Biventricular structural and functional responses to aortic constriction in a rabbit model of chronic right ventricular pressure overload

Apitz, Christian; Honjo, Osami; Humpl, Tilman; Li, Jing; Assad, Renato S.; Cho, Mi Y.; Hong, James; Friedberg, Mark K.; Redington, Andrew N.

doi:10.1016/j.jtcvs.2012.06.027

Cited by 62 publications

(59 citation statements)

References 25 publications

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“…Basically, optimal coupling efficiency is achieved if contractility is matched to vascular load (Naeije & Manes, 2014). Pulmonary artery constriction selectively elevates RV afterload leading to a hyper-contractile response of the RV which was also shown at different time points after pressure overload induction in other species (Leeuwenburgh et al, 2002;Gaynor et al, 2005;Apitz et al, 2012). These and our data suggest that the observed contractility elevation together with RV dilatation and hypertrophy is insufficient to compensate for a dramatically increased afterload leading to ventricular-arterial decoupling and diminished RV ejection volumes.…”

Section: Discussionsupporting

confidence: 80%

Maintained right ventricular pressure overload induces ventricular–arterial decoupling in mice

Böehm

Lawrie

Wilhelm

et al. 2017

Experimental Physiology

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This is the peer reviewed version of the following article: Boehm, M. et al (2016), Maintained right ventricular pressure overload induces ventricular-arterial decoupling in mice. Exp Physiol., which has been published in final form at https://doi.org/10.1113/EP085963. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving.eprints@whiterose.ac.uk https://eprints.whiterose.ac.uk/ Reuse Unless indicated otherwise, fulltext items are protected by copyright with all rights reserved. The copyright exception in section 29 of the Copyright, Designs and Patents Act 1988 allows the making of a single copy solely for the purpose of non-commercial research or private study within the limits of fair dealing. The publisher or other rights-holder may allow further reproduction and re-use of this version -refer to the White Rose Research Online record for this item. Where records identify the publisher as the copyright holder, users can verify any specific terms of use on the publisher's website. TakedownIf you consider content in White Rose Research Online to be in breach of UK law, please notify us by emailing eprints@whiterose.ac.uk including the URL of the record and the reason for the withdrawal request.This is an Accepted Article that has been peer-reviewed and approved for publication in the Experimental Physiology, but has yet to undergo copy-editing and proof correction. Please cite this article as an Accepted Article; doi: 10.1113/EP085963. This article is protected by copyright. All rights reserved. AbstractNew Findings: What is the central question of this study?The aim is to investigate whether complementary assessment of non-invasive ultrasound imaging along with closed chest-derived intra-cardiac pressure-volume catheterization is applicable to mice for an in-depth characterization of right ventricular (RV) function even upon maintained pressure overload. What is the main finding and its importance?Characterization

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Section: Discussionsupporting

confidence: 80%

Maintained right ventricular pressure overload induces ventricular–arterial decoupling in mice

Böehm

Lawrie

Wilhelm

et al. 2017

Experimental Physiology

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“…We further demonstrated that under these circumstances of isolated RV afterload, the addition of mildly increasing LV afterload by systemic epinephrine or norepinephrine in acute RV failure (suggesting that systemic vasoconstriction might be a viable strategy for the treatment of acute RV failure when LV function is well preserved) or by the addition of mild aortic banding in both acute and chronic RV afterload leads to an increase in load-independent indexes of LV and RV contractility. 49,95 These findings extend the work of Belenkie et al, 96 who demonstrated that aortic constriction during acute RV afterload leads to increased stroke volume independently of right coronary artery flow. Perhaps more clinically relevant was our observation of maladaptive fibrotic responses in both ventricles after isolated RV afterload associated with upregulation of genes classically involved in mediating fibrosis, including transforming growth factor-β1, connective tissue growth factor, and endothelin-1 in both ventricles.…”

Section: March 4 2014supporting

confidence: 82%

“…The functional compromise is accompanied in both ventricles by adverse remodeling as manifested by biventricular myocyte hypertrophy, reduced contractility, and increased fibrosis. 49,95 Although RV hypertrophy is an expected finding secondary to isolated RV afterload, the similar findings in the otherwise healthy LV are intriguing. We further demonstrated that under these circumstances of isolated RV afterload, the addition of mildly increasing LV afterload by systemic epinephrine or norepinephrine in acute RV failure (suggesting that systemic vasoconstriction might be a viable strategy for the treatment of acute RV failure when LV function is well preserved) or by the addition of mild aortic banding in both acute and chronic RV afterload leads to an increase in load-independent indexes of LV and RV contractility.…”

Section: March 4 2014mentioning

confidence: 94%

“…46,48 This aligns with the marked upregulation of connective tissue growth factor/CCN2 and other profibrotic signaling molecules during RV and LV fibrosis in our and other models of RV afterload and failure. 28,49 In contrast, miRNA 21 and 34c* may increase during LV failure but decrease in RV failure. 28 Reddy et al 30 investigated miRNAs during the transition from RV hypertrophy to RV failure and compared these with miRNA expression in LV hypertrophy or failure.…”

Section: March 4 2014mentioning

confidence: 98%

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Right Versus Left Ventricular Failure

2014

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1033V entricular failure manifests in many forms, its underlying physiology ranging from overt left ventricular (LV) systolic dysfunction to isolated right ventricular (RV) diastolic dysfunction, and the wide portfolio of resulting symptoms vary from chronic fluid retention to acute multiorgan dysfunction and death. In this review, we discuss the morphological, functional, and molecular similarities and differences in RV and LV responses to adverse loading and failure. We further discuss whether LV and RV function and failure can truly be discussed as separate entities and thereby examine interactions between the ventricles that on one hand contribute to ventricular dysfunction but on the other may be harnessed for therapeutic benefit. Embryological and Physiological Differences Between the RV and LVThe RV and LV have different embryological origins.1 The LV originates from the primary heart field; the RV, from the secondary heart field. Consequently, several genes specifically control RV formation, including, among others, Hand2 and Tbx20.2 During gestation, the RV functions as the systemic ventricle ( Figure 1A). During fetal life, in addition to supplying the modest amount of pulmonary blood flow, the RV pumps blood to the lower body and placenta and contributes more than half of the combined cardiac output.3 With the transition from fetal to postnatal physiology and with the reduction in pulmonary vascular resistance, the subpulmonary RV transforms its morphology and geometry, becoming a thin-walled chamber to adopt its postnatal physiological characteristics. 4 Because it faces a low impedance pulmonary circulation, the normal postnatal RV maintains a cardiac output equal to that of the LV at approximately a fifth of the energy cost. The trapezoidal RV pressure-volume loop reflects this difference, with few if any isovolumic periods. Consequently, RV output starts early during pressure generation and is later maintained by a "hangout period" when antegrade flow continues into the pulmonary artery despite the onset of RV relaxation.5 In contrast, the rectangular LV pressure-volume loops reflect the LV square-wave pump function with distinct and well-developed isovolumic contraction and relaxation periods.6 Likewise, RV myocytes display faster twitch velocities than LV myocytes. 7The physiological differences are reflected in morphological differences between the ventricles (Table 1). The low-pressure RV is triangular in the sagittal plane and crescent-shaped in cross section as a result of the concave RV free wall and convex interventricular septum wrapping around the high-pressured, thick-walled, bullet-shaped LV. Consequently, although the normal RV has a lower ratio of volume to surface area and a thinner wall than the LV, 8 the low cavity pressure determines a lower wall stress and lower oxygen demands.Anatomic differences are also apparent in myocardial architecture. LV subepicardial and subendocardial fibers are oblique and helical with fiber angles ranging from 30° to 80° with a mean of ≈60°, whereas ...

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“…This is for two reasons. First, antegrade diastolic flow clearly contributes (by up to 40% or 50% 15 ) to the overall cardiac output, and second, it limits the duration of pulmonary incompetence, which is so often present in these patients. Thus, maintenance and enhancement of antegrade diastolic flow are crucial to maintaining adequate cardiac output in these patients.…”

Section: Right Ventricular Diastolic Dysfunctionmentioning

confidence: 99%

Low Cardiac Output Due to Acute Right Ventricular dysfunction and Cardiopulmonary Interactions in Congenital Heart Disease (2013 Grover Conference Series)

Redington

2014

Pulm. circ.

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The importance of right ventricular dysfunction, as a driver of symptoms and outcomes in the normal biventricular circulation, is increasingly recognized. However, the pathophysiologic mechanisms underlying the role of the right ventricle in acute and chronic hemodynamic deterioration are less well understood. This review aims to clarify the impact of acute right ventricular dysfunction on biventricular interactions and, in turn, to discuss the role of cardiopulmonary interactions in the normal circulation and when modified by the presence of associated structural malformations. Such interactions may be adverse or beneficial, and a more complete understanding of their importance may result in novel therapeutic strategies and improved outcomes.

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Biventricular structural and functional responses to aortic constriction in a rabbit model of chronic right ventricular pressure overload

Cited by 62 publications

References 25 publications

Maintained right ventricular pressure overload induces ventricular–arterial decoupling in mice

Maintained right ventricular pressure overload induces ventricular–arterial decoupling in mice

Right Versus Left Ventricular Failure

Low Cardiac Output Due to Acute Right Ventricular dysfunction and Cardiopulmonary Interactions in Congenital Heart Disease (2013 Grover Conference Series)

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