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Alessia Azzu,Marco Morosin,Alexios S. Antonopoulos,Massimo Capoccia,Ulrich Rosendahl,Raad Mohiaddin 한국심초음파학회 2021 Journal of Cardiovascular Imaging (J Cardiovasc Im Vol.29 No.4
BACKGROUND: Post-pericardiectomy right ventricular (RV) failure has been reported but it remains not well-studied. To investigate imaging parameters that could predict RV function and the outcome of patients post-pericardiectomy. METHODS: We analysed data from a total of 53 CP patients undergoing pericardiectomy. Preoperative, early and at 6 months postoperative echocardiographic (echo) imaging datasets were analysed and correlated with preoperative cardiac magnetic resonance (CMR), cardiac computed tomography scans and histology. The primary endpoint of the study was RV functional status early postoperatively and at 6 months. Secondary endpoint was the need for prolonged inotropic support. RESULTS: A cause of CP was identified in 26 patients (49%). Inotropic support ≥ 48 hours was required in n = 28 (53%) of patients and was correlated with lower preoperative RV areas by echo or RV volumes by CMR (p < 0.05 for all). A pericardial score based on pericardial thickness/calcification and epicardial fat thickness had good diagnostic accuracy to identify patients requiring prolonged use of inotropes (area under the curve, 0.825; 95% confidence interval, 0.674–0.976). Pericardiectomy resulted in RV decompression and impaired RV function early postoperatively (fractional area change: 40.5% ± 8.8% preoperatively vs. 31.4% ± 10.4% early postoperatively vs. 42.5% ± 10.2% at 6 months, p < 0.001). CONCLUSIONS: We show that a smaller RV cavity size and a pericardial scoring system are associated with prolonged inotropic support in CP patients undergoing pericardiectomy. RV systolic impairment post decompression is present in most patients, but it is only transient.
Injury-Mediated Vascular Regeneration Requires Endothelial ER71/ETV2
Park, Changwon,Lee, Tae-Jin,Bhang, Suk Ho,Liu, Fang,Nakamura, Rei,Oladipupo, Sunday S.,Pitha-Rowe, Ian,Capoccia, Benjamin,Choi, Hong Seo,Kim, Tae Min,Urao, Norifumi,Ushio-Fukai, Masuko,Lee, Dongjun,Mi American Heart Association, Inc. 2016 Arteriosclerosis, thrombosis, and vascular biology Vol.36 No.1
<P>Objective Comprehensive understanding of the mechanisms regulating angiogenesis might provide new strategies for angiogenic therapies for treating diverse physiological and pathological ischemic conditions. The E-twenty six (ETS) factor Ets variant 2 (ETV2; aka Ets-related protein 71) is essential for the formation of hematopoietic and vascular systems. Despite its indispensable function in vessel development, ETV2 role in adult angiogenesis has not yet been addressed. We have therefore investigated the role of ETV2 in vascular regeneration. Approach and Results We used endothelial Etv2 conditional knockout mice and ischemic injury models to assess the role of ETV2 in vascular regeneration. Although Etv2 expression was not detectable under steady-state conditions, its expression was readily observed in endothelial cells after injury. Mice lacking endothelial Etv2 displayed impaired neovascularization in response to eye injury, wounding, or hindlimb ischemic injury. Lentiviral Etv2 expression in ischemic hindlimbs led to improved recovery of blood perfusion with enhanced vessel formation. After injury, fetal liver kinase 1 (Flk1), aka VEGFR2, expression and neovascularization were significantly upregulated by Etv2, whereas Flk1 expression and vascular endothelial growth factor response were significantly blunted in Etv2-deficient endothelial cells. Conversely, enforced Etv2 expression enhanced vascular endothelial growth factor-mediated endothelial sprouting from embryoid bodies. Lentiviral Flk1 expression rescued angiogenesis defects in endothelial Etv2 conditional knockout mice after hindlimb ischemic injury. Furthermore, Etv2(+/-); Flk1(+/-) double heterozygous mice displayed a more severe hindlimb ischemic injury response compared with Etv2(+/-) or Flk1(+/-) heterozygous mice, revealing an epistatic interaction between ETV2 and FLK1 in vascular regeneration. Conclusions Our study demonstrates a novel obligatory role for the ETV2 in postnatal vascular repair and regeneration.</P>