scholarly journals Physiological and Clinical Consequences of Right Ventricular Volume Overload Reduction After Transcatheter Treatment for Tricuspid Regurgitation

2019 ◽  
Vol 12 (15) ◽  
pp. 1423-1434 ◽  
Author(s):  
Karl-Philipp Rommel ◽  
Christian Besler ◽  
Thilo Noack ◽  
Stephan Blazek ◽  
Maximilian von Roeder ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Tricuspid Regurgitation ◽  
Volume Overload ◽  
Ventricular Volume ◽  
Right Ventricular Volume ◽  
Clinical Consequences

Prolonged repolarization in atrial septal defect: An example of mechanoelectrical feedback due to right ventricular volume overload

Heart Rhythm ◽  
2016 ◽  
Vol 13 (6) ◽  
pp. 1303-1308 ◽  
Author(s):  
Kristina Rücklová ◽  
Karel Koubský ◽  
Viktor Tomek ◽  
Peter Kubuš ◽  
Jan Janoušek
Keyword(s):  
Right Ventricular ◽  
Atrial Septal Defect ◽  
Septal Defect ◽  
Volume Overload ◽  
Ventricular Volume ◽  
Right Ventricular Volume

Normal myocardial function in severe right ventricular volume overload hypertrophy

2001 ◽  
Vol 280 (1) ◽  
pp. H11-H16 ◽  
Author(s):  
Yuji Ishibashi ◽  
Judith C. Rembert ◽  
Blase A. Carabello ◽  
Shintaro Nemoto ◽  
Masayoshi Hamawaki ◽  
...  
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Tricuspid Regurgitation ◽  
Contractile Function ◽  
Right Heart Failure ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Right Ventricular Volume ◽  
Right Heart ◽  
Severe Tricuspid Regurgitation

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 μm) nor the velocity (2.92 ± 0.12 μm/s) of sarcomere shortening differed from controls (0.179 ± 0.005 μm and 3.09 ± 0.11 μm/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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