scholarly journals A Multilayer Functionalized Drug-Eluting Balloon for Treatment of Coronary Artery Disease

Pharmaceutics ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 614
Author(s):  
Hak-Il Lee ◽  
Won-Kyu Rhim ◽  
Eun-Young Kang ◽  
Bogyu Choi ◽  
Jun-Hyeok Kim ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Ex Vivo ◽  
Multilayer Coating ◽  
Balloon Catheter ◽  
Transition Time ◽  
Coating Materials ◽  
Drug Transfer ◽  
Coated Materials ◽  
Drug Loss ◽  
Drug Eluting

Drug-eluting balloons (DEBs) have been mostly exploited as an interventional remedy for treating atherosclerosis instead of cardiovascular stents. However, the therapeutic efficacy of DEB is limited due to their low drug delivery capability to the disease site. The aim of our study was to load drugs onto a balloon catheter with preventing drug loss during transition time and maximizing drug transfer from the surface of DEBs to the cardiovascular wall. For this, a multilayer-coated balloon catheter, composed of PVP/Drug-loaded liposome/PVP, was suggested. The hydrophilic property of 1st layer, PVP, helps to separate drug layer in hydrophilic blood vessel, and the 2nd layer with Everolimus (EVL)-loaded liposome facilitates drug encapsulation and sustained release to the targeted lesions during inflation time. Additionally, a 3rd layer with PVP can protect the inner layer during transition time for preventing drug loss. The deionized water containing 20% ethanol was utilized to hydrate EVL-loaded liposome for efficient coating processes. The coating materials showed negligible toxicity in the cells and did not induce pro-inflammatory cytokine in human coronary artery smooth muscle cells (HCASMCs), even in case of inflammation induction through LPS. The results of hemocompatibility for coating materials exhibited that protein adsorption and platelet adhesion somewhat decreased with multilayer-coated materials as compared to bare Nylon tubes. The ex vivo experiments to confirm the feasibility of further applications of multilayer-coated strategy as a DEB system demonstrated efficient drug transfer of approximately 65% in the presence of the 1st layer, to the tissue in 60 s after treatment. Taken together, a functional DEB platform with such a multilayer coating approach would be widely utilized for percutaneous coronary intervention (PCI).

scholarly journals An Engineered Gene Nanovehicle Developed for Smart Gene Therapy to Selectively Inhibit Smooth Muscle Cells: An In Vitro Study

2020 ◽  
Vol 21 (4) ◽  
pp. 1530
Author(s):  
Ling-Yi Cheng ◽  
Yu-Chi Wang ◽  
Ming-Hong Chen ◽  
Fu-I Tung ◽  
Kuan-Ming Chiu ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Ex Vivo ◽  
Vascular Endothelial Cell ◽  
Balloon Catheter ◽  
In Vitro Study ◽  
Vitro Study ◽  
Stent Restenosis ◽  
Drug Eluting ◽  
In Stent Restenosis

In-stent restenosis is a serious concern for patients treated through the stenting procedure, although this can be solved using drug-eluting stents and/or drug-eluting balloon catheters. However, the chemical agents released from the drug-eluting layer for inhibiting smooth muscle cell (SMC) migration are inevitably associated with damage to vascular endothelial cell (ECs). The present in vitro study used a distinct strategy, in which a smart gene (phEGR1-PKCδ, an engineered plasmid consists of an SMC-specific promoter (human early growth response 1, hEGR1 promoter) ligated with a gene encoding apoptosis-inducing protein (protein kinase C-delta, PKCδ) was incorporated into a novel gene vehicle (Au cluster-incorporated polyethylenimine/carboxymethyl hexanoyl chitosan, PEI-Au/CHC) to form the PEI-Au/CHC/phEGR1-PKCδ complex, which was proposed for the selective inhibition of SMC proliferation. It was found that the cell viability of SMCs receiving the PEI-Au/CHC/phEGR1-PKCδ complex under simulated inflammation conditions was significantly lower than that of the ECs receiving the same treatment. In addition, the PEI-Au/CHC/phEGR1-PKCδ complex did not demonstrate an inhibitory effect on EC proliferation and migration under simulated inflammation conditions. Finally, the PEI-Au/CHC/phEGR1-PKCδ complexes coated onto a balloon catheter used in percutaneous transluminal coronary angioplasty (PTCA) could be transferred to both the ECs and the SMC layer of Sprague Dawley (SD) rat aortas ex vivo. These preliminary in vitro results suggest that the newly developed approach proposed in the present study might be a potential treatment for reducing the incidence rate of in-stent restenosis and late thrombosis in the future.

Ex vivo optical frequency domain imaging and histopathology of malapposed drug eluting stent in coronary artery

2016 ◽  
Vol 66 (6) ◽  
pp. 354-355
Author(s):  
Akiko Fujino ◽  
Hiroyuki Hao ◽  
Rika Kawakami ◽  
Yasu-aki Tsuchida ◽  
Kenichi Fujii ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Frequency Domain ◽  
Ex Vivo ◽  
Drug Eluting Stent ◽  
Optical Frequency ◽  
Optical Frequency Domain Imaging ◽  
Drug Eluting

Elevated level of circulatory sTLT1 induces inflammation through SYK/MEK/ERK signalling in coronary artery disease

2019 ◽  
Vol 133 (22) ◽  
pp. 2283-2299
Author(s):  
Apabrita Ayan Das ◽  
Devasmita Chakravarty ◽  
Debmalya Bhunia ◽  
Surajit Ghosh ◽  
Prakash C. Mandal ◽  
...  
Keyword(s):  
Risk Factors ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Chronic Inflammation ◽  
Ex Vivo ◽  
Human Subjects ◽  
Critical Role ◽  
Atherosclerotic Cardiovascular Disease ◽  
Tnf Α ◽  
Artery Disease

Abstract The role of inflammation in all phases of atherosclerotic process is well established and soluble TREM-like transcript 1 (sTLT1) is reported to be associated with chronic inflammation. Yet, no information is available about the involvement of sTLT1 in atherosclerotic cardiovascular disease. Present study was undertaken to determine the pathophysiological significance of sTLT1 in atherosclerosis by employing an observational study on human subjects (n=117) followed by experiments in human macrophages and atherosclerotic apolipoprotein E (apoE)−/− mice. Plasma level of sTLT1 was found to be significantly (P<0.05) higher in clinical (2342 ± 184 pg/ml) and subclinical cases (1773 ± 118 pg/ml) than healthy controls (461 ± 57 pg/ml). Moreover, statistical analyses further indicated that sTLT1 was not only associated with common risk factors for Coronary Artery Disease (CAD) in both clinical and subclinical groups but also strongly correlated with disease severity. Ex vivo studies on macrophages showed that sTLT1 interacts with Fcɣ receptor I (FcɣRI) to activate spleen tyrosine kinase (SYK)-mediated downstream MAP kinase signalling cascade to activate nuclear factor-κ B (NF-kB). Activation of NF-kB induces secretion of tumour necrosis factor-α (TNF-α) from macrophage cells that plays pivotal role in governing the persistence of chronic inflammation. Atherosclerotic apoE−/− mice also showed high levels of sTLT1 and TNF-α in nearly occluded aortic stage indicating the contribution of sTLT1 in inflammation. Our results clearly demonstrate that sTLT1 is clinically related to the risk factors of CAD. We also showed that binding of sTLT1 with macrophage membrane receptor, FcɣR1 initiates inflammatory signals in macrophages suggesting its critical role in thrombus development and atherosclerosis.

Unprotected Left Main Coronary Artery Percutaneous Coronary Intervention-Our Experiences at a Tertiary Hospital

2014 ◽  
Vol 6 (2) ◽  
pp. 107-111
Author(s):  
S Munwar ◽  
AHMW Islam ◽  
S Talukder ◽  
AQM Reza ◽  
T Ahmed ◽  
...  
Keyword(s):  
Percutaneous Coronary Intervention ◽  
Coronary Artery ◽  
Left Main Coronary Artery ◽  
Coronary Intervention ◽  
Drug Eluting Stent ◽  
Bare Metal ◽  
Coronary Artery Diseases ◽  
Left Main ◽  
Percutaneous Coronary ◽  
Drug Eluting

Background: Aim of the study was to evaluate the primary procedural success of percutaneous coronary intervention of unprotected left main coronary artery stenosis using either Bare-metal stents or drug eluting stent. Methods: Total 33 patients were enrolled in this very preliminary non-randomized prospective cohort study. Among them, Male: 25 and Female: 8. Total 35 stents were deployed. Mean age were for Male: 59 yrs, for Female: 62 yrs. Associated coronary artery diseases risk factors were dyslipidemia, High Blood pressure, Diabetes Mellitus, Positive family history for coronary artery diseases and smoking. Results: Among the study group; 26 (78%) were Dyslipidemic, 24(70%) were hypertensive; 17 (51.5%) patients were Diabetic, 11(33%) were smoker and 7(21%) patients had family history of Ischaemic heart disease. Female patients were more obese (BMI M 26: F 27) and developed coronary artery diseases in advance age. Common stented territory were left main: 20 (60%), Left main to left anterior descending artery 7 (22%) and Left main to left circumflex artery 6 (18%). Average length and diameter of stent was 3.5 and 18 mm respectively. Stent used: Bare Metal Stent 5 (15%), Drug Eluting Stent: 28 (85%). Among the different Drug Eluting Stents, Everolimus eluting stents were 11 (39.3%), Sirolimus eluting 10(35.7%), Paclitaxel eluting 3 (10.7%), Biolimus eluting 3 (10.7%) and Zotarolimus eluting1 (3.6%). In the present study, overall survival outcome was 94% (31 patient), mortality of cardiac cause 3% (1 patient) and 1 patient (3%) died of hepatocellular carcinoma. Conclusion: Our study has shown that percutaneous coronary intervention of the unprotected left main is a safe and effective alternative to Coronary Artery Bypass Graft (CABG). DOI: http://dx.doi.org/10.3329/cardio.v6i2.18349 Cardiovasc. j. 2014; 6(2): 107-111

Periostin promotes arterial calcification through PPARγ-related glucose metabolism reprogramming

2021 ◽  
Author(s):  
Yi Zhu ◽  
Jing-Jing Ji ◽  
Xiao-Dong Wang ◽  
Xue-Jiao Sun ◽  
Min Li ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Ex Vivo ◽  
Matrix Gla Protein ◽  
Calcium Deposition ◽  
Arterial Calcification ◽  
Agatston Score ◽  
Respiratory Chain Complexes ◽  
Ecm Remodeling ◽  
Pparγ Agonist ◽  
Lactate Levels

Extracellular matrix (ECM) exerts a list of biological functions, contributing to almost 30% of the osteogenic process. Periostin is a secreted protein that can alter ECM remodeling in response to vascular injury. However, the functional role of periostin in vascular calcification has yet to be fully described. Ex vivo, recombinant periostin accelerated thoracic aortas calcification, increased the expression of glycolysis key enzymes, and disturbed the normal oxidative phosphorylation (OXPHOS), which could be alleviated by the peroxisome proliferation-activated receptor γ (PPARγ) agonist pioglitazone. In vascular smooth muscle cells (VSMCs), recombinant periostin promoted VSMC-osteoblastic phenotype transition and calcium deposition, and suppressed PPARγ expression. Mechanistically, recombinant periostin caused over-activation of glycolysis and mitochondrial dysfunction in VSMCs, as assessed by extracellular acidification rate (ECAR), oxygen consumption rate, and mitochondrial respiratory chain complexes activities. Targeted glycolysis inhibitors reduced mitochondrial calcium overload, apoptosis, and periostin-induced VSMCs calcification. PPARγ agonists preserved glycolysis and OXPHOS in the stimulated microenvironment, and reversed periostin-promoted VSMC calcification. Furthermore, plasma periostin, lactate, and matrix Gla protein levels were measured in 274 patients who underwent computed tomography to determine coronary artery calcium score (Agatston score). Plasma periostin and lactate levels were both linked to an Agatston score of more than zero in patients with coronary artery calcification. There is also a positive correlation between plasma periostin and lactate levels. This study suggests that downregulation of PPARγ is involved in the mechanism by which periostin accelerates arterial calcification, partly through excessive glycolysis activation and unbalanced mitochondrial homeostasis.

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