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Circulation. 2007;115:1392-1397
Published online before print March 5, 2007, doi: 10.1161/CIRCULATIONAHA.106.674259
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(Circulation. 2007;115:1392-1397.)
© 2007 American Heart Association, Inc.


Interventional Cardiology

Risk Stratification, Systematic Classification, and Anticipatory Management Strategies for Stent Fracture After Percutaneous Pulmonary Valve Implantation

Johannes Nordmeyer, AS; Sachin Khambadkone, MD; Louise Coats, MRCP; Silvia Schievano, MEng; Philipp Lurz, AS; Giovanni Parenzan, MA; Andrew M. Taylor, MD, MRCP, FRCR; James E. Lock, MD; Philipp Bonhoeffer, MD

From the University College London Institute of Child Health and Great Ormond Street Hospital for Children (J.N., S.K., L.C., S.S., P.L. G.P., A.M.T., P.B.), London, United Kingdom, and Department of Cardiology (J.E.L.), Children’s Hospital, Boston, Mass.

Correspondence to Dr Philipp Bonhoeffer, Cardiothoracic Unit, Great Ormond Street Hospital for Children, Great Ormond Street, London WC1N 3JH, United Kingdom. E-mail bonhop{at}gosh.nhs.uk

Received November 3, 2006; accepted January 5, 2007.

Background— We analyzed the incidence, risk factors and treatment options for stent fracture after percutaneous pulmonary valve (PPV) implantation (PPVI).

Methods and Results— After PPVI, 123 patients had chest x-ray in anteroposterior and lateral projection, echocardiography, and clinical evaluation during structured follow-up. Of these 123 patients, 26 (21.1%) developed stent fracture 0 to 843 days after PPVI (stent fracture–free survival at 1 year, 85.1%; at 2 years, 74.5%; and at 3 years, 69.2%). Stent fracture was classified as type I: no loss of stent integrity (n=17); type II: loss of integrity with restenosis on echocardiography (n=8); and type III: separation of fragments or embolization (n=1). In a multivariate Cox regression, we analyzed various factors, of which 3 were associated with a higher risk of stent fracture: implantation into "native" right ventricular outflow tract (P=0.04), no calcification along the right ventricular outflow tract (judged with fluoroscopy, P=0.02), recoil of PPV (qualitatively, PPV diameter in frontal or lateral plane with fully inflated balloon > diameter after balloon deflation, P=0.03). Substernal PPV location, high-pressure post-PPVI dilatation of PPV, pre-PPVI right ventricular outflow tract gradients, and other indicators of PPV compression or asymmetry did not pose increased risk. Patients with type I fracture remain under follow-up. Patients with type II fracture had 2nd PPVI or are awaiting such procedure, and 1 patient with type III fracture required surgical explantation.

Conclusion— Stent fracture after PPVI can be managed effectively by risk stratification, systematic classification, and anticipatory management strategies. Serial x-ray and echocardiography are recommended for surveillance.


 

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