Acellular Human Amniotic Membrane Scaffold with 15d-PGJ2 Nanoparticles in Postinfarct Rat Model.

The difficulty in the regeneration of cardiomyocytes after myocardial infarction is a major cause of heart failure. Together, the amniotic membrane and 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) can help in the recovery of cardiomyocyte, as they present many growth factors and anti-inflammatory effect, respectively. The objective of this study is to compare the efficacy of Human Decellularized Amniotic Membrane Scaffold (AHAS) loaded with 15d-PGJ2 in improving ventricular function in a rat model of postinfarct ventricular dysfunction. Myocardial infarction was induced in 24 rats by left coronary occlusion. After a week, the animals were subjected to echocardiography for evaluation of left ventricle ejection fraction (LVEF), left ventricle end diastolic volume (LVEDV), and left ventricle end systolic volume (LVESV). Animals with ejection fraction <40% were included in the study and were randomized into three groups: control (n = 8), AHAS (n = 8) and AHAS +15d-PGJ2 (n = 8). In the AHAS group only the membrane was implanted, whereas in the AHAS +15d-PGJ2 the membrane +15d-PGJ2 was implanted on myocardial infarction. Echocardiographic evaluation was performed after 1 month. For histological analysis, heart tissue was stained with Gomori trichome, Sirius Red, the antibody against CD31 and connexin 43 (Cx43). There were no significant differences in the baseline LVEF, LVEDV, and LVESV in all groups. After 1 month, ejection fraction decreased in the control group but increased in the AHAS group and in the AHAS +15d-PGJ2 group in comparison with the control group. The LVEDV and LVESV in the AHAS and AHAS +15d-PGJ2 groups decreased compared with the control group, featuring a ventricular antiremodeling effect. Histopathology of the infarcted area identified the reduction of infarct size and collagen type 1 in the AHAS and AHAS +15d-PGJ2 groups. New blood vessels and cardiomyocytes have been identified in an infarcted area by CD31 and Cx43. AHAS +15d-PGJ2 provided an increase in the ejection fraction and prevented ventricular dilation in this postinfarction ventricular dysfunction model. Impact Statement Our study demonstrated reduction of myocardial fibrosis, proliferation of cardiomyocytes and increase in ejection fraction in rats after experimental acellular amniotic membrane scaffold (AHAS) carrying nanoparticles of 15d-PGJ2 scaffold engraftment in infarcted myocardium. AHAS grafts facilitated colonization of fibrotic myocardium regions with new contractile cells, in addition to preventing reduction of left ventricle wall thickness. This contribution is theoretically and practically relevant as current literature describes experimental studies performed on cardiac ischemic models which present conflicting results concerning cell types used in a research model.

Morphological and hemodynamic patterns of carotid stenosis treated by endarterectomy with patch closure versus stenting: a duplex ultrasound study.

OBJECTIVES: A duplex ultrasound study was performed to investigate morphological and hemodynamic patterns of carotid stenoses treated by endarterectomy with patch closure versus stenting. MATERIALS AND METHOD: Twenty-nine carotid stenoses were treated with stenting and 65 with patch closure. Duplex ultrasound parameters (luminal diameter, mm; peak systolic velocity and end-diastolic velocity, cm/s) were measured 24 hours after the procedures and also at 12 months post-procedure. Residual stenoses (immediately postprocedure) and restenoses (within 12 months of procedure) were defined as narrowings of ≥ 50% on duplex ultrasound examination. RESULTS: In stented patients, the luminal diameter of the proximal internal carotid artery increased in the interval between the 24-hour and 12-month post-procedure studies, while in the patch closure patients, the diameter decreased. Carotid hemodynamics normalized immediately after both patching and stenting and remained relatively stable thereafter up to 12 months. No statistically elevated flow velocities (in the absence of residual stenosis or restenosis) were observed in the patched or stented carotid arteries. No significant differences in residual stenosis rates were observed between the stenting group (3 cases, 10.34%) and the patch closure group (1 case, 1.53%, P = 0.08). At 12 months, 2 stenting patients (6.88%) and 2 patch closure patients (3.07%) had $50% restenosis (P = 0.58). One case of late stroke due to restenosis was observed in the stenting group; the patient died 12 months postoperatively, before receiving new intervention. CONCLUSION: Measurements over time in luminal diameter signalized differences in arterial remodeling mechanisms between patched and stented carotids. Both stenting and patch closure were associated with carotid patency and flow restoration. This study does not support a general approach to new velocity criteria indiscriminately applied to stented or patched carotids.

Morphological and hemodynamic patterns of carotid stenosis treated by endarterectomy with patch closure versus stenting: a duplex ultrasound study

OBJECTIVES: A duplex ultrasound study was performed to investigate morphological and hemodynamic patterns of carotid stenoses treated by endarterectomy with patch closure versus stenting. MATERIALS AND METHOD: Twenty-nine carotid stenoses were treated with stenting and 65 with patch closure. Duplex ultrasound parameters (luminal diameter, mm; peak systolic velocity and end-diastolic velocity, cm/s) were measured 24 hours after the procedures and also at 12 months post-procedure. Residual stenoses (immediately postprocedure) and restenoses (within 12 months of procedure) were defined as narrowings of >50 percent on duplex ultrasound examination. RESULTS: In stented patients, the luminal diameter of the proximal internal carotid artery increased in the interval between the 24-hour and 12-month post-procedure studies, while in the patch closure patients, the diameter decreased. Carotid hemodynamics normalized immediately after both patching and stenting and remained relatively stable thereafter up to 12 months. No statistically elevated flow velocities (in the absence of residual stenosis or restenosis) were observed in the patched or stented carotid arteries. No significant differences in residual stenosis rates were observed between the stenting group (3 cases, 10.34 percent) and the patch closure group (1 case, 1.53 percent, P = 0.08). At 12 months, 2 stenting patients (6.88 percent) and 2 patch closure patients (3.07 percent) had $50 percent restenosis (P = 0.58). One case of late stroke due to restenosis was observed in the stenting group; the patient died 12 months postoperatively, before receiving new intervention. CONCLUSION: Measurements over time in luminal diameter signalized differences in arterial remodeling mechanisms between patched and stented carotids. Both stenting and patch closure were associated with carotid patency and flow restoration. This study does not support a general approach to new velocity criteria indiscriminately applied to stented or patched carotids.