Noninvasive diagnosis of complications of the mitral bioprosthesis

Horowitz, M.; Goodman, Daniel J.; Hancock, E. William; Popp, Richard L.

doi:10.1016/s0022-5223(19)40217-1

Cited by 35 publications

(2 citation statements)

References 24 publications

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“…Late occurrence of low output state following valve replacement may also be connected with valve thrombosis, as occurred in one of our patients. We agree with the interpretation of Horowitz et al [21] that major valve thrombi are caused by stagnant flow in the presence of extremely impaired cardiac function, and by alterations of the clotting mechanism. Since all thrombi were related to the alloplastic parts of the prosthesis (e.g., the sewing ring and the suture line), we believe that these parts are the primary sites of thrombosis, rather than the valve tissue itself.…”

Section: Discussionsupporting

confidence: 93%

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Thrombotic complications after valve replacement with porcine heterografts

Hetzer

Gerbode

et al. 1979

World j. surg.

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The incidence of thrombotic and thromboembolic (TE) complications after Hancock valve replacement was reviewed in 140 patients with mitral valve prostheses and 150 patients with aortic valve prostheses. In patients with aortic valves, 1 embolus occurred and another patient was found at autopsy to have thrombi on a degenerated valve. Both patients had been on aspirin treatment. There was no TE event in patients receiving no anticoagulant therapy. In patients with mitral valves, 16 showed pre‐ and/or postoperative low output syndrome (Group A); 8 of these patients died and 6 had autopsies that showed major thrombi in the heterograft. In 126 long‐term survivors, 9 thromboembolic events occurred (TE incidence 5.4% per patient year). All patients with emboli had atrial fibrillation. The majority (7/9) of emboli occurred during the first 3 postoperative months. Five occurred in patients who were not on anticoagulation (Group B), and 2 occurred in patients receiving warfarin therapy (Group C). There was no thromboembolic event in patients receiving aspirin treatment (Group D). It is concluded that patients with Hancock aortic valves have a very small risk of TE, and do not need anticoagulation. Patients with Hancock mitral valves with stable hemodynamics have a decreased risk of TE and do not require anticoagulation. Patients with atrial fibrillation have an increased risk of TE and should be on warfarin for 3 months after surgery and then on aspirin therapy.

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Section: Discussionsupporting

confidence: 93%

“…This finding appears to be rare in the Hancock valves. Johnson et al [20] and Horowitz et al [21] reported such complications. Johnson's patient had been in a chronic low output state, and the 2 patients described by Horowitz had a severe postoperative low output state and renal failure, one of them associated with coagulopathy.…”

Section: Discussionmentioning

confidence: 97%