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Ann Thorac Surg 2006;82:989-995
© 2006 The Society of Thoracic Surgeons
a Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany
b Department of Cardiovascular Surgery, Semmelweis University, Budapest, Hungary
c Department of Cardiology, University of Heidelberg, Heidelberg, Germany
d Department of Cardiovascular Surgery, University of Freiburg, Freiburg, Germany
Accepted for publication April 13, 2006.
* Address correspondence to Dr Szabó, Department of Cardiac Surgery, Im Neuenheimer Feld 110, 69120 Heidelberg, Germany. (Email: dzsi{at}hotmail.com).
Presented at the Poster Session of the Forty-second Annual Meeting of The Society of Thoracic Surgeons, Chicago, IL, Jan 30–Feb 1, 2006.
BACKGROUND: Increased right ventricular afterload is a common problem after correction of various heart diseases with chronic volume overload. We determined the effects of an acute increase of right ventricular afterload in normal and chronically volume overloaded hearts.
METHODS: In 6 dogs, volume overload was induced by chronic arteriovenous shunts for 3 months. Six sham-operated animals served as controls. After closing the shunts, right ventricular systolic and end-diastolic pressure as well as end-diastolic volume were measured by conductance catheter. In addition, pressure–volume loops were recorded. Myocardial contractility was described by the slope of the end-systolic pressure–volume relationship. Afterload was increased to right ventricular systolic pressure to 35 mm Hg and to 50 mm Hg by pulmonary banding.
RESULTS: Chronic volume overload resulted in a significant increase of right ventricular systolic pressure (34 ± 2 versus 25 ± 2 mm Hg, p < 0.05), end-diastolic pressure (10.4 ± 1.7 versus 6.8 ± 0.4 mm Hg, p < 0.05), and end-diastolic volume (39 ± 2 versus 33 ± 3 mL, p < 0.05). Baseline contractility (1.47 ± 0.24 versus 1.53 ± 0.32 mm Hg/mL) did not differ. While afterload increase to 35 and 50 mm Hg led to stepwise increase in contractility (2.73 ± 0.30 mm Hg/mL and 4.15 ± 0.30 mm Hg/mL, p < 0.05 versus baseline, respectively) at unchanged end-diastolic pressure and volume in controls, it showed only a slight increase (2.11 ± 0.38 mm Hg/mL and 2.99 ± 0.29 mm Hg/mL, p < 0.05 versus sham) with concomitant increase in end-diastolic pressure (12.4 ± 2.2 mm Hg/mL and 16.3 ± 1.9 mm Hg, p < 0.05) and volume (42 ± 4 mL and 48 ± 8 mL, p < 0.05) in the chronically volume overloaded group.
CONCLUSIONS: Chronic volume overload per se does not impair right ventricular contractility. However, the inotropic adaptation (homeometric autoregulation) to an increased afterload is limited, which is partly compensated by the Frank-Starling mechanism (heterometric autoregulation).
Related Article
Ann. Thorac. Surg. 2006 82: 995.
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  P. Pokreisz, G. Marsboom, and S. Janssens Pressure overload-induced right ventricular dysfunction and remodelling in experimental pulmonary hypertension: the right heart revisited Eur. Heart J. Suppl., December 1, 2007; 9(suppl_H): H75 - H84. [Abstract] [Full Text] [PDF]
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 A. J. Parry Invited commentary. Ann. Thorac. Surg., September 1, 2006; 82(3): 995 - 995. [Full Text] [PDF]
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