Cardiac Football or Cause of Severe Tricuspid Regurgitation?

Abstract

77-YEAR-OLD, 175-cm, 71-kg man was admitted to the authors’ institution for evaluation of progressive dyspnea on exertion and reduced exercise tolerance of 2 years duration. His symptoms occasionally were accompanied by chest pressure without radiation and were relieved consistently with rest. The patient also described intermittent paroxysmal nocturnal dyspnea and recent lower-extremity swelling, but he denied orthopnea, diaphoresis, syncope, and palpitations. The patient had undergone 2-vessel coronary artery bypass graft surgery and an aortic valve replacement with a Carpentier-Edwards bioprosthetic valve (Edwards Life Sciences, Irvine, CA) for aortic insufficiency 24 years before the current admission. The patient’s past medical history also was notable for chronic atrial fibrillation (for which he received digoxin and warfarin), wellcontrolled essential hypertension (treated with carvedilol, lisinopril, and furosemide), and hyperlipidemia (treated with simvastatin). The physical examination revealed a harsh grade III of VI crescendo-decrescendo systolic murmur best heard at the 4th left intercostal space that radiated to the left axilla. A second, lower-pitched holosystolic murmur (grade II of VI) was noted at the 2nd right intercostal space. A grade II of VI early diastolic murmur also was heard at the left ventricular apex. Auscultation of the lungs indicated bilateral basilar rales. There was jugular venous distention present, and lower-extremity pitting edema was observed, but hepatojugular reflux was not elicited. Transesophageal echocardiography (TEE) was performed as part of the evaluation. The leaflets of the bioprosthesis were thickened, calcified, and sclerotic (not shown). Moderate aortic stenosis (peak gradient of 37 mmHg, area of 1.05 cm 2 ) and severe aortic insufficiency were present. The mitral valve leaflets also were calcified and showed reduced mobility concomitant with mild stenosis (area of 1.9 cm 2 ) and severe regurgitation (not shown). The TEE examination further revealed the images shown in Figures 1 through 3. What is the diagnosis? What is the mechanism responsible for the echocardiographic findings?