An ultralow dose paclitaxel coated drug balloon with an outer protective sheath for peripheral arterial disease treatment

2021 ◽  
Vol 9 (10) ◽  
pp. 2428-2435
Author(s):  
Tingchao Zhang ◽  
Gaoyang Guo ◽  
Li Yang ◽  
Yunbing Wang

In this paper, an ultralow dose paclitaxel-coated balloon was developed. Benefiting from the unique design of the meglumine matrix and outer protective sheath, its therapeutic effect was comparable to those of commercial high-dose counterparts in the swine model.

Heart ◽  
2015 ◽  
Vol 101 (5) ◽  
pp. 356-362 ◽  
Author(s):  
Robert M Stoekenbroek ◽  
S Matthijs Boekholdt ◽  
Rana Fayyad ◽  
Rachel Laskey ◽  
Matti J Tikkanen ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Jialin Pan ◽  
Wenqin Liu ◽  
Ye Chen ◽  
Chi Zhang ◽  
Cong Lin

At present, the global prevalence of peripheral arterial disease is increasing year by year, and it has become a worldwide disease. Studies have shown that transplanting endothelial progenitor cells (EPCs) into ischemic tissues can improve the tissue ischemia, thereby having a therapeutic effect on peripheral arterial diseases. This indicates that EPCs play a therapeutic effect in peripheral arterial disease. Recent studies have shown that peptidylarginine deiminase (PAD) is involved in the regulation of epigenetics and its inhibitor Cl-amidine can improve endothelium-dependent vasodilation and significantly reduce the formation of arterial thrombosis. It can also play a role in hematopoietic stem cells that share the same origin with EPCs. Therefore, we speculate that PAD4 may also have an effect on EPCs through a similar mechanism, thereby participating in the damage and repair of peripheral arterial disease. Therefore, we first detected the expression of PAD4 in EPCs of peripheral arterial disease and detected changes in the number and function of endothelial progenitor cells in peripheral blood after injecting the PAD4 inhibitor Cl-amidine into mice. A mouse model of lower limb ischemia was established to explore the effect of PAD4 on the function of EPCs in peripheral arterial disease. The results show that PAD4 is highly expressed in peripheral arterial diseases and the PAD4 inhibitor Cl-amidine can increase the number of EPCs and can treat peripheral arterial diseases by improving the proliferation, migration, and vascularization of EPCs.


2021 ◽  
Vol 37 ◽  
Author(s):  
Cihan Yücel ◽  
Mete Gürsoy ◽  
Serkan Ketenciler ◽  
Aslıhan Tenekeciğil ◽  
Feryaz Kızıltan ◽  
...  

2018 ◽  
Vol 5 (5) ◽  
pp. 5-11
Author(s):  
A. N. Krutikov ◽  
V. N. Vavilov ◽  
D. V. Korolev ◽  
E. N. Semernin ◽  
A. A. Kostareva

The review discussed issues of intermittent pneumatic compression using for peripheral arterial disease treatment. Historical information, regimes and possible mechanisms of action are discussed.


2012 ◽  
Vol 24 (8) ◽  
pp. 687-690 ◽  
Author(s):  
Mohammad Al-Jazzar ◽  
Farag A Aly ◽  
Mohammed Al-Omran ◽  
Ahmad H Alghadir ◽  
Mohamed Y Berika

2008 ◽  
Vol 99 (01) ◽  
pp. 182-189 ◽  
Author(s):  
Roger Simon ◽  
Bernd van der Loo ◽  
Tamara Kovacevic ◽  
Christiane Brockes ◽  
Valentin Rousson ◽  
...  

SummaryBeneficial effects of aggressive lipid-lowering with high-dose atorvastatin (80 mg/day) have been demonstrated in patients with coronary and cerebrovascular disease. The impact of such a therapy in patients with peripheral arterial disease (PAD) is less known so far. Here we studied the effects of high-dose atorvastatin on brachial artery endothelial function, common carotid intima-media thickness (IMT) and local progression of PAD in these patients. One hundred of 500 patients screened with documented PAD were randomly assigned to receive 80 mg of atorvastatin daily for six months or to continue on conventional medical treatment. Ninety-six percent of patients in the control group were on standard statin treatment. High resolution B-mode ultrasonography was used to study brachial artery flowmediated dilation (FMD), IMT and ankle-brachial index (ABI) at baseline and at six months. FMD and IMT at baseline and at six months were 4.1 (0.06–8.6) versus 5.0 (0.76 vs. 8.1) %, p=0.96, and 0.76 (0.66–0.82) versus 0.73 (0.63–0.81) mm, p=0.41, respectively, in the atorvastatin group, and 2.66 (-1.9 – 6.9) versus 3.65 (0.0–8.6)%, p=0.02, and 0.78 (0.71–0.90) versus 0.77 (0.70–0.90) mm, p=0.48,in the control group. ABI at baseline and at six months was not different in either group. LDL cholesterol was reduced from 2.53 (2.21–3.28) to 1.86 (1.38–2.29) mM (p<0.0001) in the atorvastatin group, whereas levels remained stable in the control group [2.38 (1.94–3.16) vs.2.33 (1.82–2.84) mM, p=0.61]. Major adverse cardiovascular events occurred in 2.1% in the atorvastatin group and 1.9% in the control group (p= 0.61). In conclusion, in this pilot trial aggressive lipid-lowering with 80 mg of atorvastatin daily for six months had no effect on brachial artery FMD in patients with PAD. IMT andABI were also similar in patients with and without high-dose atorvastatin at six months.


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