Carotid artery vasoreactivity correlates with abdominal aortic vasoreactivity in young healthy individuals but not in patients with abdominal aortic aneurysm

BACKGROUND: Sympathetic stimulation of central arteries, such as coronary and carotid arteries, cause vasodilation in healthy subjects, but vasoconstriction in those with increased cardiovascular risk. This study compared vasoreactivity to sympathetic stimulation between abdominal aorta and carotid artery in healthy young individuals (young group, n = 20), in patients with abdominal aortic aneurysm (AAA group, n = 20) and in a healthy older group, age- and gender matched with AAA group (matched group, n = 18). METHOD: All subjects underwent cold pressor test, while performing concomitantly duplex ultrasound of abdominal aorta and carotid artery vasoreactivity. Observer-independent software was used to analyze and calculate magnitude and timing of maximum vasodilation or vasoconstriction. Pearson's correlation coefficient was calculated to investigate vasoreactivity between arteries. RESULTS: Carotid artery reactivity [Interquartile range 25%, Interquartile range 75%] did not significantly differ between the young, matched and AAA group (3.5% [1.4, 4.7], 2.6% [2.0, 4.1] and 2.2% [-1.9, 3.7], respectively, p = 0.301). Abdominal aortic responsiveness demonstrated larger differences between young (4.9% [-0.2, 8.4]), matched (3.3% [-2.5, 4.4]) and individuals with AAA (0.5% [-3.9, 4.1], p = 0.059). Pooled analysis showed a significant correlation between carotid and abdominal aortic vasoreactivity (r = 0.444, p = 0.001). Subgroup analyses demonstrated significant correlation between both arteries in young (r = 0.636, p = 0.003), but not matched (r = −0.040, p = 0.866) or AAA group (r = 0.410, p = 0.129). CONCLUSIONS: Sympathetic stimulation induces powerful vasodilation of the carotid artery and abdominal aorta, which is significantly correlated in healthy individuals. No such correlation is present in abdominal aortic aneurysm patients. This suggests the aneurysm alters local abdominal aorta vasoreactivity, but not the carotid artery

Changes in Noninvasive Arterial Stiffness and Central Blood Pressure After Endovascular Abdominal Aneurysm Repair

Purpose: To evaluate the impact of elective endovascular aneurysm repair (EVAR) on the carotid-femoral pulse wave velocity (cfPWV) and central pressure waveform, through 1-year follow-up. Materials and Methods: A tonometric device was used to measure cfPWV and estimate the central pressure waveform in 20 patients with an infrarenal abdominal aortic aneurysm scheduled for elective EVAR. The evaluated central hemodynamic parameters included the central pressures, the augmentation index (AIx), and the subendocardial viability ratio (SEVR). AIx quantifies the contribution of reflected wave to the central systolic pressure, whereas SEVR describes the myocardial perfusion relative to the cardiac workload. Measurements were performed before EVAR, at discharge, and 6 weeks and 1 year after EVAR. Results: CfPWV was increased at discharge (12.4±0.4 vs 11.3±0.5 m/s at baseline; p=0.005) and remained elevated over the course of 1-year follow-up (6 weeks: cfPWV = 12.2±0.5 m/s; 1 year: cfPWV = 12.2±0.7 m/s, p<0.05). After an initial drop in systolic central pressure at discharge, all the central pressures increased thereafter up to 1 year, without significant differences compared with baseline. The same was observed for the AIx and SEVR. Conclusion: Endovascular aortic aneurysm repair caused an increase in pulse wave velocity compared with baseline, which remained elevated through 1 year follow-up, which may be related to an increased cardiovascular risk. However, no differences in central pressure, augmentation index, and subendocardial viability ration were observed during follow-up

Major adverse cardiac events after elective infrarenal endovascular aortic aneurysm repair

Objective: There is a significant cardiac morbidity and mortality after endovascular aneurysm repair (EVAR). However, information about long-term risk of cardiac events after EVAR and potential predictors is lacking. Therefore, the aim of this study was to determine incidence and predictors of major adverse cardiac events (MACE) at 1 and 5 years after elective EVAR for infrarenal abdominal aortic aneurysms. Methods: Baseline, perioperative, and postoperative information of 320 patients was evaluated. The primary outcome was the incidence of MACE after EVAR, which was defined as acute coronary syndrome, unstable angina pectoris, de novo atrial fibrillation, hospitalization for heart failure, mitral valve insufficiency, revascularization (including percutaneous coronary intervention and coronary artery bypass grafting), as well as cardiovascular and noncardiovascular death. Kaplan-Meier analyses were performed to determine incidences of MACE, MACE excluding noncardiovascular death and cardiac events by excluding noncardiovascular and vascular death from MACE. Predictors of MACE were identified using univariate and multivariate binary regression analysis. Results: Through 1 and 5 years of follow-up after EVAR, freedom from MACE was 89.4% (standard error [SE], 0.018) and 59.8% (SE, 0.033), freedom from MACE excluding noncardiovascular death was 94.7% (SE, 0.013) and 77.5% (SE, 0.030) and freedom from cardiac events was 96.0% (SE, 0.011) and 79.1% (SE, 0.030), respectively. Predictors for MACE within 1 year were American Society of Anesthesiologists (ASA) score of III or IV (odds ratio [OR], 3.17; 95% confidence interval [CI], 1.52-6.59) and larger abdominal aortic diameter (OR, 1.04; 95% CI, 1.01-1.08). A history of atrial fibrillation (OR, 0.14; 95% CI, 0.03-0.60) was a negative predictor factor. Predictors for MACE through 5 years were a history of heart failure (OR, 4.10; 95% CI 1.36-12.32) and valvular heart disease (OR, 2.31; 95% CI, 0.97-5.51), American Society of Anesthesiologists score of 3 or 4 (OR, 1.66; 95% CI, 0.96-2.88), and older age (OR, 1.04; 95% CI, 1.01-1.08). Conclusions: MACE is a common complication during the first 5 years after elective EVAR. Cardiac diseases at baseline are strong predictors for long-term MACE and potentially helpful in optimizing future postoperative long-term follow-up

A systematic review summarizing local vascular characteristics of aneurysm wall to predict for progression and rupture risk of abdominal aortic aneurysms

Objective: At present, the rupture risk prediction of abdominal aortic aneurysms (AAAs) and, hence, the clinical decision making regarding the need for surgery, is determined by the AAA diameter and growth rate. However, these measures provide limited predictive information. In the present study, we have summarized the measures of local vascular characteristics of the aneurysm wall that, independently of AAA size, could predict for AAA progression and rupture. Methods: We systematically searched PubMed and Web of Science up to September 13, 2021 to identify relevant studies investigating the relationship between local vascular characteristics of the aneurysm wall and AAA growth or rupture in humans. A quality assessment was performed using the ROBINS-I (risk of bias in nonrandomized studies of interventions) tool. All included studies were divided by four types of measures of arterial wall characteristics: metabolism, calcification, intraluminal thrombus, and compliance. Results: A total of 20 studies were included. Metabolism of the aneurysm wall, especially when measured by ultra-small superparamagnetic iron oxide uptake, and calcification were significantly related to AAA growth. A higher intraluminal thrombus volume and thickness had correlated positively with the AAA growth in one study but in another study had correlated negatively. AAA compliance demonstrated no correlation with AAA growth and rupture. The aneurysmal wall characteristics showed no association with AAA rupture. However, the metabolism, measured via ultra-small superparamagnetic iron oxide uptake, but none of the other measures, showed a trend toward a relationship with AAA rupture, although the difference was not statistically significant. Conclusions: The current measures of aortic wall characteristics have the potential to predict for AAA growth, especially the measures of metabolism and calcification. Evidence regarding AAA rupture is scarce, and, although more work is needed, aortic wall metabolism could potentially be related to AAA rupture. This highlights the role of aortic wall characteristics in the progression of AAA but also has the potential to improve the prediction of AAA growth and rupture

Effect of Different EndoAnchor Configurations on Aortic Endograft Displacement Resistance: An Experimental Study

Purpose: This study investigated the effect of different EndoAnchor configurations on aortic endograft displacement resistance in an in vitro model. Materials and Methods: An in vitro model was developed and validated to perform displacement force measurements on different EndoAnchor configurations within an endograft and silicone tube. Five EndoAnchor configurations were created: (1) 6 circumferentially deployed EndoAnchors, (2) 5 EndoAnchors within 120° of the circumference and 1 additional, contralateral EndoAnchor, (3) 4 circumferentially deployed EndoAnchors, (4) 2 rows of 4 circumferentially deployed EndoAnchors, and (5) a configuration of 2 columns of 3 EndoAnchors. An experienced vascular surgeon deployed EndoAnchors under C-arm guidance at the proximal sealing zone of the endograft. A constant force with increments of 1 newton (N) was applied to the distal end of the endograft. The force necessary to displace a part of the endograft by 3 mm was defined as the endograft displacement force (EDF). Two video cameras recorded the measurements. Videos were examined to determine the exact moment 3-mm migration had occurred at part of the endograft. Five measurements were performed after each deployed EndoAnchor for each configuration. Measurements are given as the median and interquartile range (IQR) Q1, Q3. Results: Baseline displacement force measurement of the endograft without EndoAnchors resulted in a median EDF of 5.1 N (IQR 4.8, 5.2). The circumferential distribution of 6 EndoAnchors resulted in a median EDF of 53.7 N (IQR 49.0, 59.0), whereas configurations 2 through 5 demonstrated substantially lower EDFs of 29.0 N (IQR 28.5, 30.1), 24.6 N (IQR 21.9, 27.2), 36.7 N, and 9.6 N (IQR 9.4, 10.0), respectively. Decreasing the distance between the EndoAnchors over the circumference of the endograft increased the displacement resistance. Conclusion: This in vitro study demonstrates the influence EndoAnchor configurations have on the displacement resistance of an aortic endograft. Parts of the endograft where no EndoAnchor has been deployed remain sensitive to migration. In the current model, the only configuration that rivaled a hand-sewn anastomosis was the one with 6 EndoAnchors. A circumferential distribution of EndoAnchors with small distances between EndoAnchors should be pursued, if possible. This study provides a quantification of different EndoAnchor configurations that clinicians may have to adopt in clinical practice, which can help them make a measured decision on where to deploy EndoAnchors to ensure good endograft fixation

Effect of abdominal aortic endoprostheses on arterial pulse wave velocity in an in vitro abdominal aortic flow model

OBJECTIVE Aortic pulse-wave-velocity (aPWV) is a measure for arterial stiffness, which is associated with increased cardiovascular risk. Recent evidence suggests aPWV increases after endograft-placement for aortic aneurysms. The aim of this study was to investigate the influence of different aortic endoprostheses on aPWV and structural stiffness in vitro. Approach: Three different abdominal aortic endoprostheses (AFX, Endurant II, and Nellix) were implanted in identical silicone aneurysm models. One model was left untreated, and another model contained an aortic tube graft (Gelweave). The models were placed in an in vitro flow set-up that mimics physiological flow. aPWV was measured as the transit time of the pressure wave over the flow trajectory of the suprarenal to iliac segment. Structural stiffness corrected for lumen diameter was calculated for each model. Results: aPWV was significantly lower for the control compared to the AFX, Endurant, Nellix and tube graft models (13.00±1.20, 13.40±1.17, 18.18±1.20, 16.19±1.25 and 15.41±0.87m/s, respectively (P<0.05)). Structural stiffness of the AFX model was significant lower compared to the control model (4718N/m versus 5115N/m (P<0.001), respectively), whereas all other models showed higher structural stiffness. Significance: Endograft placement resulted in a higher aPWV compared to a non-treated aortic flow model. All models showed increased structural stiffness over the flow trajectory compared to the control model, except for the AFX endoprosthesis. Future studies in patients treated with an endograft are needed to evaluate the current results in vivo