Volume 137, Issue 6 , Page 1573, June 2009
Experimental ventricular pressure overload in young animals induces cardiomyocyte hypertrophy in addition to hyperplasia of contractile and noncontractile elements of the myocardium
Article Outline
CTSNet classification: 18
To the Editor:
Since the early 1990s, we have been working with experimental right ventricular hypertrophy using young goats aged 4 to 8 weeks to achieve right (subpulmonary) ventricular retraining by means of a balloon catheter or an adjustable pulmonary artery banding system.1, 2, 3 We have consistently found a hypertrophic response of the cardiomyocytes. Moreover, we have also demonstrated that the right ventricle responds not only with hypertrophy of the myocardial fibers but also with hyperplasia of the contractile and interstitial components of the myocardium.3 Recently, Leeuwenburgh and colleagues4 demonstrated the development of a hyperplastic rather than a hypertrophic myocardial response in young animals submitted to chronic right ventricular pressure overload. Their findings deserve some comments because previous studies also showed a hypertrophic response, even in young animals. Anversa and associates,5 studying 30 normal Wistar rats at 1, 5, and 11 days of age, found that left ventricular cardiomyocytes presented both hypertrophy and hyperplasia, attributing these to the physiologic pressure overload imposed on that chamber after birth.
Based on the age of the lambs (2–3 weeks), the duration of pressure overload (8-week period), and the reported data from the study by Leeuwenburgh and colleagues,4 we are surprised about the fact that the authors did not find any signal of myocardial fiber hypertrophy. Moreover, even considering the hyperplastic response alone, no mention was made regarding the presence or absence of proliferating (proliferating cell nuclear antigen–labeled) interstitial cells. If, as the authors stated, “more of the same tissue” was found in the trained myocardium, in addition to proliferating cardiomyocytes, they should have found some hyperplasia of cells from the interstitial compartment of the heart. In fact, this was a prominent feature of our experimental model of pressure overload in young animals.3 The number of interstitial and vessel cells labeled by the cell proliferation marker Ki67 in our study was 14 and 18 times greater, respectively, than that of the cardiomyocytes under 2 different protocols of ventricular systolic overload (continuous and intermittent).3
References
- Reversible pulmonary trunk banding with a balloon catheter: assessment of rapid pulmonary ventricular hypertrophy. J Thorac Cardiovasc Surg. 2000;120:66–72
- Reversible pulmonary trunk banding II. An experimental model for rapid pulmonary ventricular hypertrophy. J Thorac Cardiovasc Surg. 2002;124:999–1006
- Reversible pulmonary trunk banding III: assessment of myocardial adaptive mechanisms—contribution of cell proliferation. J Thorac Cardiovasc Surg. 2007;133:1510–1516
- Chronic right ventricular pressure overload results in a hyperplastic rather than a hypertrophic myocardial response. J Anat. 2008;212:286–294
- . Morphometric study of early postnatal development in the left and right ventricular myocardium of the rat. Hypertrophy, hyperplasia and binucleation of myocytes. Circ Res. 1980;46:495–502
PII: S0022-5223(09)00218-9
doi:10.1016/j.jtcvs.2009.01.021
© 2009 The American Association for Thoracic Surgery. Published by Elsevier Inc. All rights reserved.
Volume 137, Issue 6 , Page 1573, June 2009
