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12 June 2026 : Case report  Japan

[In Press] Severe Tricuspid Regurgitation: Traumatic Papillary Muscle Rupture Mimicking Infective Endocarditis—A Case Report

Challenging differential diagnosis, Management of emergency care, Rare disease

Soichiro Kobayashi12E, Taku Omori ORCID logo1E, Daisuke Izumi23E, Toshiya Tokui4E, Atsunobu Kasai2E, Kaoru Dohi1E

DOI: 10.12659/AJCR.952267

Am J Case Rep In Press; DOI: 10.12659/AJCR.952267  

Available online: 2026-06-12, In Press, Corrected Proof

Publication in the "In-Press" formula aims at speeding up the public availability of the pending manuscript while waiting for the final publication. The assigned DOI number is active and citable. The availability of the article in the Medline, PubMed and PMC databases as well as Web of Science will be obtained after the final publication according to the journal schedule

Abstract

BACKGROUND
Differentiating traumatic tricuspid regurgitation (TR) from infective endocarditis (IE) is clinically crucial in patients presenting with abnormal tricuspid valve findings after blunt chest trauma. Particularly, papillary muscle rupture caused by trauma can produce mobile valvular structures that closely resemble vegetations, making accurate diagnosis challenging in the acute setting.
CASE REPORT
A man in his 60s with pulmonary sarcoidosis was admitted after a 5-m fall, sustaining multiple fractures. Preoperative transthoracic echocardiography revealed a 7-mm mobile structure on the anterior tricuspid leaflet with flail motion and severe TR. Because of fever, IE was suspected; however, blood cultures and further investigations excluded IE. A diagnosis of traumatic TR due to papillary muscle rupture was made. Although the patient was hemodynamically stable under medical therapy, the heart team recommended surgery to prevent long-term heart failure. Four months after fracture repair, tricuspid valve repair with artificial chordae and annuloplasty was performed. The surgical findings were fully consistent with the preoperative diagnosis, and pathological examination of the ruptured papillary muscle demonstrated coagulative necrosis without significant inflammatory infiltration, supporting a traumatic etiology. At 4-year follow-up, he remains stable without signs of heart failure exacerbation.
CONCLUSIONS
Accurate differentiation between traumatic TR due to papillary muscle rupture and IE is essential, as misclassification may lead to unnecessary antimicrobial therapy or delayed surgical intervention. This case highlights how mobile traumatic lesions can closely mimic vegetations and underscores the importance of comprehensive evaluation to guide appropriate management and optimize outcomes.

Keywords: Cardiovascular Diseases; Case Reports; Heart Valve Diseases; Traumatology

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American Journal of Case Reports eISSN: 1941-5923
American Journal of Case Reports eISSN: 1941-5923