By convention, the ascending aorta is measured by echo from leading edge to leading edge. “Leading edge” connotes the edge of the aortic wall that is closest to the probe (at the top of the inverted “V” of the ultrasound image). By transthoracic echo (TTE), the leading edges are the outer anterior wall and inner posterior wall. By transesophageal echo (TEE), the leading edges are the outer posterior wall and inner anterior wall. Aortic measurements should be taken (by convention) in diastole (when the aorta is moving least). Simple TTE is 70 to 85% sensitive in diagnosing ascending aortic dissection. TEE sensitivity approaches 100%, though the tracheal carina imposes a blind spot on TEE, impeding visualization of distal ascending aorta and proximal aortic arch. While computed tomography angiography may be superior for defining full anatomic extent of aortic dissection, echocardiography is superior in assessing functional consequences such as mechanism and severity of aortic regurgitation, evidence of myocardial ischemia when complicated by coronary dissection, or evidence of tamponade physiology when pericardial effusion is present. Reverberation artifact can mimic a dissection flap. A true flap moves independently of the outer aortic wall which can be confirmed by M-mode. Color flow respects a true flap but does not respect a reverberation artifact. Assessment for bicuspid aortic valve (BAV) morphology should be done in systole, not diastole. In diastole, when the valve is closed, the raphé can make a bicuspid valve appear trileaflet. Doming in the parasternal long axis (PLAX) view and an eccentric closure line on PLAX M-mode should also raise suspicion for BAV.

Arteriovenous fistulae (AVF) fail to mature in female patients compared with male patients, leading to inferior outcomes and decreased utilization. As our mouse AVF model recapitulates sex differences in human AVF maturation, we hypothesized that sex hormones mediate these differences during AVF maturation. C57Bl/6 mice (9-11 week) underwent aortocaval AVF surgery and gonadectomy. AVF hemodynamics were measured via ultrasound (days 0-21). Blood was collected for FACS, and tissue for immunofluorescence and ELISA (days 3,7); wall thickness was assessed using histology (day 21). Inferior vena cava (IVC) shear stress was higher in male mice (p=0.0028) after gonadectomy, and they had increased wall thickness (22.0 ± 1.8 um vs. 12.7 ± 1.2; p<0.0001). Conversely, females had decreased thickness (6.8 ± 0.6 um vs. 15.3 ± 0.9; p=0.0002). Intact females had higher proportions of circulating CD3+ T cells on day 3 (p=0.0043), CD4+ (p=0.0003) and CD8+ T cells (p=0.005) on day 7, and CD11b+ monocytes on day 3 (p = 0.0046). After gonadectomy, these differences disappeared. In the fistula wall of intact female mice, CD3+ T cells (p=0.025), CD4+ T cells (p=0.0178), CD8+ T cells (p=0.0571), and CD68+ macrophages (p=0.0078) increased in the fistula wall on day 3 and 7. This disappeared after gonadectomy. Further, female mice had higher IL-10 (p=0.0217) and TNF-α levels (p=0.0417) in their AVF walls than males. Sex hormones mediate AVF maturation and suggest that hormone receptor signaling may be a target to improve AVF maturation.

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Background: Arteriovenous fistulae (AVF) fail to mature, that is dilate and thicken, in women more than in men, leading to inferior outcomes and decreased utilization in women. As our mouse AVF model recapitulates human AVF maturation, including decreased maturation and patency in female mice, we hypothesize that sex hormones mediate sex differences during AVF maturation. Methods: C57Bl/6 mice (9-11 months) were treated with sham or aortocaval AVF surgery; some were pretreated with gonadectomy 1 week prior to surgery. AVF diameter was measured via ultrasound (days 0-21). Blood was collected for FACS, and tissue examined using immunofluorescence or ELISA (days 3,7); wall thickness was assessed using histology (day 21). Results: At baseline, female and male mice had similar inferior vena cava (IVC) diameter (p=0.611) and wall thickness (p=0.491). After AVF creation, female mice had increased normalized IVC diameter (p=0.0012), flow velocity (p=0.0013), and shear stress (p=0.002; days 3-21; n=10); however, there was no difference in wall thickness (female, 15.8±0.2 um; male, 12.4±2.3 um; p=0.638; n=10). There were also increased circulating CD11b+ macrophages in female compared with male mice (31.8 ± 4.0% vs 18.7 ± 1.9%; p=0.001; day 3; n=22) and CD4+ T cells (57.9 ± 2.9% vs 34.5 ± 6.1%, p=0.0001). In the AVF wall there were increased CD45+ cells on immunofluorescence in females (22.5 ± 1.5 cells/hpf vs 13 ± 2 cells/hpf, p=0.063; day 3; n=4) as well as increased IL-10 immunoreactivity (3.98 ± 0.44 ng/ug vs 2.49 ± 0.47 ng/ug; p=0.076). In mice with gonadectomy, baseline IVC diameter, velocity, and shear stress were similar between female and male mice. After gonadectomy, male mice had increased AVF wall thickness than intact males (24.2 ± 1.6 um vs 12.4 ± 2.3; p=0.014); conversely, female mice had decreased thickness than intact females (6.1 ± 0.6 um vs 15.8 ± 0.2; p=0.005). There was loss of differences among circulating immune cells after gonadectomy (CD11b, p=0.0882; CD4, p=0.7095). Conclusions: Sex differences in hemodynamics and inflammation are present during venous remodeling, whereas these differences disappear after gonadectomy. Sex hormones mediate AVF maturation and suggest that hormone receptor signaling may be a target to improve AVF maturation.

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