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Anatomic Relationship of the Complex Tricuspid Valve, Right Ventricle, and Pulmonary VasculatureA Review

Educational Objective
To describe the anatomy and physiology of the right ventricle, right atrium, and tricuspid valve as they relate to tricuspid regurgitation.
1 Credit CME
Key Points

Question  What are the anatomic, physiologic, and hemodynamic determinants of progressive tricuspid regurgitation?

Findings  In this narrative review, the complex relationship between the tricuspid valve apparatus and structure and function of the right side of the heart are described, as well as pulmonary vascular hemodynamics, starting with the anatomic construct, which determines these interactions. Abnormalities of any component can lead to a cascade of events that result in progressive tricuspid regurgitation.

Meaning  Understanding the pathophysiology of tricuspid regurgitation gives insight into clinical outcomes and the timing of interventions.


Importance  Severe functional or secondary tricuspid regurgitation (TR) is associated with poor long-term outcomes in natural history studies as well as specific disease states. An understanding of the physiologic causes of the TR is lacking precluding a systematic approach to treatment.

Observations  The complex anatomic relationship between the tricuspid valve apparatus and structure of the right side of the heart lends insight into the functional changes seen with secondary TR. The association of these changes with changes in pulmonary vascular hemodynamics can lead to a cascade of events that result in disease progression.

Conclusions and Relevance  Appreciating the role of pulmonary vascular hemodynamics on right ventricular and tricuspid valve morphology and function improves our understanding of the pathophysiology of secondary TR. The limitations of current therapeutic approaches for secondary TR have stimulated interest in improving outcomes with this morbid disease. Changes in timing or approach to intervention require a more comprehensive understanding of the pathophysiology.

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Article Information

Corresponding Author: Rebecca T. Hahn, MD, Columbia University Medical Center, New York-Presbyterian Hospital, 177 Fort, Washington Ave, New York, NY 10032 (rth2@columbia.edu).

Accepted for Publication: February 6, 2019.

Published Online: April 17, 2019. doi:10.1001/jamacardio.2019.0535

Author Contributions: Drs Hahn and Delhaas had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.

Concept and design: All authors.

Acquisition, analysis, or interpretation of data: Waxman, Denti.

Drafting of the manuscript: All authors.

Critical revision of the manuscript for important intellectual content: Waxman, Denti, Delhaas.

Statistical analysis: Denti.

Administrative, technical, or material support: Denti.

Supervision: Denti.

Conflict of Interest Disclosures: Dr Hahn reports speaker fees from Boston Scientific Corporation and Baylis Medical Company, Inc; nonfinancial support for being a speaker and consultant for Edwards Lifescience and Philips Healthcare; consulting for Abbott Structural, Medtronic, Navigate, and Siemens Healthcare; nonfinancial support from 3mensio and GE Healthcare; and is the chief scientific officer for the Echocardiography Core Laboratory at the Cardiovascular Research Foundation for multiple industry-sponsored trials, for which she receives no direct industry compensation. Dr Waxman serves on steering committees for clinical trials sponsored by United Therapeutics, Medtronic, Gossamer Bio, and Acceleron Pharma and does not receive any direct compensation. No other disclosures were reported.

Additional Contributions: We thank Dmitry Levin, BA, University of Washington, Center for CardioVascular Innovation, for creating Figure 1. He was not compensated for this work.

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