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• W2118162364 abstract "HomeCirculationVol. 123, No. 16Response to Letter Regarding Article, “Differential Cardiac Remodeling in Preload Versus Afterload” Free AccessReplyPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReplyPDF/EPUBResponse to Letter Regarding Article, “Differential Cardiac Remodeling in Preload Versus Afterload” Karl Toischer, Adam G. Rokita, Bernhard Unsöld, Samuel Sossalla, Alexander Becker, Tim Seidler, Cornelia Grebe, Lena Preuß, Shamindra N. Gupta, Kathie Schmidt, Stephan E. Lehnart, Katrin Schäfer, Lars S. Maier and Gerd Hasenfuss Wuqiang Zhu, Sean P. Reuter and Loren J. Field Georgios Kararigas and Vera Regitz-Zagrosek Nils Teucher Martina Krüger and Wolfgang A. Linke Johannes Backs Karl ToischerKarl Toischer Search for more papers by this author , Adam G. RokitaAdam G. Rokita Search for more papers by this author , Bernhard UnsöldBernhard Unsöld Search for more papers by this author , Samuel SossallaSamuel Sossalla Search for more papers by this author , Alexander BeckerAlexander Becker Search for more papers by this author , Tim SeidlerTim Seidler Search for more papers by this author , Cornelia GrebeCornelia Grebe Search for more papers by this author , Lena PreußLena Preuß Search for more papers by this author , Shamindra N. GuptaShamindra N. Gupta Search for more papers by this author , Kathie SchmidtKathie Schmidt Search for more papers by this author , Stephan E. LehnartStephan E. Lehnart Search for more papers by this author , Katrin SchäferKatrin Schäfer Search for more papers by this author , Lars S. MaierLars S. Maier Search for more papers by this author and Gerd HasenfussGerd Hasenfuss Search for more papers by this author Wuqiang ZhuWuqiang Zhu Search for more papers by this author , Sean P. ReuterSean P. Reuter Search for more papers by this author and Loren J. FieldLoren J. Field Search for more papers by this author Georgios KararigasGeorgios Kararigas Search for more papers by this author and Vera Regitz-ZagrosekVera Regitz-Zagrosek Search for more papers by this author Nils TeucherNils Teucher Search for more papers by this author Martina KrügerMartina Krüger Search for more papers by this author and Wolfgang A. LinkeWolfgang A. Linke Search for more papers by this author Johannes BacksJohannes Backs Search for more papers by this author Originally published26 Apr 2011https://doi.org/10.1161/CIRCULATIONAHA.110.017566Circulation. 2011;123:e421We would like to thank Reil et al for their interesting discussion. They argue that wall stress of mice with transversal aortic constriction (TAC) may have been higher than those of mice with aortocaval shunt (shunt), which would be supported by lack of brain natriuretic peptide expression in shunt. We believe that we can disprove the arguments and the conclusion of Reil et al for the following reasons: After 1 week of increased load under both conditions, hypertrophy, as measured by left ventricular weight per tibia length, is similarly increased in both models, and this holds true for myocyte minimal fiber diameter as well (Figure 1 of our article).1It was recently shown under well-controlled in vitro conditions that myocardial expression of brain natriuretic peptide increases only with afterload, not with preload.2 Accordingly, it was shown by Yamamoto et al3 that strain of neonatal myocytes during systole significantly increased brain natriuretic peptide expression, whereas strain during diastole did not.We believe that wall stress-time integral is the major determinant of load-dependent gene expression, whereas arterial elastance reflects arterial load impact on the left ventricle.4 Accordingly, Ea has been shown to be reduced in human aortic regurgitation.5 It is hard to believe that hypertrophy-inducing load of the left ventricle under the condition of severe shunt would be reduced to 42.5% of control as calculated by Reil et al. This should induce atrophy instead of hypertrophy.The argument that the pericardium would reduce preload is interesting. However, to our knowledge, pericardial forces are largely unknown in mice. Unlike in human or large animal models, the mouse pericardium is thin. Therefore, the contribution to left ventricular end-diastolic pressure generation should be rather low. In addition, volume overload occurs in all heart chambers in our shunt model. Therefore, calculation of the transmural gradient (left ventricular end-diastolic pressure minus right atrial pressure) would lead to a low gradient, and the left ventricular pressure might be underestimated.Finally, the argument that the isovolumetric decay of left ventricular diastolic pressure was not included in the wall stress calculation is well taken. Accordingly, to estimate the impact of inclusion of isovolumetric decay, we recalculated diastolic and total wall stress. The diastole was divided in the part of the isovolumetric decay and in the residual part, and total wall stress was newly calculated. Mean total wall stress was then 9.68±0.22 mm Hg in sham, 15.17±1.17 mm Hg in shunt (P<0.05 versus sham), and 15.43±0.66 mm Hg in TAC (P<0.01 versus sham). Mean total wall stress was increased in shunt by 57% and in TAC by 59% (P=0.86 shunt versus TAC). Therefore, inclusion of the isovolumetric decay in the calculation of diastolic wall stress does not lead to a significantly higher wall stress in TAC compared with shunt.In conclusion, afterload leads to maladaptive hypertrophy, whereas preload has a more favorable phenotype. This results from distinct differences in hypertrophic signal activation with both forms of load despite comparable increases in stress-time integral.Karl Toischer, MDAdam G. Rokita, MDBernhard Unsöld, MDSamuel Sossalla, MDAlexander Becker, MDTim Seidler, MDCornelia Grebe, PhDLena Preuß, MScShamindra N. Gupta, MScKathie Schmidt, MScStephan E. Lehnart, MDKatrin Schäfer, MDLars S. Maier, MDGerd Hasenfuss, MD Department of Cardiology and Pulmonology Heart Center Georg-August-University Goettingen, GermanyWuqiang Zhu, MD, PhDSean P. Reuter, TALoren J. Field, PhD Wells Center for Pediatric Research and Krannert Institute of Cardiology Indiana University School of Medicine Indianapolis, INGeorgios Kararigas, PhDVera Regitz-Zagrosek, MD Institute of Gender in Medicine (GiM) Charité - Universitätsmedizin Berlin Berlin, GermanyNils Teucher, MD Department of Cardiac Surgery Georg-August-University Goettingen, GermanyMartina Krüger, PhDWolfgang A. Linke, PhD Department of Cardiovascular Physiology Ruhr University Bochum, GermanyJohannes Backs, MD Department of Internal Medicine III University of Heidelberg Heidelberg, GermanyDisclosuresNone.References1. Toischer K, Rokita AG, Unsöld B, Zhu W, Kararigas G, Sossalla S, Reuter SP, Becker A, Teucher N, Seidler T, Grebe C, Preuss L, Gupta SN, Schmidt K, Lehnart SE, Krüger M, Linke WA, Backs J, Regitz-Zagrosek V, Schäfer K, Field LJ, Maier LS, Hasenfuss G. Differential cardiac remodeling in preload versus afterload. Circulation. 2010; 122:993–1003.LinkGoogle Scholar2. Toischer K, Kögler H, Tenderich G, Grebe C, Seidler T, Van PN, Jung K, Knöll R, Körfer R, Hasenfuss G. Elevated afterload, neuroendocrine stimulation, and human heart failure increase BNP levels and inhibit preload-dependent SERCA upregulation. Circ Heart Fail. 2008; 1:265–271.LinkGoogle Scholar3. Yamamoto K, Dang QN, Maeda Y, Huang H, Kelly RA, Lee RT. Regulation of cardiomyocyte mechanotransduction by the cardiac cycle. Circulation. 2001; 103:1459–1464.LinkGoogle Scholar4. Kelly RP, Ting CT, Yang TM, Liu CP, Maughan WL, Chang MS, Kass DA. Effective arterial elastance as index of arterial vascular load in humans. Circulation. 1992; 86:513–521.LinkGoogle Scholar5. Segers P, Morimont P, Kolh P, Stergiopulos N, Westerhof N, Verdonck P. Arterial elastance and heart-arterial coupling in aortic regurgitation are determined by aortic leak severity. Am Heart J. 2002; 144:568–576.CrossrefMedlineGoogle Scholar eLetters(0)eLetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. Comments are reviewed for appropriate use of tone and language. Comments are not peer-reviewed. Acceptable comments are posted to the journal website only. Comments are not published in an issue and are not indexed in PubMed. Comments should be no longer than 500 words and will only be posted online. References are limited to 10. Authors of the article cited in the comment will be invited to reply, as appropriate.Comments and feedback on AHA/ASA Scientific Statements and Guidelines should be directed to the AHA/ASA Manuscript Oversight Committee via its Correspondence page.Sign In to Submit a Response to This Article Previous Back to top Next FiguresReferencesRelatedDetails April 26, 2011Vol 123, Issue 16 Advertisement Article InformationMetrics © 2011 American Heart Association, Inc.https://doi.org/10.1161/CIRCULATIONAHA.110.017566 Originally publishedApril 26, 2011 PDF download Advertisement SubjectsComputational BiologyContractile FunctionGene Expression and RegulationMyocardial Biology" @default.
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