Predicting the Risk for Acute Type B Aortic Dissection in Hypertensive Patients Using Anatomic Variables

Shirali, Aditya S.; Bischoff, Moritz S.; Lin, Hung‐Mo; Oyfe, Irina; Lookstein, R.; Griepp, Randall B.; Luozzo, Gabriele Di

doi:10.1016/j.jcmg.2012.07.018

Cited by 61 publications

(58 citation statements)

References 14 publications

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“…In our current studies, main cause of AAA rupture [42,43], thus, we mainly performed our experiments in VSMCs in vitro Hypertension is an important risk factor in the genesis of AAD in humans [44]. Ang II also markedly elevates blood pressure in the AAD model.…”

Section: Discussionmentioning

confidence: 99%

Ursodeoxycholic Acid Attenuates Acute Aortic Dissection Formation in Angiotensin II-Infused Apolipoprotein E-Deficient Mice Associated with Reduced ROS and Increased Nrf2 Levels

Liu¹,

Wang²,

Wang³

et al. 2016

Cell Physiol Biochem

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Background/Aims: Acute aortic dissection (AAD) is characterized by excessive smooth muscle cell (SMC) loss, extracellular matrix (ECM) degradation and inflammation. In response to certain stimulations, oxidative stress is activated and regulates apoptosis and inflammation. Excessive apoptosis promotes aortic inflammation and degeneration, leading to AAD formation. This study aimed to clarify role of oxidative stress in the pathogenesis of AAD and whether the antioxidant ursodeoxycholic acid (UDCA) attenuates AAD formation. Methods: Angiotensin II (Ang II) was infused in 8-months male ApoE^-/- mice for one week to establish a model of AAD. UDCA (10 mg/kg/day) was administered via intragastric gavage for 3 consecutive days before AngII infusion and also during the AngII infusion for another consecutive 7 days. Results: Ang II-infusion resulted in the incidence of AAD at a rate of 35% (13/37) and UDCA markedly reduced the incidence of AAD to 16% (6/37), accompanied with reduced maximal aortic diameter measured at the suprarenal region of the abdominal aorta. Additionally, UDCA pretreatment prevented Ang II induced generations of reactive oxygen species (ROS) and apoptosis of vascular smooth muscle cells (VSMCs) both in vivo and in. vitro Mechanistically, we found UDCA markedly increased Nrf2 expression in VSMCs and prevented Ang II induced expression of NADPH subunits (p47, p67 and gp91) in Nrf2-dependent manner and rescued the activity of redox enzymes (Cu/Zn-SOD, Mn-SOD and CAT), thereby inhibiting apoptosis of VSMCs. Conclusion: These results demonstrate that UDCA prevented AAD formation by reducing apoptosis of VSMCs caused by oxidative stress in Nrf2 dependent manner and suggest that UDCA might have clinical potential to suppress AAD formation.

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Section: Discussionmentioning

confidence: 99%

Ursodeoxycholic Acid Attenuates Acute Aortic Dissection Formation in Angiotensin II-Infused Apolipoprotein E-Deficient Mice Associated with Reduced ROS and Increased Nrf2 Levels

Liu¹,

Wang²,

Wang³

et al. 2016

Cell Physiol Biochem

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“…One such procedural recommendation is to intensively treat the RA ostium (9, 19), especially the superior part, which is thought to be particularly rich in ganglia and sympathetic nerves. Placement of single electrode catheters in the proximal part of the renal arteries can be challenging and may be unstable and without sufficient wall contact (20, 21), raising the question about whether patients really derive benefit from such attempts? Herein, for the first time to our knowledge, we provided quantitative data on nerve and ganglia distribution near the ostium that can help guide the decision as to preferential treatment sites.…”

Section: Discussionmentioning

confidence: 99%

Innervation Patterns May Limit Response to Endovascular Renal Denervation

Tzafriri¹,

Mahfoud

Keating³

et al. 2014

Journal of the American College of Cardiology

113

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BACKGROUND Renal denervation is a new interventional approach to treat hypertension with variable results. OBJECTIVES The purpose of this study was to correlate response to endovascular radiofrequency ablation of renal arteries with nerve and ganglia distributions. We examined how renal neural network anatomy affected treatment efficacy. METHODS A multielectrode radiofrequency catheter (15 W/60 s) treated 8 renal arteries (group 1). Arteries and kidneys were harvested 7 days post-treatment. Renal norepinephrine (NEPI) levels were correlated with ablation zone geometries and neural injury. Nerve and ganglion distributions and sizes were quantified at discrete distances from the aorta and were compared with 16 control arteries (group 2). RESULTS Nerve and ganglia distributions varied with distance from the aorta (p < 0.001). A total of −75% of nerves fell within a circumferential area of 9.3, 6.3, and 3.4 mm of the lumen and 0.3, 3.0, and 6.0 mm from the aorta. Efficacy (NEPI 37 ng/g) was observed in only 1 of 8 treated arteries where ablation involved all 4 quadrants, reached a depth of 9.1 mm, and affected 50% of nerves. In 7 treated arteries, NEPI levels remained at baseline values (620 to 991 ng/g), ≤20% of the nerves were affected, the ablation areas were smaller (16.2 ± 10.9 mm2) and present in only 1 to 2 quadrants at maximal depths of 3.8 ± 2.7 mm. CONCLUSIONS Renal denervation procedures that do not account for asymmetries in renal periarterial nerve and ganglia distribution may miss targets and fall below the critical threshold for effect. This phenomenon is most acute in the ostium but holds throughout the renal artery, which requires further definition.

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“…Increased aortic tortuosity is associated with a poorer prognosis in aortic diseases (Franken et al, 2015; Hatakeyama et al, 2001; Morris et al, 2011; Shirali et al, 2013), but the detailed mechanisms leading to tortuosity are still unknown (Morris, 2015). However, elastic fibers are altered in most cases of aortic tortuosity (Morris, 2015).…”

Section: Discussionmentioning

confidence: 99%

Function of Ltbp-4L and fibulin-4 in survival and elastogenesis in mice

Bultmann-Mellin

Essers

Heijingen

et al. 2016

Disease Models &Amp; Mechanisms

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LTBP-4L and LTBP-4S are two isoforms of the extracellular matrix protein latent-transforming growth factor beta-binding protein 4 (LTBP-4). The mutational inactivation of both isoforms causes autosomal recessive cutis laxa type 1C (ARCL1C) in humans and an ARCL1C-like phenotype in Ltbp4−/− mice, both characterized by high postnatal mortality and severely affected elastogenesis. However, genetic data in mice suggest isoform-specific functions for Ltbp-4 because Ltbp4S−/− mice, solely expressing Ltbp-4L, survive to adulthood. This clearly suggests a requirement of Ltbp-4L for postnatal survival. A major difference between Ltbp4S−/− and Ltbp4−/− mice is the matrix incorporation of fibulin-4 (a key factor for elastogenesis; encoded by the Efemp2 gene), which is normal in Ltbp4S−/− mice, whereas it is defective in Ltbp4−/− mice, suggesting that the presence of Ltbp-4L might be required for this process. To investigate the existence of a functional interaction between Ltbp-4L and fibulin-4, we studied the consequences of fibulin-4 deficiency in mice only expressing Ltbp-4L. Resulting Ltbp4S−/−;Fibulin-4R/R mice showed a dramatically reduced lifespan compared to Ltbp4S−/− or Fibulin-4R/R mice, which survive to adulthood. This dramatic reduction in survival of Ltbp4S−/−;Fibulin-4R/R mice correlates with severely impaired elastogenesis resulting in defective alveolar septation and distal airspace enlargement in lung, and increased aortic wall thickness with severely fragmented elastic lamellae. Additionally, Ltbp4S−/−;Fibulin-4R/R mice suffer from aortic aneurysm formation combined with aortic tortuosity, in contrast to Ltbp4S−/− or Fibulin-4R/R mice. Together, in accordance with our previous biochemical findings of a physical interaction between Ltbp-4L and fibulin-4, these novel in vivo data clearly establish a functional link between Ltbp-4L and fibulin-4 as a crucial molecular requirement for survival and elastogenesis in mice.

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Predicting the Risk for Acute Type B Aortic Dissection in Hypertensive Patients Using Anatomic Variables

Cited by 61 publications

References 14 publications

Ursodeoxycholic Acid Attenuates Acute Aortic Dissection Formation in Angiotensin II-Infused Apolipoprotein E-Deficient Mice Associated with Reduced ROS and Increased Nrf2 Levels

Ursodeoxycholic Acid Attenuates Acute Aortic Dissection Formation in Angiotensin II-Infused Apolipoprotein E-Deficient Mice Associated with Reduced ROS and Increased Nrf2 Levels

Innervation Patterns May Limit Response to Endovascular Renal Denervation

Function of Ltbp-4L and fibulin-4 in survival and elastogenesis in mice

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