Diabetes and Its Effect on Abdominal Aortic Aneurysm Growth Rate in Hispanic Patients

Betancourt-Garcia, Monica M.; Vatcheva, Kristina; Thakur, Amrit; Gupta, Prateek K.; Postevka, Eugene; Martínez, Ricardo; Forse, R. Armour

doi:10.1016/j.avsg.2019.06.004

Cited by 8 publications

(3 citation statements)

References 26 publications

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“…Thus, diabetes is considered to have a protective effect on AAA. 20 , 21 , 22 , 23 Therefore, it is possible that locally induced matrix stabilization such as the PGG treatment we have reported, could effectively slow AAA progression and lower the incidence of AAA rupture.…”

Section: Discussionmentioning

confidence: 96%

Chemical stabilization of the extracellular matrix attenuates growth of experimentally induced abdominal aorta aneurysms in a large animal model

Simionescu

Casco

Turner³

et al. 2020

JVS-Vascular Science

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Objective The goal of the present study was to test the safety and efficacy of chemical stabilization of the arterial extracellular matrix as a novel nonoperative treatment of abdominal aortic aneurysms (AAAs) in a clinically relevant large animal model. Methods To achieve matrix stabilization, we used 1,2,3,4,6-pentagalloylglucose (PGG), a noncytotoxic polyphenolic agent capable of binding to and stabilizing elastin and collagen against the action of degrading enzymes. We first optimized the therapeutic PGG formulation and time of exposure by in vitro testing on porcine aortas using phenol histologic staining with iron chloride, elastic recoil assays, and PGG quantification as a function of tissue thickness. We then induced AAAs in 16 swine using sequential balloon angioplasty and elastase/collagenase and calcium chloride treatment of the infrarenal segment. We monitored AAA induction and development using digital subtraction angiography. At 2 weeks after induction, after the AAAs had reached ∼66% arterial expansion, the swine were randomly assigned to 2 groups. In the treatment group, we delivered PGG to the aneurysmal aorta endoluminally using a weeping balloon and evaluated the AAA diameters using digital subtraction angiography for another 10 weeks. The control swine did not receive any treatment. For the safety evaluation, we collected blood and performed comprehensive metabolic panels and complete blood counts every 2 to 3 weeks for all the animals. The swine were routinely monitored for neurologic and physical attributes such as behavior, inactivity, alertness, appetite, discomfort, and weight gain. After euthanasia and full necropsy, we analyzed the AAA tissue samples for PGG content, elastic recoil, and histologic features. Results In vitro, a single 2.5-minute intraluminal delivery of 0.3% PGG to the swine aorta was sufficient for PGG to diffuse through the entire thickness of the porcine arterial tissues and to bind with high affinity to the elastic lamellae, as seen by positive iron chloride staining, a reduction of elastic recoil, and an increase in PGG content. In vivo, the control swine AAA tissues were thickened and showed the typical aspects of AAA, including chronic inflammation, adventitial reactivity, smooth muscle cell proliferation, elastic lamellae degradation, and medial and adventitial calcification. Similar aspects were noted in the PGG-treated arteries, except for the lack of calcification and an apparent diminished hyperplasia. PGG treatment was effective in reducing AAA expansion and reversing the process of AAA dilation by reducing the aortic diameters to ≤30% by week 12 ( P < .05). PGG was specifically localized to the aneurysmal segments as seen by histologic examination, the reduction of elastic recoil, and an increase in PGG content. PGG treatment did not affect the swine's neurologic or physical attributes, weight, blood chemistry, blood cells, or functionality of remote orga...

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Section: Discussionmentioning

confidence: 96%

Chemical stabilization of the extracellular matrix attenuates growth of experimentally induced abdominal aorta aneurysms in a large animal model

Simionescu

Casco

Turner³

et al. 2020

JVS-Vascular Science

View full text Add to dashboard Cite

show abstract

“…While the growth pattern of AAA in both diabetic and non-diabetic group was found to be mostly linear, 40% of those in diabetic group was found to have an indeterminate growth pattern compared to 19% in non-diabetic group, further proving that diabetes slowed down the growth of AAA [ 16 ]. Another study analyzed data collected from mostly Mexican American patients and found the AAA expansion rate per month to be 65% lower in patients with diabetes compared to those without diabetes [ 47 ]. Specifically, the growth rate was 0.07mm per month and 0.21mm per month in diabetic and non-diabetic patients, respectively [ 47 ].…”

Section: Methodsmentioning

confidence: 99%

“…Another study analyzed data collected from mostly Mexican American patients and found the AAA expansion rate per month to be 65% lower in patients with diabetes compared to those without diabetes [ 47 ]. Specifically, the growth rate was 0.07mm per month and 0.21mm per month in diabetic and non-diabetic patients, respectively [ 47 ].…”

Section: Methodsmentioning

confidence: 99%

Diabetes and Abdominal Aortic Aneurysm: Is the Protective Effect on AAA Due to Antidiabetic Medications Alone, Due to the Disease Alone, or Both?

Shanmuganathan,

K. Agrawal

2024

Arch Intern Med Res

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Diabetes is a metabolic disease that may result in multiple microvascular and macrovascular diseases. Interestingly, many studies have demonstrated the inverse relationship between diabetes and the development and expansion of abdominal aortic aneurysm (AAA). One hypothesis is that the aortic wall stiffness resulting from hyperglycemia and advanced glycation end products could delay the development and growth of AAA. Other studies have proposed that the concurrent use of antidiabetic medications which promote anti-inflammatory cytokines while hindering pro-inflammatory cytokines may potentially be the reason for this protective effect of diabetes on AAA. Contrastingly, the presence of diabetes has been found to have a negative effect on the outcome of AAA following its repair which may be due to elevated blood glucose negatively affecting the healing process. The current literature has also demonstrated the negative impact of the use of fluoroquinolones on AAA. This comprehensive review critically reviewed and summarized the role of diabetes, anti-diabetes medications and fluoroquinolones on AAA, and on the effect of diabetes and certain anti-diabetes medications on outcomes following its repair.

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Metformin Prescription Associated with Reduced Abdominal Aortic Aneurysm Growth Rate and Reduced Chemokine Expression in a Swedish Cohort

Unosson

Wågsäter

Bjarnegård

et al. 2021

Annals of Vascular Surgery

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Background: Recent reports suggest that the negative association between diabetes mellitus and abdominal aortic aneurysm (AAA) may be driven by metformin, the world's most common antidiabetic drug rather than diabetes per se. We sought to investigate the association among AAA growth rate, chemokine profile, and metformin prescription in a contemporary Swedish cohort. Methods: Patients under surveillance for small AAA were identified at 4 Swedish vascular centers with active AAA screening programs. Annual AAA growth rate, medical history, and prescribed medications were recorded for linear regression analysis. In a subset of patients with AAA and control subjects without AAA or diabetes, plasma samples were available and analyzed for 40 inflammatory chemokines. Results: A total of 526 patients were included for AAA growth analysis: 428 without type 2 diabetes mellitus (T2DM), 65 with T2DM and metformin prescription, and 33 with T2DM but without metformin prescription. Patients were included from 2005 to 2017 with mean follow-up of 3.2 (1.7) years and median annual AAA growth rate 1.6 mm, range À4.8 to 15.4 mm. Mean (standard deviation) annual AAA growth rates were 2.3 (2.2) mm in non-T2DM patients versus 1.1 (1.1) mm in patients with T2DM with metformin prescription and 1.6 (1.4) mm among those with T2DM without metformin prescription. With non-T2DM patients as reference in an unadjusted and 2 adjusted models, metformin prescription was significantly associated with reduced AAA growth rate (P < 0.001, P ¼ 0.005, and P ¼ 0.024, respectively), but not T2DM without metformin prescription (P ¼ 0.137, P ¼ 0.331, and P ¼ 0.479, respectively). Among 240 patients with AAA (152 without T2DM, 51 with T2DM and metformin, and 37 with T2DM without metformin) and 59 without AAA or T2DM, metformin prescription was associated with reduced expression of chemokines representing all classes of leukocytes. Conclusions: Metformin prescription is associated with reduced AAA growth rate, possibly mediated by broad anti-inflammatory effects. A randomized controlled trial is needed to determine what role metformin may play in AAA disease, particularly in the absence of T2DM.

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Diabetes and Its Effect on Abdominal Aortic Aneurysm Growth Rate in Hispanic Patients

Cited by 8 publications

References 26 publications

Chemical stabilization of the extracellular matrix attenuates growth of experimentally induced abdominal aorta aneurysms in a large animal model

Chemical stabilization of the extracellular matrix attenuates growth of experimentally induced abdominal aorta aneurysms in a large animal model

Diabetes and Abdominal Aortic Aneurysm: Is the Protective Effect on AAA Due to Antidiabetic Medications Alone, Due to the Disease Alone, or Both?

Metformin Prescription Associated with Reduced Abdominal Aortic Aneurysm Growth Rate and Reduced Chemokine Expression in a Swedish Cohort

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