Key result
Despite massive tricuspid regurgitation causing overt right heart failure, intrinsic right ventricular contractile function remained normal.
Why the study?
Does severe right ventricular volume overload from tricuspid regurgitation cause intrinsic myocardial contractile dysfunction in a dog model?
Does severe right ventricular volume overload from tricuspid regurgitation cause intrinsic myocardial contractile dysfunction in a dog model?
Despite massive tricuspid regurgitation causing overt right heart failure, intrinsic right ventricular contractile function remains normal at the cellular level, contrasting with the depressed function seen in left ventricular volume overload.
Answers are grounded in this paper and cite their sources.
Intrinsic RV contractility preserved despite TR-induced RHF in dogs; challenges LV volume-overload paradigm and leaves open human translation.
Severe left ventricular volume overloading causes myocardial and cellular contractile dysfunction. Whether this is also true for severe right ventricular volume overloading was unknown. We therefore created severe tricuspid regurgitation percutaneously in seven dogs and then observed them for 3.5-4.0 yr. All five surviving operated dogs had severe tricuspid regurgitation and right heart failure, including massive ascites, but they did not have left heart failure. Right ventricular cardiocytes were isolated from these and from normal dogs, and sarcomere mechanics were assessed via laser diffraction. Right ventricular cardiocytes from the tricuspid regurgitation dogs were 20% longer than control cells, but neither the extent (0.171 +/- 0.005 microm) nor the velocity (2.92 +/- 0.12 microm/s) of sarcomere shortening differed from controls (0.179 +/- 0.005 microm and 3.09 +/- 0.11 microm/s, respectively). Thus, despite massive tricuspid regurgitation causing overt right heart failure, intrinsic right ventricular contractile function was normal. This finding 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 depressed.
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Ishibashi et al. (2001) studied Severe right ventricular volume overload hypertrophy (n=7). Percutaneously created severe tricuspid regurgitation vs. Normal dogs was evaluated on Extent and velocity of sarcomere shortening. Despite massive tricuspid regurgitation causing overt right heart failure, intrinsic right ventricular contractile function remained normal.
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