Percutaneous endovascular delivery of calcium chloride to the intact porcine carotid artery: A novel animal model of arterial calcification

Abrão, Sergio Ricardo; Campos, Carlos M.; Cavalcante, Rafael; Eggermont, Jeroen; Lemos, Pedro A.; Lederman, Alex; Silva, Erasmo S. da; Aun, Ricardo; Belczak, Sérgio Quilici; Abizaid, Alexandre; Brito, Fábio Sândoli de

doi:10.1002/ccd.29070

Cited by 3 publications

(4 citation statements)

References 26 publications

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“…This is because no stable and mature models of calcified coronary artery in large animals have been established yet. In a previous study, media calcification was induced by exposing a porcine carotid artery to a low concentration of calcium chloride 22 . However, this method could not be accomplished in the coronary artery.…”

Section: Discussionmentioning

confidence: 99%

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In vivo evaluation of intravascular lithotripsy in a healthy porcine coronary model

Yin

Wang

Chen

et al. 2023

Cathet Cardio Intervent

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Objectives In this study, we aimed to investigate the vascular response to an intravascular lithotripsy (IVL) shockwave balloon in a healthy porcine coronary artery model. Background IVL is a novel clinical technique for modifying heavily calcified atherosclerotic plaques. Methods A total of 24 porcine coronary arteries were treated with IVL or plain old balloon angioplasty (POBA). Histology, histomorphometry, quantitative coronary angiography analysis (QCA), and optical coherence tomography (OCT) were performed postprocedure and at 1‐month follow‐up (1M‐FU). Results There was no significant difference in the late lumen loss and diameter stenosis (determined by QCA) and the minimal lumen area (evaluated by OCT) of the IVL and POBA groups at 1M‐FU. Pathological analysis revealed that the lumen and neointima areas were similar between the two groups. However, the medial and adventitial layers were more prominent in the IVL than in the POBA group. The injury score and inflammation of the media and adventitia increased dramatically in the IVL group postprocedure and at 1M‐FU. At 1M‐FU, media fibrin deposition and adventitial fibrosis were also significantly increased in the IVL group. However, there was no significant difference in neointima fibrin deposition, endothelialization, and thrombosis between both groups. Layered separation of the media and adventitia was observed in the IVL group. Conclusion The findings indicate that the IVL balloon did not cause serious intimal hyperplasia and endothelial damage compared with the effects of POBA in the healthy coronary artery. However, shock waves may cause unique damage to the vascular media and adventitia in the coronary artery, which was not observed in the peripheral artery.

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Section: Discussionmentioning

confidence: 99%

“…In a previous study, media calcification was induced by exposing a porcine carotid artery to a low concentration of calcium chloride. 22 However, this method could not be accomplished in the coronary artery. The blood flow could not be completely blocked due to the many branches arising from the coronary artery.…”

Section: Discussionmentioning

confidence: 99%

In vivo evaluation of intravascular lithotripsy in a healthy porcine coronary model

Yin

Wang

Chen

et al. 2023

Cathet Cardio Intervent

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“…The most common preclinical disease model for atherosclerosis, which closely mimics calcification, is Apoe −/− mice ( 31 ). More recently, a model utilizing calcium chloride to induce calcification has been established ( 32 ). Using these models to further test Wnt targeted calcification treatments may be a logical next step.…”

Section: Discussionmentioning

confidence: 99%

Wnt Signaling in Vascular Calcification

Bundy

Boone

Simpson

2021

Front. Cardiovasc. Med.

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Cardiovascular disease is a worldwide epidemic and considered the leading cause of death globally. Due to its high mortality rates, it is imperative to study the underlying causes and mechanisms of the disease. Vascular calcification, or the buildup of hydroxyapatite within the arterial wall, is one of the greatest contributors to cardiovascular disease. Medial vascular calcification is a predictor of cardiovascular events such as, but not limited to, hypertension, stiffness, and even heart failure. Vascular smooth muscle cells (VSMCs), which line the arterial wall and function to maintain blood pressure, are hypothesized to undergo a phenotypic switch into bone-forming cells during calcification, mimicking the manner by which mesenchymal stem cells differentiate into osteoblast cells throughout osteogenesis. RunX2, a transcription factor necessary for osteoblast differentiation and a target gene of the Wnt signaling pathway, has also shown to be upregulated when calcification is present, implicating that the Wnt cascade may be a key player in the transdifferentiation of VSMCs. It is important to note that the phenotypic switch of VSMCs from a healthy, contractile state to a proliferative, synthetic state is necessary in response to the vascular injury surrounding calcification. The lingering question, however, is if VSMCs acquire this synthetic phenotype through the Wnt pathway, how and why does this signaling occur? This review seeks to highlight the potential role of the canonical Wnt signaling pathway within vascular calcification based on several studies and further discuss the Wnt ligands that specifically aid in VSMC transdifferentiation.

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“…A recent study describes the technique of endovascular administration of calcium chloride to the carotid arteries of pigs to model arterial calcification. Via catheter administration, a short exposure (9 mins) resulted in extensive circumferential parietal calcification, as confirmed by imaging modalities (intravascular ultrasound and optical coherence tomography) and histological assessments [ 85 ]. Despite clear advantages, pigs are not commonly used due to limitations around size, housing, and often prohibitive costs.…”

Section: Experimental Models For Early Phase Drug Discovery: Enhancin...mentioning

confidence: 99%

Translating atherosclerosis research from bench to bedside: navigating the barriers for effective preclinical drug discovery

et al. 2022

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Cardiovascular disease (CVD) remains the leading cause of death worldwide. An ongoing challenge remains the development of novel pharmacotherapies to treat CVD, particularly atherosclerosis. Effective mechanism-informed development and translation of new drugs requires a deep understanding of the known and currently unknown biological mechanisms underpinning atherosclerosis, accompanied by optimization of traditional drug discovery approaches. Current animal models do not precisely recapitulate the pathobiology underpinning human CVD. Accordingly, a fundamental limitation in early-stage drug discovery has been the lack of consensus regarding an appropriate experimental in vivo model that can mimic human atherosclerosis. However, when coupled with a clear understanding of the specific advantages and limitations of the model employed, preclinical animal models remain a crucial component for evaluating pharmacological interventions. Within this perspective, we will provide an overview of the mechanisms and modalities of atherosclerotic drugs, including those in the preclinical and early clinical development stage. Additionally, we highlight recent preclinical models that have improved our understanding of atherosclerosis and associated clinical consequences and propose model adaptations to facilitate the development of new and effective treatments.

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Percutaneous endovascular delivery of calcium chloride to the intact porcine carotid artery: A novel animal model of arterial calcification

Cited by 3 publications

References 26 publications

In vivo evaluation of intravascular lithotripsy in a healthy porcine coronary model

In vivo evaluation of intravascular lithotripsy in a healthy porcine coronary model

Wnt Signaling in Vascular Calcification

Translating atherosclerosis research from bench to bedside: navigating the barriers for effective preclinical drug discovery

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