coronary-angiography-during-ex-situ-heart-perfusion-in-a-porcine-model

Coronary Angiography During Ex-Situ Heart Perfusion in a Porcine Model

Heart transplantation is the gold standard treatment for advanced heart failure. The procurement of extended criteria donors (ECD) increases due to the ...

Groupe Hospitalier Paris Saint Joseph

To investigate the physiological correlates of indices of RV function in a model of chronic pressure overload.

Non-invasive indices of right ventricular function are markers of ventricular-arterial coupling rather than ventricular contractility: insights from a porcine model of chronic pressure overload.

Ventricular-arterial coupling is a measure of the relationship between ventricular contractility and afterload. We sought to determine the relationship between ventricular-arterial coupling and right ventricular (RV) remodeling in a novel porcine model of progressive pulmonary hypertension (PH).

Right ventricular plasticity in a porcine model of chronic pressure overload.

Right ventricular (RV) response to exercise or pharmacological stress is not well documented in pulmonary hypertension (PH). We investigated the relationship between RV reserve and ventricular-arterial coupling. Surgical ligation of the left pulmonary artery was performed in 13 Large White piglets (PH group), thereafter weekly embolisations of the right lower lobe were performed for 5 weeks. A control group of six piglets underwent sham procedures. Right heart catheterisation and echocardiography were performed at week 6. Pressure-volume loops were recorded before and after dobutamine infusion. Induction of experimental PH resulted in a higher mean ± sd pulmonary artery pressure (34 ± 9 versus 14 ± 2 mmHg; p<0.01) and in a lower ventricular-arterial coupling efficiency (0.66 ± 0.18 versus 1.24 ± 0.17; p<0.01) compared with controls at 6 weeks. Dobutamine-induced relative changes in RV stroke volume index (SVI) and end-systolic elastance were lower in the PH group (mean ± SD 47 ± 5% versus 20 ± 5%, p<0.01, and 81 ± 37% versus 32 ± 14%, p<0.01, respectively). Change in SVI was strongly associated with resting ventricular-arterial coupling (R(2)=0.74; p<0.01). RV reserve was associated with ventricular-arterial coupling in a porcine model of chronic pressure overload.

Right ventricular reserve in a piglet model of chronic pulmonary hypertension.

Chronic thromboembolic pulmonary hypertension results from chronic mechanical obstruction of the pulmonary arteries after acute venous thromboembolism. However, the mechanisms that result in the progression from unresolved thrombus to fibrotic vascular remodeling are unknown. We hypothesized that pulmonary artery endothelial cells contribute to this phenomenon via paracrine growth factor and cytokine signaling.

Abnormal pulmonary endothelial cells may underlie the enigmatic pathogenesis of chronic thromboembolic pulmonary hypertension.

Mechanisms of right ventricular (RV) adaptation to chronic pressure overload are not well understood. We hypothesized that a lower capillary density (CD) to stroke work ratio would be associated with more fibrosis and RV maladaptive remodeling.

The importance of capillary density-stroke work mismatch for right ventricular adaptation to chronic pressure overload.

Right ventricular (RV) failure is the main prognostic factor in pulmonary hypertension, and ventricular capillary density (CD) has been reported to be a marker of RV maladaptive remodeling and failure. Our aim was to determine whether right intracoronary endothelial progenitor cell (EPC) infusion can improve RV function and CD in a piglet model of chronic thromboembolic pulmonary hypertension (CTEPH).

Autologous endothelial progenitor cell therapy improves right ventricular function in a model of chronic thromboembolic pulmonary hypertension.

We aimed to assess the mitochondrial respiratory capacities in the right ventricle in the setting of ventricular remodeling induced by pressure overload.

Right ventricular mitochondrial respiratory function in a piglet model of chronic pulmonary hypertension.

Angiophagy has been described as a non-fibrinolytic mechanism of pulmonary artery (PA) patency restoration after distal (<50 µm in diameter) pulmonary embolism in mice. We hypothesized that angiophagy could achieve muscularized PA patency restoration after pulmonary embolism in piglets and humans. Angiophagy was defined by pathological assessment as the moving of an embolic specimen from the lumen to the interstitium according to three stages in a pig model of chronic thromboembolic pulmonary hypertension (CTEPH) 6 to 10 weeks after embolization with enbucrilate: the embolic specimen is (I) covered by endothelial cells, (II) covered by endothelial cells and smooth muscle cells, and (III) located in the adventitia. In animals, we observed the three stages of the pulmonary angiophagy of enbucrilate emboli in <300 µm PA. Stages II and III were observed in 300 to 1000 μm PA, and only Stage I was observed in larger-diameter PA (>1000 μm). In lung samples from patients with histories of pulmonary embolisms, we observed PA angiophagy stigma for embolic specimens derived from blood clots and from bone marrow emboli. This study provides an original pathological description and staging of PA angiophagy in a large animal model of CTEPH and in humans after pulmonary embolism.

Description, Staging and Quantification of Pulmonary Artery Angiophagy in a Large Animal Model of Chronic Thromboembolic Pulmonary Hypertension.

Percutaneous closure of paravalvular leak (PVL) has emerged as an alternative to surgical management in selected cases. Achieving complete PVL occlusion, while respecting prosthesis function remains challenging. A multimodal imaging analysis of PVL morphology before and during the procedure is mandatory to select an appropriate device. We aim to explore the additional value of 3D printing in predicting device related adverse events including mechanical valve leaflet blockade, risk of device embolization and residual shunting.

Article	Year
Non-invasive indices of right ventricular function are markers of ventricular-arterial coupling rather than ventricular contractility: insights from a porcine model of chronic pressure overl... European heart journal cardiovascular Imaging\| PubMed ID: 23677917	2013
Right ventricular plasticity in a porcine model of chronic pressure overload. The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation\| PubMed ID: 24290166	2014
Right ventricular reserve in a piglet model of chronic pulmonary hypertension. The European respiratory journal\| PubMed ID: 25504996	2015
Abnormal pulmonary endothelial cells may underlie the enigmatic pathogenesis of chronic thromboembolic pulmonary hypertension. The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation\| PubMed ID: 27793518	2017
The importance of capillary density-stroke work mismatch for right ventricular adaptation to chronic pressure overload. The Journal of thoracic and cardiovascular surgery\| PubMed ID: 28712579	2017
Autologous endothelial progenitor cell therapy improves right ventricular function in a model of chronic thromboembolic pulmonary hypertension. The Journal of thoracic and cardiovascular surgery\| PubMed ID: 30669226	2019
Right ventricular mitochondrial respiratory function in a piglet model of chronic pulmonary hypertension. The Journal of thoracic and cardiovascular surgery\| PubMed ID: 30979421	2019
Description, Staging and Quantification of Pulmonary Artery Angiophagy in a Large Animal Model of Chronic Thromboembolic Pulmonary Hypertension. Biomedicines\| PubMed ID: 33187154	2020
3D-Printing to Plan Complex Transcatheter Paravalvular Leaks Closure. Journal of clinical medicine\| PubMed ID: 36012997	2022

Benoît Decante

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