|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Ann Thorac Surg 2002;73:761
© 2002 The Society of Thoracic Surgeons
a Division of Cardiothoracic Surgery, University of California, San Diego, 200 West Arbor Dr, San Diego, CA 92103-8892, USA
e-mail: pthistlethwaite{at}ucsd.edu
This study by Dr Menzel and coworkers represents another contribution to the growing body of literature which suggests that tricuspid regurgitation secondary to thromboembolic pulmonary hypertension is relieved by pulmonary endarterectomy. In their small series of 39 patients, 33 patients experienced variable degrees of relief of tricuspid regurgitation by echocardiographic assessment after operation. The resolution of valvular dysfunction occurred in the immediate postoperative period, and none of the patients required tricuspid valve repair or replacement.
It is well known that patients with severe pulmonary hypertension develop functional tricuspid regurgitation due to annular dilatation and right ventricular volume overload [1, 2]. Pulmonary endarterectomy is one of the few procedures in cardiothoracic surgery where operation remote to any valvular structure results in resolution of severe tricuspid regurgitation. This operation usually causes dramatic reduction in pulmonary vascular resistance and right ventricular pressure. The question remains, however, why a small subset of patients undergoing this operation do not show improvement in tricuspid regurgitation and whether these patients can be identified preoperatively for risk/benefit stratification.
We have recently demonstrated in a series of over 200 patients undergoing pulmonary endarterectomy at the University of California, San Diego that one of the factors affecting the resolution of tricuspid regurgitation and hemodynamic outcome after pulmonary endarterectomy is the type and location of thromboembolic pathology in the pulmonary artery tree encountered at the time of operation [3]. Patients with intimal thickening/fibrosis and organized thrombus/fresh clot in the main or lobar pulmonary arteries showed almost complete resolution of tricuspid regurgitation, while patients with pathology limited to segmental arteries or who had a distal small vessel vasculopathic process did not show similar valvular or hemodynamic improvement. Isolated small vessel arteriolar disease (medical hyperplasia and hypertrophy) like that seen in primary pulmonary hypertension was not improved by blind pulmonary endarterectomy. This suggests that tricuspid valve outcome is determined by the degree of surgically accessible disease encountered at the time of operation.
Long-term remodeling of the right ventricle and pulmonary vascular bed after this operation and its effect on tricuspid valve function remain to be determined. Nonetheless, it is clear in the majority of patients undergoing pulmonary endarterectomy, that tricuspid valve repair/replacement is unnecessary for early restoration of valve function. The presented study underscores the intricate balance between thromboembolic pulmonary hypertension, right heart function, and tricuspid valve anatomy and gives definitive evidence that pulmonary endarterectomy corrects tricuspid valve regurgitation in this complex group of patients.
References
Related Article
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |