Right-Ventricular Adaptation in Setting of Pressure Overload after Intramyocardial Delivery of Mononuclear Cells

2018 ◽  
Vol 227 (4) ◽  
pp. S54-S55
Author(s):  
Kimberly Holst ◽  
Saji Oommen ◽  
Susana Cantero-Peral ◽  
Pouya Hemmati ◽  
Joseph A. Dearani ◽  
...  
Circulation ◽  
1995 ◽  
Vol 91 (9) ◽  
pp. 2359-2370 ◽  
Author(s):  
Sheng-Jing Dong ◽  
Adrian P. Crawley ◽  
John H. MacGregor ◽  
Yael Fisher Petrank ◽  
Dale W. Bergman ◽  
...  

Circulation ◽  
1997 ◽  
Vol 95 (9) ◽  
pp. 2312-2317 ◽  
Author(s):  
Dongsheng Fan ◽  
Thomas Wannenburg ◽  
Pieter P. de Tombe

2021 ◽  
Vol 2021 (2) ◽  
Author(s):  
Gini Priyadharshini Jeyashanmugaraja ◽  
Evgeny Shloknik ◽  
Deborah Tosin Akanya ◽  
Kristin Stawiarski ◽  
Christopher Winterbottom ◽  
...  

ABSTRACT A 63-year-old woman was admitted with severe respiratory distress requiring mechanical ventilation and shock requiring vasopressor support. She was found to have COVID-19 pneumonia. Focused cardiac ultrasound performed for evaluation of shock was significant for right ventricular dilation and dysfunction with signs of right ventricular pressure overload. Given worsening shock and hypoxemia systemic thrombolysis was administered for presumed massive pulmonary embolism with remarkable improvement of hemodynamics and respiratory failure. In next 24 h patient’s neurologic status deteriorated to the point of unresponsiveness. Emergent computed tomography showed multiple ischemic infarcts concerning for embolic etiology. Focused cardiac ultrasound with agitated saline showed large right to left shunt due to a patent foramen ovale. This was confirmed by transesophageal echocardiogram, 5 months later. This case highlights strengths of focused cardiac ultrasound in critical care setting and in patients with COVID-19 when access to other imaging modalities can be limited.


Author(s):  
Jurate Bidviene ◽  
Denisa Muraru ◽  
Francesco Maffessanti ◽  
Egle Ereminiene ◽  
Attila Kovács ◽  
...  

AbstractOur aim was to assess the regional right ventricular (RV) shape changes in pressure and volume overload conditions and their relations with RV function and mechanics. The end-diastolic and end-systolic RV endocardial surfaces were analyzed with three-dimensional echocardiography (3DE) in 33 patients with RV volume overload (rToF), 31 patients with RV pressure overload (PH), and 60 controls. The mean curvature of the RV inflow (RVIT) and outflow (RVOT) tracts, RV apex and body (both divided into free wall (FW) and septum) were measured. Zero curvature defined a flat surface, whereas positive or negative curvature indicated convexity or concavity, respectively. The longitudinal and radial RV wall motions were also obtained. rToF and PH patients had flatter FW (body and apex) and RVIT, more convex interventricular septum (body and apex) and RVOT than controls. rToF demonstrated a less bulging interventricular septum at end-systole than PH patients, resulting in a more convex shape of the RVFW (r = − 0.701, p < 0.0001), and worse RV longitudinal contraction (r = − 0.397, p = 0.02). PH patients showed flatter RVFW apex at end-systole compared to rToF (p < 0.01). In both groups, a flatter RVFW apex was associated with worse radial RV contraction (r = 0.362 in rToF, r = 0.482 in PH at end-diastole, and r = 0.555 in rToF, r = 0.379 in PH at end-systole, respectively). In PH group, the impairment of radial contraction was also related to flatter RVIT (r = 0.407) and more convex RVOT (r = − 0.525) at end-systole (p < 0.05). In conclusion, different loading conditions are associated to specific RV curvature changes, that are related to longitudinal and radial RV dysfunction.


2019 ◽  
Vol 116 (10) ◽  
pp. 1700-1709 ◽  
Author(s):  
Mario Boehm ◽  
Xuefei Tian ◽  
Yuqiang Mao ◽  
Kenzo Ichimura ◽  
Melanie J Dufva ◽  
...  

Abstract Aims The temporal sequence of events underlying functional right ventricular (RV) recovery after improvement of pulmonary hypertension-associated pressure overload is unknown. We sought to establish a novel mouse model of gradual RV recovery from pressure overload and use it to delineate RV reverse-remodelling events. Methods and results Surgical pulmonary artery banding (PAB) around a 26-G needle induced RV dysfunction with increased RV pressures, reduced exercise capacity and caused liver congestion, hypertrophic, fibrotic, and vascular myocardial remodelling within 5 weeks of chronic RV pressure overload in mice. Gradual reduction of the afterload burden through PA band absorption (de-PAB)—after RV dysfunction and structural remodelling were established—initiated recovery of RV function (cardiac output and exercise capacity) along with rapid normalization in RV hypertrophy (RV/left ventricular + S and cardiomyocyte area) and RV pressures (right ventricular systolic pressure). RV fibrotic (collagen, elastic fibres, and vimentin+ fibroblasts) and vascular (capillary density) remodelling were equally reversible; however, reversal occurred at a later timepoint after de-PAB, when RV function was already completely restored. Microarray gene expression (ClariomS, Thermo Fisher Scientific, Waltham, MA, USA) along with gene ontology analyses in RV tissues revealed growth factors, immune modulators, and apoptosis mediators as major cellular components underlying functional RV recovery. Conclusion We established a novel gradual de-PAB mouse model and used it to demonstrate that established pulmonary hypertension-associated RV dysfunction is fully reversible. Mechanistically, we link functional RV improvement to hypertrophic normalization that precedes fibrotic and vascular reverse-remodelling events.


PLoS ONE ◽  
2013 ◽  
Vol 8 (7) ◽  
pp. e70802 ◽  
Author(s):  
Navin K. Kapur ◽  
Vikram Paruchuri ◽  
Mark J. Aronovitz ◽  
Xiaoying Qiao ◽  
Emily E. Mackey ◽  
...  

2003 ◽  
Vol 13 (4) ◽  
pp. 384-386 ◽  
Author(s):  
Munesh Tomar ◽  
Sitaraman Radhakrishnan ◽  
Savitri Shrivastava

We report two instances of transient isolated right-sided myocardial hypertrophy in patients with an intact ventricular septum, normal thickness of the posterior wall of the left ventricle, and normal ventricular function, diagnosed by echocardiography on the third day of life. The two neonates, born at 36 and 38 weeks gestation respectively, had perinatal distress. Both were diagnosed as having isolated right ventricular hypertrophy with mild pulmonary hypertension, which disappeared in both cases within 8 weeks without any specific therapy. Though the cause of the ventricular hypertrophy remains unclear, we believe that it is the consequence of remodeling of pulmonary vasculature secondary to acute perinatal distress, resulting in persistent pulmonary hypertension and producing pressure overload on the right ventricle, and hence right ventricular hypertrophy. The finding of early and transient right ventricular hypertrophy, with normal left-sided structures and normal ventricular function, has thus far failed to gain attention in the paediatric cardiologic literature.


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