and load measures, in separate models, with aneurysm growth. Variables considered in the models were: age, sex, BSA, mean arterial pressure, baseline aneurysm size, aneurysm etiology and location, follow-up time, concordant/discordant nature of the imaging modalities and history of hypertension, diabetes and smoking. Interaction terms for age, sex, and aneurysm etiology with each hemodynamic measure were tested in the models. Seventy five percent of subjects were men. Mean±SD age, baseline aneurysm size and follow-up time were 62.8±11.4 years, 46.5±3.9 mm and 2.3±0.9 years, respectively. Aneurysm growth rate was 0.34±0.36 mm/year in men and 0.73±0.84 mm/year in women (P=0.040). Results of the linear regression models are summarized in the Table. Measures of aortic stiffness, central BP and pulsatile arterial load independently predicted future aneurysm expansion. Conversely, brachial BP and steady arterial load did not. None of the interaction terms were significant, suggesting that results are equally applicable to all ages, both sexes, and all TAA etiologies. Potential applications of our findings are summarized in the Figure. Measures of aortic function, including aortic stiffness and pulsatile hemodynamics, independently predict future TAA growth and provide novel insights into disease activity. Moreover, some of the hemodynamic measures were superior to baseline aneurysm size (which is the standard for clinical assessment) in the prediction of future aneurysm expansion. Our findings demonstrate a potential role for non-invasive hemodynamic assessment as a means to better predict TAA disease activity and refine risk stratification in patients with TAA.View Large Image Figure ViewerDownload Hi-res image Download (PPT)

P5604Combining aortic size with measures of aortic stiffness and pulsatile hemodynamics enhances prediction of future thoracic aortic aneurysm expansion

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

Sex Differences in Thoracic Aortic Aneurysm Growth.

Women with thoracic aortic aneurysms (TAAs) have higher risk of acute aortic syndromes and death than men. We have shown that TAA growth is accelerated in women, helping explain the sex differences in TAA outcomes. Since aortic stiffness reflects the health of the aorta, we sought to determine the sex-specific role of aortic stiffness on TAA growth. One hundred thirty unoperated people with TAA were recruited. Maximal aneurysm size at the oldest and latest imaging studies was measured to calculate TAA growth rate. Aortic stiffness was assessed by carotid-femoral pulse wave velocity (cfPWV) using applanation tonometry. Multivariable linear regression adjusted for confounders assessed the association of cfPWV with TAA growth. Seventy-three percent of subjects were men. Mean±SD age, baseline aneurysm size, follow-up time, and cfPWV were 62.5±11.5 years, 45.3±4.0 mm, 3.3±3.0 years and 9.6±3.5 m/s, and not different based on sex. TAA growth rate was 0.96±1.00 mm/y in women and 0.45±0.58 mm/y in men ( P=0.006). In the whole group, cfPWV was independently associated with TAA growth (β±SE: 0.06±0.02, P=0.02). However, in sex-specific analyses cfPWV was independently associated with faster aneurysm growth in women (β±SE: 0.21±0.09, P=0.03), but not in men (β±SE: -0.002±0.02, P=0.94), with a significant sex×cfPWV interaction ( P<0.0001). In patients with TAA, aneurysm growth is more than twice as fast in women than men, and aortic stiffness is associated with greater TAA growth in women, but not in men. Our findings highlight greater aortic stiffness as an important correlate of TAA expansion in women.

SEX DIFFERENCES IN THORACIC AORTIC ANEURYSM GROWTH: ROLE OF AORTIC STIFFNESS

Thoracic Aortic Aneurysm (TAA) is a deadly disease, affecting adults of all ages. Presently, the only parameter available for risk prediction is TAA size. However, many individuals suffer an aortic dissection with aneurysms that are smaller than guideline-based cutoffs for repair. Further, women with thoracic aortic aneurysms (TAAs) have faster aneurysm growth and greater risk of acute aortic syndromes and death than men. Since the stiffness of the aorta reflects the health of its wall, we hypothesized that aortic stiffness would be independently associated with TAA growth, and that sex would significantly modify this association. One hundred and thirty unoperated TAA subjects were recruited. Maximal aneurysm size at the oldest and latest imaging studies was measured; aneurysm growth rate was calculated as mm/year. Aortic stiffness was assessed by carotid-femoral pulse wave velocity (cfPWV) using applanation tonometry. Unadjusted and multivariable linear regression analyses assessed the association of cfPWV with TAA growth. Models were adjusted for age, sex, body size, aneurysm etiology and location, baseline aneurys size, follow-up time, mean arterial pressure, history of hypertension, diabetes and smoking, and concordant/ discordant nature of the imaging modality. We also tested the interaction term sex*cfPWV in the prediction of TAA growth. Seventy four percent of subjects were men. Mean±SD age, baseline aneurysm size and follow-up time were 62.9±11.8 years, 45.3±4.0 mm and 3.3±3.0 years, respectively, and not different by sex. cfPWV was 9.8±4.3 m/s in women and 9.5±3.2 m/s in men (P=0.70). TAA growth rate was 1.0±1.0 mm/year in women and 0.4±0.6 mm/year in men (P=0.006). Unadjusted regression results are depicted in the Figure. In multivariable linear regression, cfPWV was independently associated with TAA growth (β±SE for 1 m/s increase in cfPWV: 0.06±0.02, P=0.02). Other independent predictors of faster aneurysm growth were female sex and longer follow-up time (P<0.05 for each), but not baseline aneurysm size (P=0.28). The sex*cfPWV interaction term was significant (P<0.0001), thus sex-specific models were performed. cfPWV was independently associated with faster aneurysm growth in women (β±SE: 0.21±0.09, P=0.03), but not in men (β±SE: -0.001±0.024, P=0.94). Among TAA patients, higher aortic stiffness is independently associated with faster aneurysm growth, and findings are specific to women. Our findings highlight poorer aortic wall health, reflected by greater aortic stiffness, as a potential mechanism for TAA expansion, especially in women. Aortic stiffness assessment may represent a future target for TAA-related risk stratification, monitoring and therapeutics aimed at containing TAA growth.

113 Is obstructive sleep apnea (OSA) a risk factor for the progression of thoracic aortic aneurysm (TAA)?

Introduction: Care of aortic aneurysms (AA) consists of regular imaging follow-up and managing cardiovascular risk factors. OSA has been proposed to be associated with accelerated expansion of abdominal AA in observational studies. The purpose of this ongoing study is to evaluate whether OSA has an influence on the progression of thoracic aortic aneurysm (TAA). Methods: In total, 340 people with known TAA are to be included in this prospective, observational study. In women the TAA is defined as aortic diameter > 39mm at the level of Sinus valsalvae and >42mm at the level of the ascending aorta. The values for men are >44mm and >46 mm, respectively. Each participant undergoes a home sleep study at baseline and at the 3-year follow-up. OSA is defined as Apnea-Hypopnea-Index (AHI) ≥ 5/h, and its severity classified into mild, moderate or severe according to the guidelines by the American Academy of Sleep Medicine (AASM). Each participant receives an annual TAA assessment by transthoracic echocardiography. The primary outcome is the yearly expansion rate of TAA in relation to OSA severity. The secondary outcomes encompass aortic events (ruptures, dissections), endovascular repairs and rapid progressions of TAA. Results: To date, 228 patients have been recruited, 20 patients have dropped out during follow-up and 5 have reached a secondary outcome (TAA surgery). Out of 203 still active participants, 148 have reached the first follow-up (1 year) and 88 the second one (2 years). In total, 12 patients were started on continuous positive air pressure therapy (CPAP) during follow-up - these were considered as a separate AHI category. The baseline characteristics are listed in table 1. The one-year progression rates were similar in all subgroups. After 2 years, the mean systolic TAA progression rate at Sinus valsalve (0.051 ± 0.107cm) was significantly greater in moderate-to-severe OSA (AHI≥15/h) than in participants with an AHI < 15/h (0.014 ± 0.098cm) or in the CPAP subgroup (-0.003 ± 0.055cm). A similar trend was observed for the ascending aorta. Conclusions: Moderate-to-severe OSA seems to increase the TAA expansion rate at the level of Sinus valsalvae, whereas CPAP seems to be an effective countermeasure. It might therefore be beneficial to routinely screen and treat for OSA in the management of TAA.Table 1Population CharacteristicsPopulation CharacteristicsFeatureTotal (203 participants)2nd follow-up at +2 years (88 partcipants)N%N%Males168(82.76%)74(84.09%)Smokers and Ex-Smokers117(57.64%)46(52.27%)Arterial Hypertension151(74.38%)62(70.46%)Diabetes Mellitus13(6.4%)6(6.81%)Adipositas36(17.73%)17(19.32%)Dyslipidemia115(56.65%)48(54.55%)Stroke28(13.79%)17(19.32%)Coronary Heart Disease46(22.66%)20(22.73%)Other know Aneurysms8(3.94%)2(2.27%)Chronic Obstructive Pulmonary Disease13(6.4%)5(5.68%)Atrial Fibrillation45(22.17%)20(22.73%)Renal Failure22(10.84%)11(12.50%)Family History of Vascular Incidents47(23.15%)28(31.82%)Family History of Aortic Aneurysms20(9.85%)8(0.09%)AHI < 577(37.93%)29(32.96%)AHI 5-1561(30.05%)27(30.68%)AHI 15-3040(19.7%)14(15.91%)AHI > 3025(12.32%)9(10.23%)CPAP12(5.91%)9(10.23%) Open table in a new tab

Expansion rate of descending thoracic aortic aneurysms.

Surveillance is mandatory for all patients with a thoracic aortic aneurysm (TAA). The frequency of surveillance imaging, however, is not evidence-based, as few data exist regarding TAA growth rates. This study aimed to determine the rate of TAA expansion and to inform surveillance intervals based on TAA diameter. Patients with a TAA for whom morphological data were available from serial CT scans were studied. Annualized growth rates based on diameter at presentation and time taken to reach a theoretical intervention threshold of 55 mm were calculated. The number of patients who would have achieved the threshold undetected was determined based on simulated imaging intervals of 6 months, 1, 2 and 3 years. A total of 2916 scans from 995 patients were analysed. The mean aortic expansion rate was 2·76 mm per year for all patients, with an exponential increase observed at sizes above 45 mm. Only 3·9 per cent of patients with a starting diameter of 30-39 mm and 5·3 per cent of those with a diameter of 40-44 mm achieved threshold size within 2 years. Conversely, the probability of expansion to more than 55 mm was 74·5 per cent in 2 years for patients with a starting diameter of 50-54 mm, rising to 85·7 per cent at 3 years. Based on a threshold of 55 mm for intervention, most patients with a maximum aortic diameter below 40 mm could safely undergo surveillance at 2-yearly intervals. Above 45 mm, annual surveillance is recommended. Patients with a diameter greater than 50 mm could be optimized for possible repair, if this is clinically appropriate.

Systematic Review of the Growth Rates and Influencing Factors in Thoracic Aortic Aneurysms

The growth rates of thoracic aortic aneurysms (TAAs) and factors influencing their expansion are poorly understood. This study aimed to review systematically published literature describing TAA expansion and examine factors that may be associated with this. A comprehensive search of MEDLINE and Embase databases was performed until 30 April 2015. Studies describing rates of TAA growth were identified and systematically reviewed. Outcomes of interest were TAA growth rates and associated factors. Study quality was assessed using Scottish Intercollegiate Guidelines Network quality checklists for cohort studies. Eleven publications, involving 1383 patients, met the eligibility criteria and were included in the review. Included studies were generally low in quality. Aneurysm measurement and growth-rate estimation techniques were inconsistently reported. Mean growth rates for all TAAs ranged from 0.2 to 4.2 mm/year. Mean growth rates for ascending and aortic arch aneurysms ranged from 0.2 to 2.8 mm/year, while those for descending and thoracoabdominal aneurysms ranged from 1.9 to 3.4 mm/year in studies reporting according to anatomical location. Large aneurysm size, distal aneurysm locations, presence of Marfan's syndrome, and bicuspid aortic valve were consistently associated with accelerated TAA growth. Presence of chronic dissection and chronic obstructive pulmonary disorder were also implicated as risk factors for faster TAA growth. Associations between medical comorbidity and aneurysm expansion were conflicting. Previous aortic surgery and anticoagulants were reported to have a protective effect on aneurysm growth in two studies. There is a shortfall in the understanding of TAA expansion rates. Existing studies are heterogeneous in methodology and reported outcomes. Identified unifying themes suggest that TAAs grow at a slow rate with large presenting diameter, distal aneurysm, and history of bicuspid aortic valve or Marfan's syndrome serving as main risk factors for accelerated aneurysm growth. High-quality studies with a standardised approach to TAA growth assessment are required.

Thoracic aortic aneurysm expansion due to late distal stent graft-induced new entry.

This study analyzed the mechanism and risk factors of thoracic aortic aneurysm expansion due to late distal stent graft-induced new entry (dSINE). This late complication of thoracic endovascular aneurysm repair (TEVAR) for aortic dissection is under-recognized but potentially life-threatening. In 142 patients who underwent TEVAR with endovascular entry sealing for acute and chronic aortic type B dissection, using commercially available straight (nontapered) stent-grafts, we examined the oversizing rate, the aortic taper ratio, and the need for reintervention. Nine of 142 patients developed thoracic aortic aneurysm expansion due to dSINE after TEVAR. The median follow-up was 47.5 ± 37.4 months. There was a significant difference in the distal stent-aorta angle between the patients with and without dSINE (149.08 ± 15.09° vs. 166.72 ± 12.47°, P < 0.005). Patients with dSINE showed a significantly higher taper ratio of the true lumen of the aorta (40.9 ± 14.13% vs. 25.36 ± 20.2%, P < 0.05). There was also a significant difference in the oversizing of the stent-graft in the distal landing zone (95.88 ± 49.3% vs. 55.94 ± 36.23%, P < 0.01). All patients with dSINE underwent a secondary endograft procedure without any complications or deaths. In 7 cases we used a custom-made, highly tapered stent-graft. Lifelong follow-up of patients is mandatory after TEVAR. A stent-graft with a tapered design should be used in aortic dissection to avoid oversizing and devastating late complications.

Prediction of thoracic aortic aneurysm expansion: validation of formulae describing growth

Background. The expansion rate of thoracic aortic aneurysms may be an important and clinically relevant index of the risk of rupture. The aims of this study were to assess the validity of three published exponential equations that predict expansion rate in a separate sample population, and to calculate an expansion rate formula for this cohort of patients. Methods. We studied 88 consecutive patients undergoing serial computed tomographic or magnetic resonance imaging scanning to monitor thoracic aortic aneurysm progression. In interval scans of at least 6 months, we measured minimum coronal aortic diameter at seven set levels and maximal diameter, yielding 780 segment-intervals. Results. The linear expansion rate (mean 2.6 mm/year) increased with incremental aortic diameter (aortic diameter <40 mm: 2.0; 40–49 mm: 2.3; 50–59 mm: 3.6; ≥60 mm: 5.6 mm/year; p < 0.01). Regression analysis showed close correlation between predicted and sample data, but there were significant differences between observed and expected measurements. The Yale formula underestimated growth by 0.8 mm, while Mt. Sinai and Osaka formulae overestimated actual change by 1.5 and 0.2 mm, respectively. The expansion rate derived from our population was: last diameter = initial diameter × e (0.00367 × time) ( r = 0.617). Conclusions. Although formulae derived from one thoracic aortic aneurysm sample population may not extrapolate exactly to others, there is close concordance of results for patient populations in three different continents.