Computational fluid dynamicaccuracy in mimicking changes in blood hemodynamics in patients with acute type IIIb aortic dissection treated with TEVAR

Background: We aimed to verify the accuracy of the Computational Fluid Dynamics (CFD) algorithm for blood flow reconstruction for type IIIb aortic dissection (TBAD) before and after thoracic endovascular aortic repair (TEVAR). Methods: We made 3D models of the aorta and its branches using pre- and post-operative CT data from five patients treated for TBAD. The CFD technique was used to quantify the displacement forces acting on the aortic wall in the areas of endograft, mass flow rate/velocity and wall shear stress (WSS). Calculated results were verified with ultrasonography (USG-Doppler) data. Results: CFD results indicated that the TEVAR procedure caused a 7-fold improvement in overall blood flow through the aorta (p = 0.0001), which is in line with USG-Doppler data. A comparison of CFD results and USG-Doppler data indicated no significant change in blood flow through the analysed arteries. CFD also showed a significant increase in flow rate for thoracic trunk and renal arteries, which was in accordance with USG-Doppler data (accuracy 90% and 99.9%). Moreover, we observed a significant decrease in WSS values within the whole aorta after TEVAR compared to pre-TEVAR (1.34 ± 0.20 Pa vs. 3.80 ± 0.59 Pa, respectively, p = 0.0001). This decrease was shown by a significant reduction in WSS and WSS contours in the thoracic aorta (from 3.10 ± 0.27 Pa to 1.34 ± 0.11Pa, p = 0.043) and renal arteries (from 4.40 ± 0.25 Pa to 1.50 ± 0.22 Pa p = 0.043). Conclusions: Post-operative remodelling of the aorta after TEVAR for TBAD improved hemodynamic patterns reflected by flow, velocity and WSS with an accuracy of 99%

Lower levels of Caveolin-1 and higher levels of endothelial nitric oxide synthase are observed in abdominal aortic aneurysm patients treated with simvastatin

This study was undertaken to verify whether simvastatin modulates Cav-1/eNOS expression, and if this modulation is associated with changes in pro- and anti-inflammatory cytokine and Toll-like receptor 4 (TLR4) level in abdominal aortic aneurysm (AAA). It is a 1:2 case-control study of non-statin (n=12) and simvastatin-treated patients (n=24) who underwent open AAA repair. Simvastatin treatment decreased Cav-1 (p0.05) and increased IL-10 concentration (p=0.055); however, TLR4 expression was unaffected, suggesting that simvastatin influences Cav-1 and eNOS in the AAA wall by other mechanisms. Simvastatin may modulate Cav-1 and eNOS expression in the aneurysmal wall, indicating a potentially beneficial role for statins in AAA patients

Comparing maximum diameter and volume when assessing the growth of small abdominal aortic aneurysms using longitudinal CTA data : cohort study

Background: Monitoring of abdominal aortic aneurysms (AAAs) is currently based on serial measurements of maximum aortic diameter. Additional assessment of aneurysm volume has previously been proposed to possibly improve growth prediction and treatment decisions. To evaluate the use of supplementing volume measurements, the authors aimed to characterise the growth distribution of AAA volume and to compare the growth rates of the maximum diameter and volume at the patient level. Methods: Maximum diameter and volume were monitored every 6 months in 84 patients with small AAAs, with a total of 331 computed tomographic angiographies (with initial maximum diameters of 30-68 mm). A previously developed statistical growth model for AAAs was applied to assess the growth distribution of volume and to compare individual growth rates for volume and for maximum diameter. Results: The median (25-75% quantile) expansion in volume was 13.4 (6.5-24.7) % per year. Cube root transformed volume and maximum diameter showed a closely linear association with a within-subject correlation of 0.77. At the surgery threshold maximum diameter of 55 mm, the median (25-75% quantile) volume was 132 (103-167) ml. In 39% of subjects, growth rates for volume and maximum diameter were equivalent, in 33% growth was faster in volume and in 27% growth was faster in maximum diameter. Conclusion: At the population level, volume and maximum diameter show a substantial association such that the average volume is approximately proportional to the average maximum diameter raised to a power of three. At the individual level, however, in the majority of patient's AAAs grow at different pace in different dimensions. Hence, closer monitoring of aneurysms with sub-critical diameter but suspicious morphology may benefit from complementing maximum diameter by volume or related measurements

Medicine / Does the choice of intraoperative fluid modify abdominal aneurysm repair outcomes? : A cohort analysis

Intraoperatively administered hydroxyethyl starch could be a risk indicator for postoperative acute kidney injury (AKI) in vascular surgical patients. In a single-center retrospective cohort analysis, we assessed the impact of hydroxyethyl starch and other risk indicators on AKI and mortality in 1095 patients undergoing elective open abdominal aneurysm repair (AAA-OR) or endovascular aortic repair (EVAR). We established logistic regression models to determine the effect of various risk indicators, including hydroxyethyl starch, on AKI, as well as Cox proportional hazard models to assess the effect on mortality. The use of intravenous hydroxyethyl starch was not associated with an increased risk of AKI or mortality. Patients undergoing EVAR were less likely to develop AKI (4% vs 18%). Multivariate risk indicators associated for AKI included suprarenal or pararenal aortic cross-clamp [odds ratio (OR), 4.44; 95% confidence interval (95% CI), 2.5387.784; P < .001] and procedure length (OR, 1.005; 95% CI, 1.0031.007; P < .001), and favored EVAR (OR, 0.351; 95% CI, 0.1180.654; P < .01). Main multivariate risk indicators associated with mortality included patients needing an urgent procedure [hazard ratio (HR), 2.294; 95% CI, 1.5413.413; P < .001], those with suprarenal or pararenal aortic cross-clamp (HR, 1.756; 95% CI, 1.2472.472; P < .01), and patients undergoing EVAR (HR, 1.654; 95% CI, 1.2922.118; P < .001). We found neither a benefit nor a negative effect of hydroxyethyl starch on the risk of AKI or mortality. Instead, other variables and comorbidities were found to be relevant for the development of postoperative AKI and survival. Nevertheless, clinicians should be aware of the high risk of postoperative AKI, particularly among those undergoing AAA-OR procedures.(VLID)489229

Alterations of the renin angiotensin system in human end-stage heart failure before and after mechanical cardiac unloading by LVAD support

Heart transplantation is often an unrealizable therapeutic option for end-stage heart failure, which is why mechanical left ventricular assist devices (LVADs) become an increasingly important therapeutic alternative. Currently, there is a lack of information about molecular mechanisms which are influenced by LVADs, particularly regarding the pathophysiologically critical renin angiotensin system (RAS). We, therefore, determined regulation patterns of key components of the RAS and the beta-arrestin signaling pathways in left ventricular (LV) tissue specimens from 8 patients with end-stage ischemic cardiomyopathy (ICM) and 12 patients with terminal dilated cardiomyopathy (DCM) before and after LVAD implantation and compared them with non-failing (NF) left ventricular tissue samples: AT1R, AT2R, ACE, ACE2, MasR, and ADAM17 were analyzed by polymerase chain reaction. ERK, phosphorylated ERK, p38, phosphorylated p38, JNK, phosphorylated JNK, GRK2, beta-arrestin 2, PI3K, Akt, and phosphorylated Akt were determined by Western blot analysis. Angiotensin I and Angiotensin II were quantified by mass spectrometry. Patients were predominantly middle-aged (53 +/- 10 years) men with severely impaired LV function (LVEF 19 +/- 8%), when receiving LVAD therapy for a mean duration of 331 +/- 317 days. Baseline characteristics did not differ significantly between ICM and DCM patients. By comparing failing with non-failing left ventricles, i.e., before LVAD implantation, a downregulation of AT1R, AT2R, and MasR and an upregulation of ACE, ACE2, GRK, beta-arrestin, ERK, PI3K, and Akt were seen. Following LVAD support, then angiotensin I, ACE2, GRK, and beta-arrestin were downregulated and AT2R, JNK, and p38 were upregulated. ACE, angiotensin II, AT1R, ADAM17, MasR, ERK, PI3K, and Akt remained unchanged. Some regulation patterns were influenced by the underlying etiology of heart failure, the severity of LV dysfunction at baseline, and the duration of LVAD therapy. Key components of the RAS and beta-arrestin signaling pathways were divergently altered in failing left ventricles both before and after LVAD implantation, whereas a remarkable fraction remained unchanged. This indicates a rather incomplete molecular reverse remodeling, whose functional relevance has to be further evaluated