Browsing by Subject "Aortic Diseases"

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    Drebrin regulates angiotensin II-induced aortic remodelling.
    (Cardiovascular research, 2018-11) Zhang, Lisheng; Wu, Jiao-Hui; Huang, Tai-Qin; Nepliouev, Igor; Brian, Leigh; Zhang, Zhushan; Wertman, Virginia; Rudemiller, Nathan P; McMahon, Timothy J; Shenoy, Sudha K; Miller, Francis J; Crowley, Steven D; Freedman, Neil J; Stiber, Jonathan A

    Aims

    The actin-binding protein Drebrin is up-regulated in response to arterial injury and reduces smooth muscle cell (SMC) migration and proliferation through its interaction with the actin cytoskeleton. We, therefore, tested the hypothesis that SMC Drebrin inhibits angiotensin II-induced remodelling of the proximal aorta.

    Methods and results

    Angiotensin II was administered via osmotic minipumps at 1000 ng/kg/min continuously for 28 days in SM22-Cre+/Dbnflox/flox (SMC-Dbn-/-) and control mice. Blood pressure responses to angiotensin II were assessed by telemetry. After angiotensin II infusion, we assessed remodelling in the proximal ascending aorta by echocardiography and planimetry of histological cross sections. Although the degree of hypertension was equivalent in SMC-Dbn-/- and control mice, SMC-Dbn-/- mice nonetheless exhibited 60% more proximal aortic medial thickening and two-fold more outward aortic remodelling than control mice in response to angiotensin II. Proximal aortas demonstrated greater cellular proliferation and matrix deposition in SMC-Dbn-/- mice than in control mice, as evidenced by a higher prevalence of proliferating cell nuclear antigen-positive nuclei and higher levels of collagen I. Compared with control mouse aortas, SMC-Dbn-/- aortas demonstrated greater angiotensin II-induced NADPH oxidase activation and inflammation, evidenced by higher levels of Ser-536-phosphorylated NFκB p65 subunits and higher levels of vascular cell adhesion molecule-1, matrix metalloproteinase-9, and adventitial macrophages.

    Conclusions

    We conclude that SMC Drebrin deficiency augments angiotensin II-induced inflammation and adverse aortic remodelling.
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    Fibroblast growth factor 23 is not associated with and does not induce arterial calcification.
    (Kidney international, 2013-06) Scialla, Julia J; Lau, Wei Ling; Reilly, Muredach P; Isakova, Tamara; Yang, Hsueh-Ying; Crouthamel, Matthew H; Chavkin, Nicholas W; Rahman, Mahboob; Wahl, Patricia; Amaral, Ansel P; Hamano, Takayuki; Master, Stephen R; Nessel, Lisa; Chai, Boyang; Xie, Dawei; Kallem, Radhakrishna R; Chen, Jing; Lash, James P; Kusek, John W; Budoff, Matthew J; Giachelli, Cecilia M; Wolf, Myles; Chronic Renal Insufficiency Cohort Study Investigators
    Elevated fibroblast growth factor 23 (FGF23) is associated with cardiovascular disease in patients with chronic kidney disease. As a potential mediating mechanism, FGF23 induces left ventricular hypertrophy; however, its role in arterial calcification is less clear. In order to study this, we quantified coronary artery and thoracic aorta calcium by computed tomography in 1501 patients from the Chronic Renal Insufficiency Cohort (CRIC) study within a median of 376 days (interquartile range 331-420 days) of baseline. Baseline plasma FGF23 was not associated with the prevalence or severity of coronary artery calcium after multivariable adjustment. In contrast, higher serum phosphate levels were associated with prevalence and severity of coronary artery calcium, even after adjustment for FGF23. Neither FGF23 nor serum phosphate were consistently associated with thoracic aorta calcium. We could not detect mRNA expression of FGF23 or its coreceptor, klotho, in human or mouse vascular smooth muscle cells, or normal or calcified mouse aorta. Whereas elevated phosphate concentrations induced calcification in vitro, FGF23 had no effect on phosphate uptake or phosphate-induced calcification regardless of phosphate concentration or even in the presence of soluble klotho. Thus, in contrast to serum phosphate, FGF23 is not associated with arterial calcification and does not promote calcification experimentally. Hence, phosphate and FGF23 promote cardiovascular disease through distinct mechanisms.
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    Primary aortoduodenal fistula caused by severe atherosclerosis, not by aneurysm.
    (The American journal of cardiovascular pathology, 1993-01) Gallagher, DM; Mendelson, T; Krupski, WC; Finkbeiner, WE
    Primary aortoduodenal fistula is an uncommon cause of massive upper gastrointestinal hemorrhage usually due to pressure erosion of an abdominal aortic aneurysm into the third portion of the duodenum. This report describes a case of a 59-year-old man who died of massive gastrointestinal hemorrhage due to a primary aortoduodenal fistula. This case is unique in that the fistula formed as a result of complex atherosclerotic disease of the abdominal aorta, with adventitial chronic inflammation and foreign body reaction against atheromatous plaque, and not from an aneurysm. We were unable to identify any other reports of aortoduodenal fistulas developing spontaneously in the absence of aneurysmal disease of the aorta.
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    Utility of virtual monoenergetic images derived from a dual-layer detector-based spectral CT in the assessment of aortic anatomy and pathology: A retrospective case control study.
    (Clinical imaging, 2018-11) Chalian, Hamid; Kalisz, Kevin; Rassouli, Negin; Dhanantwari, Amar; Rajiah, Prabhakar
    OBJECTIVES:To evaluate the ability of the retrospectively generated virtual monoenergetic images (VMIs) from a dual-layer detector-based spectral computed tomography (SDCT) to augment aortic enhancement for the evaluation of aortic anatomy and pathology. METHODS:98 patients with suboptimal aortic enhancement (≤200 HU) were retrospectively identified from SDCT scans. VMI from 40 to 80 keV were generated. Attenuation, noise, SNR, and CNR were measured at seven levels in the aorta. Image quality was graded on a 5-point scale, 5 being the best. From the VMI, an ideal set was chosen with mean vascular attenuation above 200 HU while maintaining diagnostic quality. Image parameters and quality of this ideal-set were compared to the standard 120-kVp images. RESULTS:The mean attenuation of all seven measured anatomical regions was 156.6 ± 61.7 HU in the 120-kVp images. Attenuation of the VMI from 40 to 70 keV were higher than the 120-kVp image, measuring 439.2 ± 215.3 HU, 298.5 ± 140.6 HU, 213.4 ± 94.3 HU, and 164.7 ± 90.2 HU, for 40 keV, 50 keV, 60 keV, and 70 keV, respectively (p value <0.01 for 40, 50, 60 keV; 0.07 for 70 keV). SNR and CNR showed similar trends. The 50 keV VMI had the best image quality (4.48 ± 0.84 vs. 2.24 ± 0.92 on 120-kVp images, p < 0.001). Attenuation, CNR, and SNR increased by 90.6%, 85.0%, and 108.1% at 50 keV compared to 120-kVp. CONCLUSIONS:A contrast-enhanced CT study can be optimized for the assessment of the aorta by using low-energy VMI obtained using SDCT. At the optimal monoenergetic level, attenuation, SNR, CNR and image quality were significantly higher than that of conventional polyenergetic images.