scholarly journals Single access in complex angioplasty using the ventricular support system Impella CP™

2021 ◽  
Vol 29 ◽  
pp. 1-3
Author(s):  
Marcelo Ribeiro ◽  
Luis Dallan ◽  
Gustavo Neves ◽  
Luciana Simoni ◽  
Carlos Campos ◽  
...  
Keyword(s):  
Peripheral Artery Disease ◽  
Support System ◽  
Femoral Artery ◽  
Peripheral Artery ◽  
New Techniques ◽  
Single Access ◽  
Arterial Access ◽  
Left Femoral Artery ◽  
Ventricular Support ◽  
Artery Disease

The volume of complex coronary interventions has grown in Brazil and worldwide. Since they are performed in patients at increasingly higher risks, new techniques have been developed when interventional cardiologists are faced with uncommon situations, such as no safe arterial access for the procedure. We report a case of a patient with severe peripheral artery disease and occluded right femoral artery, in whom a single access (left femoral artery) was used for positioning the Impella™ and the guidewire for angioplasty.

Abstract 17955: Thereapeutic Angiogenesis Induced by Human Trx-1 Gene in Mice Hind Limb Ischemia Model: Preclinical Study for Treatment of Peripheral Artery Disease

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Mahesh Thirunavukkarasu ◽  
Inam A Shaikh ◽  
Vaithinathan Selvaraju ◽  
J.Alexandar Palesty ◽  
Nilanjana Maulik
Keyword(s):  
Gene Therapy ◽  
Peripheral Artery Disease ◽  
Femoral Artery ◽  
Hind Limb ◽  
Blood Perfusion ◽  
Limb Ischemia ◽  
Heme Oxygenase 1 ◽  
Peripheral Artery ◽  
Artery Ligation ◽  
Artery Disease

Introduction: Peripheral artery disease affects 12-20% Americans over the age of 60. Thioredoxin-1 (Trx-1) is a class of small redox proteins. We have demonstrated earlier that Trx-1 reduces oxidative stress resulting in less inflammation and increased angiogenesis in cardiac muscle via heme oxygenase-1 (HO-1) and VEGF after myocardial infarction. In the current study, we evaluate the effect of Trx-1 on post-ischemic hindlimb recovery. Methods: Peripheral artery disease was mimicked using a hindlimb ischemia (HLI) model. Wild type (WT) and Trx-1 transgenic (Trx-1Tg/+) mice (8-12 weeks old) were subjected to femoral artery ligation. Following surgery, mice were observed for 5 weeks. Serial laser doppler images were obtained, and perfusion ratios between the ischemic and non-ischemic limbs were calculated at set time intervals. The perfusion ratios were compared between WT and Trx-1Tg/+ groups. Immunohistochemical analysis of the skeletal muscle was performed to quantify the extent of fibrosis, capillary and arteriolar density 35 days after surgery. In addition, another set of experiments was designed with Ad.Trx-1 gene therapy after femoral artery ligation to study the molecular mechanism of neovascularization with Trx-1. Results: The recovery of hind limb perfusion was significantly increased in Trx-1Tg/+ mice at day 7 (0.19 ± 0.03 vs. 0.36 ± 0.07 (n=12-9), day-21 (0.37 ± 0.05 vs. 0.62 ± 0.03 (n=12-9), and day 28 (0.40 ± 0.04 vs. 0.79 ± 0.04 (n=10-9); p<0.05). Capillary density [1265 ± 87.8 vs. 762.4 ± 86.6 counts/mm2 ; (n=5); p<0.05] and arteriolar density [36.2 ± 2.96 vs. 22± 1.33 counts/mm2 ; (n=5); p<0.05] staining showed significant increase in Trx-1Tg/+ mice as compared to WT mice. Picrosirrus Red and immunofluorescence staining showed decreased fibrosis [8.3 ± 0.46 vs. 22.2 ± 1.04 (n=5); p<0.0001] and increased HO-1 expression respectively in Trx-1Tg/+ mice group as compared to WT mice, respectively. Trx-1 gene therapy study also revealed by Western blot analysis, increased Trx-1 (4.2 fold) and HO-1 (8.2 fold) expression in Ad.Trx-1-HLI as compared to Ad.LacZ-HLI. Conclusions: Our results suggest that Trx-1 is a potential therapeutic agent to increase blood perfusion and angiogenesis for the treatment of critical limb ischemia patients.

Sensory neuron inositol-1,4,5-trisphosphate (IP3) receptors contribute to chronic mechanoreflex sensitization in rats with simulated peripheral artery disease

2021 ◽  
Author(s):  
Korynne S. Rollins ◽  
Alec L E Butenas ◽  
Auni C Williams ◽  
Steven W. Copp
Keyword(s):  
Skeletal Muscle ◽  
Receptor Antagonist ◽  
Sensory Neuron ◽  
Peripheral Artery Disease ◽  
Femoral Artery ◽  
Pressor Response ◽  
Peripheral Artery ◽  
Exercise Pressor Reflex ◽  
Pressor Reflex ◽  
Artery Disease

The mechanoreflex is exaggerated in patients with peripheral artery disease (PAD) and in a rat model of simulated PAD in which a femoral artery is chronically (~72hrs) ligated. We found recently that, in rats with a ligated femoral artery, blockade of thromboxane A2 (TxA2) receptors on the sensory endings of thin fiber muscle afferents reduced the pressor response to 1 Hz repetitive/dynamic hindlimb skeletal muscle stretch (a model of mechanoreflex activation isolated from contraction-induced metabolite production). Conversely, we found no effect of TxA2 receptor blockade in rats with freely perfused femoral arteries. Here we extended the isolated mechanoreflex findings in "ligated" rats to experiments evoking dynamic hindlimb skeletal muscle contractions. We also investigated the role played by inositol 1-4-5-trisphosphate (IP3) receptors, receptors associated with intracellular signaling linked to TxA2 receptors, in the exaggerated response to dynamic mechanoreflex and exercise pressor reflex activation in ligated rats. Injection of the TxA2 receptor antagonist daltroban into the arterial supply of the hindlimb reduced the pressor response to 1 Hz dynamic contraction in ligated but not "freely perfused" rats. Moreover, injection of the IP3 receptor antagonist xestospongin C into the arterial supply of the hindlimb reduced the pressor response to 1 Hz dynamic stretch and contraction in ligated but not freely perfused rats. These findings demonstrate that, in rats with a ligated femoral artery, sensory neuron TxA2 receptor and IP3 receptor mediated signaling contributes to a chronic sensitization of the mechanically activated channels associated with the mechanoreflex and the exercise pressor reflex.

Abstract 17179: Blunted Vasoreactivity and Loss of Flow Reserve Contribute to Impaired Arteriogenesis in Diabetic Peripheral Artery Disease

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_1) ◽  
Author(s):  
XinLu Wang ◽  
Michael Simons ◽  
William Sessa ◽  
Zhen W Zhuang
Keyword(s):  
Peripheral Artery Disease ◽  
Femoral Artery ◽  
Unmet Need ◽  
Diabetic Mice ◽  
Feeding Artery ◽  
Peripheral Artery ◽  
Flow Reserve ◽  
Collateral Arteries ◽  
Chronic Hyperglycemia ◽  
Artery Disease

Introduction: Given the uncertainty around the exact pathophysiological mechanisms of diabetic peripheral artery disease (PAD), patients continue to have extremely poor prognoses. Our study attempted to address this critical unmet need. Hypothesis: We hypothesize that vasoreactivity in the feeding artery and impaired peripheral flow reserve are two primary causes of impaired arteriogenesis in these patients. Methods: The distal right femoral artery was ligated 2 weeks after streptozocin (STZ, n=12) or citrate buffer (n=12) treatment in wild-type (WT) mice. The contralateral hindlimbs were used as a negative control. 2 weeks post-hindlimb ischemia (HLI), the endothelial (EC)-dependent and EC-independent vasodilatation of the feeding artery was investigated using a Vevo 770 preclinical ultrasound scanner. Peripheral flow reserve was also assessed by pulse wave Doppler after 60 ul adenosine (3mg/ml) was administered systemically. A microCT angiography was performed to quantify collateral arteries. Gastrocnemius muscles were taken both for immunohistochemical examination in the evaluation of angiogenesis. Results: Femoral diameters at rest were similar between both control and diabetic models. In the non-ischemic limb, diabetes markedly blunted endothelial and smooth muscle cell (SMC) vasodilation reaction in the proximal femoral artery when compared with control mice [[acetylcholine (Ach): 286.3 ±16 μm versus 370±30 μm; sodium nitroprusside (SNP): 285±24.5 μm versus 350±30 μm, p<0.01]. In the ischemic hindlimb, chronic ischemia impaired vasodilation in diabetic mice when compared with control mice (Ach: 255±16 μm versus 330±40 μm; SNP: 340±50 μm versus 253±22 μm, p<0.05). In diabetic mice, peripheral flow reserve was impaired (1.27±0.27 in controls vs 0.87±0.13 in diabetes, p<0.05), with arteriole rarefaction and increased capillary/muscle ratio. Conclusions: This study demonstrated that chronic hyperglycemia negatively affects collateral development at different levels: 1 ) dysregulation of the feeding artery; 2 ) impaired arteriogenesis and increased angiogenesis; and 3 ) loss of peripheral flow reserve.

scholarly journals Exaggerated cardiovascular responses to treadmill running in rats with peripheral arterial insufficiency

2018 ◽  
Vol 314 (1) ◽  
pp. H114-H121 ◽  
Author(s):  
J. Matthew Kuczmarski ◽  
Kellee Unrath ◽  
Gail D. Thomas
Keyword(s):  
Blood Flow ◽  
Peripheral Artery Disease ◽  
Femoral Artery ◽  
Muscle Blood Flow ◽  
Cardiovascular Responses ◽  
Treadmill Running ◽  
Female Rats ◽  
Peripheral Artery ◽  
Flow Capacity ◽  
Artery Disease

Patients with atherosclerotic peripheral artery disease have an augmented pressor response to treadmill walking, but the underlying mechanisms remain poorly understood and difficult to isolate because of the confounding presence of numerous cardiovascular risk factors. In the present study, we tested the hypothesis that a chronic deficit in muscle blood flow capacity would be sufficient to trigger an exaggerated pressor response to dynamic exercise. Sprague-Dawley rats (5 male and 5 female) were instrumented with radiotelemetry devices to measure the cardiovascular responses to treadmill running before and after bilateral femoral artery ligation, which has been previously shown to reduce the blood flow capacity of distal hindlimb muscles by >60%. Treadmill running evoked reproducible increases in mean arterial pressure (MAP) and heart rate (HR), which were significantly augmented 3 days after femoral artery ligation in both male rats [ΔMAP: +10 ± 1 (SE) vs. +18 ± 3 mmHg and ΔHR: +94 ± 12 vs. +148 ± 15 beats/min, P < 0.05] and female rats (ΔMAP: +16 ± 3 vs. +30 ± 5 mmHg and ΔHR: +128 ± 20 vs. +178 ± 19 beats/min, P < 0.05). Similar exaggerated MAP and HR responses were observed at repeated intervals between 3 and 65 days postligation. These findings indicate that a chronic deficit in muscle blood flow capacity is an important, persistent cause of the abnormal pressor and cardioaccelerator responses to dynamic exercise in both male and female rats with peripheral arterial insufficiency. NEW & NOTEWORTHY Using radiotelemetry to assess cardiovascular effects of exercise, we showed that femoral artery obstruction in male and female rats is an important, persistent cause of exaggerated pressor and cardioaccelerator responses to treadmill running. This translational model reproduces the abnormal cardiovascular response to exercise seen in patients with peripheral artery disease. Listen to this article’s corresponding podcast at http://ajpheart.podbean.com/e/treadmill-bp-in-simulated-peripheral-artery-disease/ .

Sign in / Sign up

Export Citation Format

Share Document