Fabian Nietlispach1, John G Webb2, Jian Ye3, Anson Cheung3, Samuel V Lichtenstein3, Ronald G Carere2, Ronen Gurvitch2, Christopher R Thompson2, Avi J Ostry4, Lise Matzke5, Michael F Allard6. 1. Division of Cardiology, St. Paul's Hospital, Vancouver, British Columbia, Canada; Swiss Cardiovascular Center, Bern University Hospital, Bern, Switzerland. 2. Division of Cardiology, St. Paul's Hospital, Vancouver, British Columbia, Canada. 3. Division of Cardiac Surgery, St. Paul's Hospital, Vancouver, British Columbia, Canada. 4. Department of Pathology and Laboratory Medicine, University of British Columbia/St Paul's Hospital, Vancouver, British Columbia, Canada. 5. Department of Pathology and Laboratory Medicine, University of British Columbia/St Paul's Hospital, Vancouver, British Columbia, Canada; University of British Columbia James Hogg Research Centre, St. Paul's Hospital, Vancouver, British Columbia, Canada. 6. Department of Pathology and Laboratory Medicine, University of British Columbia/St Paul's Hospital, Vancouver, British Columbia, Canada; University of British Columbia James Hogg Research Centre, St. Paul's Hospital, Vancouver, British Columbia, Canada. Electronic address: mike.allard@pathology.ubc.ca.
Abstract
OBJECTIVES: This study sought to report on the pathology of transcatheter aortic valves explanted at early and late time points after transcatheter aortic valve implantation. BACKGROUND: Information on pathological findings following transcatheter aortic valve implantation is scarce, particularly late after transcatheter aortic valve implantation. METHODS: This study included 20 patients (13 men, median age 80 years [interquartile range: 72 to 84] years) with previous transcatheter aortic valve implantation with a valve explanted at autopsy (n = 17) or surgery (n = 3) up to 30 months after implantation (10 transapical and 10 transfemoral procedures). RESULTS: Structural valve degeneration was not seen, although fibrous tissue ingrowth was observed at later time points with minimal effects on cusp mobility in 1 case. Minor alterations in valve configuration or placement were observed in up to 50% of cases, but they were not accompanied by substantial changes in valve function or reliably associated with chest compressions. Vascular or myocardial injury was common, especially within 30 days of transcatheter aortic valve implantation (about 69%), with the latter associated with left coronary ostial occlusion by calcified native aortic valve tissue in 2 cases. Mild to severe myocardial amyloidosis was present in nearly 33% of cases and likely played a role in the poor outcome of 3 patients. Endocarditis, migration of the valve, and embolization during the procedure led to surgical valve removal. CONCLUSIONS: Structural degeneration was not seen and minor alterations of valve configuration or placement did not affect valve function and were not reliably caused by chest compressions. Vascular or myocardial injury is very common early after transcatheter aortic valve implantation and myocardial amyloidosis represents a relatively frequent potentially significant comorbid condition.
OBJECTIVES: This study sought to report on the pathology of transcatheter aortic valves explanted at early and late time points after transcatheter aortic valve implantation. BACKGROUND: Information on pathological findings following transcatheter aortic valve implantation is scarce, particularly late after transcatheter aortic valve implantation. METHODS: This study included 20 patients (13 men, median age 80 years [interquartile range: 72 to 84] years) with previous transcatheter aortic valve implantation with a valve explanted at autopsy (n = 17) or surgery (n = 3) up to 30 months after implantation (10 transapical and 10 transfemoral procedures). RESULTS:Structural valve degeneration was not seen, although fibrous tissue ingrowth was observed at later time points with minimal effects on cusp mobility in 1 case. Minor alterations in valve configuration or placement were observed in up to 50% of cases, but they were not accompanied by substantial changes in valve function or reliably associated with chest compressions. Vascular or myocardial injury was common, especially within 30 days of transcatheter aortic valve implantation (about 69%), with the latter associated with left coronary ostial occlusion by calcified native aortic valve tissue in 2 cases. Mild to severe myocardial amyloidosis was present in nearly 33% of cases and likely played a role in the poor outcome of 3 patients. Endocarditis, migration of the valve, and embolization during the procedure led to surgical valve removal. CONCLUSIONS:Structural degeneration was not seen and minor alterations of valve configuration or placement did not affect valve function and were not reliably caused by chest compressions. Vascular or myocardial injury is very common early after transcatheter aortic valve implantation and myocardial amyloidosis represents a relatively frequent potentially significant comorbid condition.
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