The Forgotten Valve
2015; Lippincott Williams & Wilkins; Volume: 132; Issue: 7 Linguagem: Inglês
10.1161/circulationaha.115.016315
ISSN1524-4539
AutoresMohammed Al‐Hijji, Jung Tak Park, Abdallah El Sabbagh, Muhammad Amin, Joseph J. Maleszewski, Daniel D. Borgeson,
Tópico(s)Cardiac Structural Anomalies and Repair
ResumoHomeCirculationVol. 132, No. 7The Forgotten Valve Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplemental MaterialFree AccessResearch ArticlePDF/EPUBThe Forgotten ValveIsolated Severe Tricuspid Valve Stenosis Mohammed Al-Hijji, MD, Jae Yoon Park, MD, Abdallah El Sabbagh, MD, Muhammad Amin, MD, PhD, Joseph J. Maleszewski, MD and Daniel D. Borgeson, MD Mohammed Al-HijjiMohammed Al-Hijji From Mayo Clinic, Division of Cardiovascular Diseases, Rochester, MN (M.A.-H., J.Y.P., A.E.S., D.D.B.); and Mayo Clinic, Division of Cardiovascular Pathology, Rochester, MN (M.A., J.J.M.). , Jae Yoon ParkJae Yoon Park From Mayo Clinic, Division of Cardiovascular Diseases, Rochester, MN (M.A.-H., J.Y.P., A.E.S., D.D.B.); and Mayo Clinic, Division of Cardiovascular Pathology, Rochester, MN (M.A., J.J.M.). , Abdallah El SabbaghAbdallah El Sabbagh From Mayo Clinic, Division of Cardiovascular Diseases, Rochester, MN (M.A.-H., J.Y.P., A.E.S., D.D.B.); and Mayo Clinic, Division of Cardiovascular Pathology, Rochester, MN (M.A., J.J.M.). , Muhammad AminMuhammad Amin From Mayo Clinic, Division of Cardiovascular Diseases, Rochester, MN (M.A.-H., J.Y.P., A.E.S., D.D.B.); and Mayo Clinic, Division of Cardiovascular Pathology, Rochester, MN (M.A., J.J.M.). , Joseph J. MaleszewskiJoseph J. Maleszewski From Mayo Clinic, Division of Cardiovascular Diseases, Rochester, MN (M.A.-H., J.Y.P., A.E.S., D.D.B.); and Mayo Clinic, Division of Cardiovascular Pathology, Rochester, MN (M.A., J.J.M.). and Daniel D. BorgesonDaniel D. Borgeson From Mayo Clinic, Division of Cardiovascular Diseases, Rochester, MN (M.A.-H., J.Y.P., A.E.S., D.D.B.); and Mayo Clinic, Division of Cardiovascular Pathology, Rochester, MN (M.A., J.J.M.). Originally published18 Aug 2015https://doi.org/10.1161/CIRCULATIONAHA.115.016315Circulation. 2015;132:e123–e125A 67-year-old white man with a history of coronary artery disease status, post–3-vessel coronary artery bypass grafting (13 years earlier) and ischemic heart disease, presented with fatigue and dyspnea on exertion for 6 months. He had undergone chronic resynchronization therapy defibrillator placement 9 months before. He denied any weight gain, paroxysmal nocturnal dyspnea, orthopnea, or lower extremity edema. On physical examination, jugular venous pressure was elevated at 12 cm H2O with prominent a and v waves and positive hepatojugular reflux. He had a grade II/VI systolic ejection murmur at the right upper sternal border and a I/IV holosystolic murmur at the right lower sternal border. His lungs were clear to auscultation, and he had no lower extremity edema.ECG demonstrated sinus rhythm at a ventricular rate of 90 beats/min. The pulmonary function test and overnight oximetry were within normal limits. The treadmill exercise test was notable for cardiac limitation with peak Vo2 of 14.5 mL·kg–1·min–1 (56% predicted) and abnormal pulmonary response with high Ve/Vco2 and decrease in oxygen saturation to 85% with exercise from 94% at rest. Transthoracic echocardiogram was notable for severe tricuspid valve stenosis (TS) (diastolic mean gradient 7 mm Hg at a heart rate of 86 beats/min) with mild regurgitation (Figure 1; online-only Data Supplement Movies I and II). Valve morphology was difficult to ascertain owing to a device lead. There was leftward displacement of an atrial septal aneurysm consistent with elevated right atrial mean pressures (online-only Data Supplement Movie III). Otherwise, right ventricular size was normal with borderline decreased systolic function and an estimated right ventricular systolic pressure of 31 mm Hg with normal left ventricular size and a calculated ejection fraction of 49%. Transesophageal echocardiogram demonstrated an atrial septal aneurysm with a large patent foramen ovale resulting in a significant right-to-left shunt at rest (Figure 2; online-only Data Supplement Movie IV). Unfortunately, the tricuspid and pulmonary valve leaflets were not well visualized.Download figureDownload PowerPointFigure 1. A, Continuous-wave Doppler flow obtained by TTE of the tricuspid valve before CRT-D implantation showing maximum inflow velocity of 0.6 m/s and mean gradient across the valve ≈0.5 mm Hg (arrow pointing at the TV inflow signal). B, Continuous-wave Doppler flow of severe tricuspid valve stenosis after CRT-D implantation. The maximum velocity is 1.8 m/s and mean gradient across the tricuspid valve is 7 mm Hg (arrow pointing at the TV inflow signal). CRT-D indicates cardiac resynchronization defibrillator, total system; TTE, transthoracic echocardiogram; and TV, tricuspid valve.Download figureDownload PowerPointFigure 2. Color Doppler still-frame image from transesophageal echocardiogram showing large patent foramen ovale with flow (black arrow) from the right to the left atrium.He was further evaluated with left and right heart catheterization, which was notable for elevated mean right atrial pressures at rest and exercise, 5 mm Hg and 19 mm Hg, respectively. There was diastolic transtricuspid gradient of 5 mm Hg at rest, rising to 14 mm Hg with exercise (Figure 3), consistent with TS. His pulmonary artery pressure and pulmonary capillary wedge pressure were normal at rest and during exercise. Infusion of agitated saline during exercise revealed robust right-to-left shunting across the interatrial septum with concomitant decrease in arterial oxygen saturation from 92% at rest to 88% with exercise.Download figureDownload PowerPointFigure 3. Right atrial and right ventricular pressure waveforms measured during right heart catheterization at rest (A) and with exercise (B) demonstrate increase in transtricuspid gradient from 5 mm Hg to 14 mm Hg. (Gradient is shown with double-head arrow sign.)Given these findings, the patient was taken to the operating room for redo thoracotomy. On such, the large patent foramen ovale and septal aneurysm were visualized, and a severely stenotic tricuspid valve (reported orifice size about the tip of a small finger), as well, with a nonadherent pacemaker lead across the valve. He underwent tricuspid valve replacement with the use of a 33-mm Hancock bioprosthesis and closure of patent foramen ovale without complication. Gross examination of the valve in the pathology laboratory revealed markedly abnormal valvular tissue, characterized by abnormal leaflet thickening with mild to moderate fibrotic fusion of both the valvular and subvalvular apparati (Figure 4). These features, in combination, were suggestive of a postinflammatory process.Download figureDownload PowerPointFigure 4. A, Gross image of excised thickened native tricuspid valve before replacement with a 33-mm Hancock bioprosthesis. B, Tissue section of the resected tricuspid valve exhibits fibrotic thickening of the leaflet tissue with mild to moderate nongranulomatous lymphoplasmacytic inflammation and scattered thick-walled blood vessels. These findings are consistent with postinflammatory disease.Our patient had a rare presentation of dyspnea on exertion related to hypoxemia with activity in the setting of severe TS and persistent right-to-left shunt from coexistent patent foramen ovale. During exercise, there was an isolated right atrial pressure rise leading to a significant right-to-left atrial pressure gradient and, hence, right-to-left shunt. Given the shunt physiology, the patient did not sense a relief of symptoms with oxygen therapy. After the operation, his symptoms resolved substantially.Tricuspid valve stenosis is an uncommon clinical entity that can be seen in the setting of rheumatic heart disease, carcinoid syndrome, metabolic or enzymatic abnormalities, or infective endocarditis.1 There are few reported cases of pacemaker-mediated TS caused by various mechanisms, including focal tricuspid valve leaflet fibrosis from laceration or perforation and fusion of looped leads with the tricuspid valve apparatus.2,3 The main treatment for symptomatic severe TS is interventional. Tricuspid valve surgery is preferable over balloon commissurotomy because the latter can create or worsen tricuspid regurgitation.4 The pathological findings were consistent with postinflammatory disease, which in a single-center study was observed in 92% of pathological specimens of severe TS.5 However, the exact etiology of isolated severe TS due to postinflammatory disease remains unclear as in our patient.DisclosuresNone.FootnotesThe online-only Data Supplement is available with this article at http://circ.ahajournals.org/lookup/suppl/doi:10.1161/CIRCULATIONAHA.115.016315/-/DC1.Correspondence to Mohammed Al-Hijji, MD, Mayo Clinic, Division of Cardiovascular Diseases, Department of Medicine, Gonda 6, 200 First St SW, Rochester, MN 55905. E-mail [email protected]References1. Bruce CJ, Connolly HM.Right-sided valve disease deserves a little more respect.Circulation. 2009; 119:2726–2734. doi: 10.1161/CIRCULATIONAHA.108.776021.LinkGoogle Scholar2. Ribeiro H, Magalhães P, Ferreira C, Baptista A, Margato R, Carvalho S, Rosa P, Mateus P, Ferreira A, Moreira JI.[Pacemaker lead-induced tricuspid stenosis: a report of two cases].Rev Port Cardiol. 2012; 31:305–308. doi: 10.1016/j.repc.2012.02.008.CrossrefMedlineGoogle Scholar3. Skoric B, Baricevic Z, Brida M, Samardzic J, Jurin H, Milicic D.Dynamic tricuspid valve stenosis induced with a pacemaker lead: a case report.J Heart Valve Dis. 2014; 23:142–144.MedlineGoogle Scholar4. Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP, Guyton RA, O'Gara PT, Ruiz CE, Skubas NJ, Sorajja P, Sundt TM, Thomas JD; ACC/AHA Task Force Members. 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines.Circulation. 2014; 129:e521–e643. doi: 10.1161/CIR.0000000000000031.LinkGoogle Scholar5. Hauck AJ, Freeman DP, Ackermann DM, Danielson GK, Edwards WD.Surgical pathology of the tricuspid valve: a study of 363 cases spanning 25 years.Mayo Clin Proc. 1988; 63:851–863.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Atchison T and Emani S (2022) Hemodynamic Assessment of Tricuspid Valve Disease Tricuspid Valve Disease, 10.1007/978-3-030-92046-3_4, (33-41), . van Buuren F, Gati S, Sharma S, Papadakis M, Adami P, Niebauer J, Pelliccia A, Rudolph V, Börjesson M, Carre F, Solberg E, Heidbuchel H, Caselli S, Corrado D, Serratosa L, Biffi A, Pressler A, Schmied C, Panhuyzen-Goedkoop N, Rasmussen H, La Gerche A, Faber L, Bogunovic N, D'Ascenzi F and Mellwig K (2021) Athletes with valvular heart disease and competitive sports: a position statement of the Sport Cardiology Section of the European Association of Preventive Cardiology, European Journal of Preventive Cardiology, 10.1093/eurjpc/zwab058, 28:14, (1569-1578), Online publication date: 20-Dec-2021. Sharma Y, Panda P, Uppal L and Debi U (2020) Case of calcific tricuspid and pulmonary valve stenosis, BMJ Case Reports, 10.1136/bcr-2020-235190, 13:9, (e235190), Online publication date: 1-Sep-2020. Salinas N, Killinger G, Segovia A, Ledesma M and Rodríguez Correa C (2022) Estenosis tricuspídea relacionada a catéter endocavitario. Una complicación poco frecuente., Revista de Ecocardiografía Práctica y Otras Técnicas de Imagen Cardíaca, 10.37615/retic.v5n1a11, 5:1, (49-52) August 18, 2015Vol 132, Issue 7 Advertisement Article InformationMetrics © 2015 American Heart Association, Inc.https://doi.org/10.1161/CIRCULATIONAHA.115.016315PMID: 26283605 Originally publishedAugust 18, 2015 Keywordsforamen ovale, patenttricuspid valve stenosisPDF download Advertisement SubjectsCardiovascular SurgeryDiagnostic TestingEchocardiographyHeart Failure
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