Elevated Strain and Structural Disarray Occur at the Right Ventricular Apex

  • V. Hariharan
  • J. Provost
  • S. Shah
  • E. Konofagou
  • H. Huang
Article

Abstract

The right ventricular apex (RVA) is a potential hot spot for development of cardiac rhythm anomalies. Many conditions, including arrhythmogenic right ventricular cardiomyopathy and Brugada’s syndrome affect the RVA, and further, the RVA remains an incompletely characterized pacing region. Whether there are structural reasons underlying these conduction properties remains unsettled. In the current study, we characterize the mechanical strains and structural attributes of the right ventricular wall, and test the hypothesis that the right ventricular apex experiences heterogeneous strain distributions and altered fiber organization, and is thus susceptible to conduction alterations. Electromechanical wave imaging (EWI), or elastography, of hearts was used to quantify mechanical strains occurring through a cardiac cycle. Histological and immunofluorescence imaging techniques were used to examine cardiac wall structure and arrangement of junctional proteins. Right ventricular mechanical strains were elevated and sustained throughout systole, compared to the left ventricle and septum. Heterogeneous strain distributions, myocardial fiber disarray, and altered junctional protein localization occured at the RVA. Disarray and altered strain distributions suggest decreased structural strength at the right ventricular apex in particular and increased mechanical impositions in the right ventricle, respectively. Thus, these data demonstrate why the right ventricular apex may be particularly vulnerable to conduction abnormalities.

Keywords

Cardiac structure Cardiomyopathy Structure/function Ultrasound Elastography 

Abbreviations

ARVC

Arrhythmogenic Right Ventricular Cardiomyopathy

RV

Right ventricle

LV

Left ventricle

RVA

Right ventricular apex

Notes

Acknowledgments

We thank Mahyar Zoghi for his assistance. This work was supported in part by NIH HL102361, and the National Science Foundation Graduate Research Fellowship.

Conflict of interest

None

References

  1. 1.
    Asimaki, A., H. Tandri, H. D. Huang, et al. A new diagnostic test for arrhythmogenic right ventricular cardiomyopathy. N. Engl. J. Med. 360(11):1075–1084, 2009.CrossRefGoogle Scholar
  2. 2.
    Furman, S., and J. B. Schwedel. An intracardiac pacemaker for Stokes-Adams seizures. N. Engl. J. Med. 261:943–948, 1959.CrossRefGoogle Scholar
  3. 3.
    Grover, M., and S. A. Glantz. Endocardial pacing site affects left ventricular end-diastolic volume and performance in the intact anesthetized dog. Circ. Res. 53(1):72–85, 1983.Google Scholar
  4. 4.
    Hayashi, M., S. Takatsuki, P. Maison-Blanche, et al. Ventricular repolarization restitution properties in patients exhibiting type 1 Brugada electrocardiogram with and without inducible ventricular fibrillation. J. Am. Coll. Cardiol. 51(12):1162–1168, 2008.CrossRefGoogle Scholar
  5. 5.
    Ho, S. Y., and P. Nihoyannopoulos. Anatomy, echocardiography, and normal right ventricular dimensions. Heart 92:I2–I13, 2006.CrossRefGoogle Scholar
  6. 6.
    Kallel, F., and J. Ophir. A least-squares strain estimator for elastography. Ultrason. Imaging 19(3):195–208, 1997.Google Scholar
  7. 7.
    Kaplan, S. R., J. J. Gard, N. Protonotarios, et al. Remodeling of myocyte gap junctions in arrhythmogenic right ventricular cardiomyopathy due to a deletion in plakoglobin (Naxos disease). Heart Rhythm. 1(1):3–11, 2004.CrossRefGoogle Scholar
  8. 8.
    Konofagou, E. E., S. Fung-Kee-Fung, J. Luo, and M. Pernot. Imaging the mechanics and electromechanics of the heart. Conf. Proc. IEEE Eng. Med. Biol. Soc. Suppl:6648–6651, 2006.Google Scholar
  9. 9.
    Kwong, K. F., R. B. Schuessler, K. G. Green, et al. Differential expression of gap junction proteins in the canine sinus node. Circ. Res. 82(5):604–612, 1998.Google Scholar
  10. 10.
    Leclercq, C., D. Gras, A. Le Helloco, L. Nicol, P. Mabo, and C. Daubert. Hemodynamic importance of preserving the normal sequence of ventricular activation in permanent cardiac pacing. Am. Heart J. 129(6):1133–1141, 1995.CrossRefGoogle Scholar
  11. 11.
    Lee, W. N., J. Provost, K. Fujikura, J. Wang, and E. E. Konofagou. In vivo study of myocardial elastography under graded ischemia conditions. Phys. Med. Biol. 56(4):1155–1172, 2011.CrossRefGoogle Scholar
  12. 12.
    Lobo, F. V., H. A. Heggtveit, J. Butany, M. D. Silver, and J. E. Edwards. Right ventricular dysplasia: morphological findings in 13 cases. Can. J. Cardiol. 8(3):261–268, 1992.Google Scholar
  13. 13.
    Marcus, F. I., G. H. Fontaine, G. Guiraudon, et al. Right ventricular dysplasia—a report of 24 adult cases. Circulation 65(2):384–398, 1982.CrossRefGoogle Scholar
  14. 14.
    Navarrete, A. Idiopathic ventricular tachycardia arising from the right ventricular apex. Europace 10(11):1343–1345, 2008.CrossRefGoogle Scholar
  15. 15.
    Provost, J., W. N. Lee, K. Fujikura, and E. E. Konofagou. Electromechanical wave imaging of normal and ischemic hearts in vivo. IEEE Trans. Med. Imaging 29(3):625–635, 2010.Google Scholar
  16. 16.
    Sen-Chowdhry, S., M. D. Lowe, S. C. Sporton, and W. J. McKenna. Arrhythmogenic right ventricular cardiomyopathy: clinical presentation, diagnosis, and management. Am. J. Med. 117(9):685–695, 2004.CrossRefGoogle Scholar
  17. 17.
    Sheehan, F., and A. Redington. The right ventricle: anatomy, physiology and clinical imaging. Heart 94(11):1510–1515, 2008.CrossRefGoogle Scholar
  18. 18.
    Takayama, Y., K. D. Costa, and J. W. Covell. Contribution of laminar myofiber architecture to load-dependent changes in mechanics of LV myocardium. Am. J. Physiol. Heart C. 282(4):H1510–H1520, 2002.Google Scholar
  19. 19.
    Thiene, G., A. Nava, D. Corrado, L. Rossi, and N. Pennelli. Right ventricular cardiomyopathy and sudden death in young people. N. Engl. J. Med. 318(3):129–133, 1988.CrossRefGoogle Scholar
  20. 20.
    Usyk, T. P., R. Mazhari, and A. D. McCulloch. Effect of laminar orthotropic myofiber architecture on regional stress and strain in the canine left ventricle. J. Elasticity 61(1–3):143–164, 2000.MATHCrossRefGoogle Scholar
  21. 21.
    Wang, S. G., W. N. Lee, J. Provost, J. W. Luo, and E. E. Konofagou. A composite high-frame-rate system for clinical cardiovascular imaging. IEEE Trans. Ultrason. Ferroelectr. Freq. Control. 55(10):2221–2233, 2008.CrossRefGoogle Scholar

Copyright information

© Biomedical Engineering Society 2012

Authors and Affiliations

  • V. Hariharan
    • 1
  • J. Provost
    • 1
  • S. Shah
    • 1
  • E. Konofagou
    • 1
  • H. Huang
    • 1
  1. 1.Department of Biomedical EngineeringColumbia UniversityNew YorkUSA

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