Normal myocardial function in severe right ventricular volume overload hypertrophy

Severe left ventricular volume overloading causes myocardial and cellular c ontractile dysfunction. Whether this is also true for severe right ventricu lar volume overloading was unknown. We therefore created severe tricuspid r egurgitation percutaneously in seven dogs and then observed them for 3.5-4. 0 yr. All five surviving operated dogs had severe tricuspid regurgitation a nd right heart failure, including massive ascites, but they did not have le ft heart failure. Right ventricular cardiocytes were isolated from these an d from normal dogs, and sarcomere mechanics were assessed via laser diffrac tion. Right ventricular cardiocytes from the tricuspid regurgitation dogs w ere 20% longer than control cells, but neither the extent (0.171 +/- 0.005 mum) nor the velocity (2.92 +/- 0.12 mum/s) of sarcomere shortening differe d from controls (0.179 +/- 0.005 mm and 3.09 +/- 0.11 mum/s, respectively). Thus, despite massive tricuspid regurgitation causing overt right heart fa ilure, intrinsic right ventricular contractile function was normal. This fi nding for the severely volume-overloaded right ventricle stands in distinct contrast to our finding for the left ventricle severely volume overloaded by mitral regurgitation, wherein intrinsic contractile function is depresse d.