Skip to main content
Log in

Left Ventricular Size and Shape: Determinants of Mechanical Signal Transduction Pathways

  • Published:
Heart Failure Reviews Aims and scope Submit manuscript

Abstract

Heart failure may be viewed as a progressive disorder that is impelled, at least in part, by progressive left ventricular (LV) remodeling. In the present discussion we will review the role of LV remodeling in the pathogenesis of heart failure, with a focus on the contribution that changes in LV size and shape play in the development and progression of the progression of heart failure. The clinical implication of this review is that existing neurohormonal strategies may not completely prevent disease progression in the failing heart, and that adjunctive strategies that are designed to specifically prevent and/or attenuate LV remodeling may play an important role in the clinical treatment of heart failure.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Similar content being viewed by others

References

  1. Eisenhofer G, Friberg P, Rundqvist B, Quyyumi AA, Lambert G, Kaye DM, Kopin IJ, Goldstein DS, Esler MD. Cardiac sympathetic nerve function in congestive heart failure. Circulation 1996;93:1677–1676.

    PubMed  Google Scholar 

  2. Eichhorn EJ, Bristow M. Medical therapy can improve the biological properties of the chronically failing heart: A new era in the treatment of heart failure. Circulation 1997;94:2285–2296.

    Google Scholar 

  3. Hasking GJ, Esler MD, Jennings GL, Burton D, Korner PI. Norepinephrine spillover to plasma in patients with congestive heart failure: evidence of increased overall and cardiorenal sympathetic nervous activity. Circulation 1986;73(4):615–621.

    PubMed  Google Scholar 

  4. Dzau VJ, Packer M, Lilly LS, Swartz SL, Hollenberg NK, Williams GH. Prostaglandins in severe congestive heart failure: Relation to activation of the renin-angiotensin system and hyponatremia. N Engl J Med 1984;310:347–352.

    PubMed  Google Scholar 

  5. Dzau VJ, Colucci WS, Hollenberg NK, Williams GH. Relation of the renin-angiotensin-aldosterone system to clinical state in congestive heart failure. Circulation 1981;63:645–651.

    PubMed  Google Scholar 

  6. Cohn JN. Structural basis for heart failure: Ventricular remodeling and its pharmacological inhibition. Circulation 1995;91:2504–2507.

    PubMed  Google Scholar 

  7. Mann DL. Mechanisms and models in heart failure: a combinatorial approach. Circulation 1999;100:999–1088.

    PubMed  Google Scholar 

  8. Linzbach AJ. Heart Failure from the Point of View of Quantitative Anatomy. Am J Cardiol 1960;5:370–382.

    Article  PubMed  Google Scholar 

  9. Ross JrJ. Afterload mismatch in aortic and mitral valve disease: implications for surgical therapy. J Am Coll Cardiol 1985;5:811–826.

    PubMed  Google Scholar 

  10. Ross JJ. Mechanisms of cardiac contraction. What roles for preload, afterload and inotropic state in heart failure? Eur Heart J 1983;(4 Suppl A):19–28:19–28.

  11. Hirota Y, Saito T, Kita Y, Shimizu G, Kino M, Kawamura K. [The natural history of dilated cardiomyopathy and pathophysiology of congestive heart failure]. J Cardiogr Suppl 1986;67–76.

  12. Pouleur H, Rousseau MF, van Eyll C, Melin J, Youngblood M, Yusuf S. Cardiac mechanics during development of heart failure. SOLVD Investigators. Circulation 1993;87:IV14–IV20.

    PubMed  Google Scholar 

  13. Vatner SF. Reduced subendocardial myocardial perfusion as one mechanism for congestive heart failure. Am J Cardiol 1988;62:94E–98E.

    Article  PubMed  Google Scholar 

  14. Shannon RP, Komamura K, Shen YT, Bishop SP, Vatner SF. Impaired regional subendocardial coronary flow reserve in conscious dogs with pacing-induced heart failure. Am J Physiol 1993;265:H801–H809.

    PubMed  Google Scholar 

  15. LeGrice IJ, Takayama Y, Holmes JW, Covell JW. Impaired subendocardial function in tachycardia-induced cardiac failure. Am J Physiol 1995;268:H1788–H1794.

    PubMed  Google Scholar 

  16. Kapadia S, Oral H, Lee J, Nakano M, Taffet GE, Mann DL. Hemodynamic regulation of tumor necrosis factor-α gene and protein expression in adult feline myocardium. Circ Res 1997;81:187–195.

    PubMed  Google Scholar 

  17. Sadoshima JI, Xu Y, Slayter HS, Izumo S. Autocrine release of angiotensin II mediates stretch-induced hypertrophy of cardiac myocytes in vitro. Cell 1993;75:977–984.

    Article  PubMed  Google Scholar 

  18. Ruwhof C, Van der LA. Mechanical stress-induced cardiac hypertrophy: mechanisms and signal transduction pathways. Cardiovasc Res 2000;47:23–37.

    Article  PubMed  Google Scholar 

  19. Force T, Michael A, Kilter H, Haq S. Stretch-activated pathways and left ventricular remodeling. J Card Fail 2002;8:S351–S358.

    Article  PubMed  Google Scholar 

  20. Mann DL. Basic mechanisms of left ventricular remodeling: the contribution of wall stess. J Card Fail 2005;10:S202–S206.

    Article  Google Scholar 

  21. Kono T, Sabbah HN, Rosman H, Alam M, Jafri S, Goldstein S. Left ventricular shape is the primary determinant of functional mitral regurgitation in heart failure. J Am Coll Cardiol 1992;20:1594–1598.

    PubMed  Google Scholar 

  22. Douglas PS, Morrow R, Ioli A, Reicheck N. Left ventricular shape, afterload, and survival in idiopathic dilated cardiomyopathy. J Am Coll Cardiol 1989;13:311–315.

    PubMed  Google Scholar 

  23. Vasan RS, Larson MG, Benjamin EJ, Evans JC, Levy D. Left ventricular dilation and the tisk of congestive heart failure in people without myocardial infarction. N Engl J Med 1997;336:1350–1355.

    Article  PubMed  Google Scholar 

  24. White HD, Norris RM, Brown MA, Brandt PW, Whitlock RM, Wild CJ. Left ventricular end-systolic volume as the major determinant of survival after recovery from myocardial infarction. Circulation 1987;76:44–51.

    PubMed  Google Scholar 

  25. St.John Sutton MS, Pfeffer MA, Plappert T, Rouleau J-L, Moye LA, Dagenais GR, Lamar GA, Klein M, Sussex B, Goldman S, Menapace Jr FJ, Parker JO, Lewis S, Sestier F, Gordon DF, McEwan P, Bernstein V, Braunwald E. Quantitative two-dimensional echocardiographic measurements are major predictors of adverse cardiovascular events after acute myocardial infarction. The protective effects of captopril. Circulation 1994;89:68–75.

    PubMed  Google Scholar 

  26. Ho KK, Pinsky JL, Kannel WB, Levy D. The epidemiology of heart failure: the Framingham Study. J Am Coll Cardiol 1993;22:6A–13A.

    PubMed  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Rights and permissions

Reprints and permissions

About this article

Cite this article

Mann, D.L. Left Ventricular Size and Shape: Determinants of Mechanical Signal Transduction Pathways. Heart Fail Rev 10, 95–100 (2005). https://doi.org/10.1007/s10741-005-4636-y

Download citation

  • Issue Date:

  • DOI: https://doi.org/10.1007/s10741-005-4636-y

Keywords

Navigation