Predictors and Impact of Myocardial Injury€After Transcatheter Aortic Valve Replacement

Fro Ca Un Va **I zzS On {{ BACKGROUND Cardiac biomarker release signifying myocardial injury post-transcatheter aortic valve replacement (TAVR) is common, yet its clinical impact within a large TAVR cohort receiving differing types of valve and procedural approaches is unknown. OBJECTIVES This study sought to determine the incidence, clinical impact, and factors associated with cardiac biomarker elevation post TAVR. METHODS This multicenter study included 1,131 consecutive patients undergoing TAVR with balloon-expandable (58%) or self-expandable (42%) valves. Transfemoral and transapical (TA) approaches were selected in 73.1% and 20.3% of patients, respectively. Creatine kinase-myocardial band (CK-MB) measurements were obtained at baseline and at several time points within the initial 72 h post TAVR. Echocardiography was performed at baseline and at 6to 12-month followup. RESULTS Overall, 66% of the TAVR population demonstrated some degree of myocardial injury as determined by a rise in CK-MB levels (peak value: 1.6-fold [interquartile range (IQR): 0.9 to 2.8-fold]). A TA approach and major procedural complications were independently associated with higher peak of CK-MB levels (p < 0.01 for all), which translated into impaired systolic left ventricular function at 6 to 12 months post TAVR (p < 0.01). A greater rise in CK-MB levels independently associated with an increased 30-day, late (median of 21 [IQR: 8 to 36] months) overall and cardiovascular mortality (p < 0.001 for all). Any increase in CK-MB levels was associated with poorer clinical outcomes, and there was a stepwise rise in late mortality according to the various degrees of CK-MB increase after TAVR (p < 0.001). CONCLUSIONS Some degree of myocardial injury was detected in two-thirds of patients post TAVR, especially in those undergoing TA-TAVR or presenting with major procedural complications. A greater rise in CK-MB levels associated with greater acute and late mortality, imparting a negative impact on left ventricular function. (J Am Coll Cardiol 2015;66:2075–88) © 2015 by the American College of Cardiology Foundation. m the *Quebec Heart and Lung Institute, Laval University, Quebec City, Quebec, Canada; yHospital Universitario Clínico San rlos, Madrid, Spain; zHospital Universitario Virgen de la Victoria, Universidad de Málaga, Málaga, Spain; xHeart Institute-InCor, iversity of São Paulo, São Paulo, Brazil; kHospital Clinico Universitario de Valladolid, Valladolid, Spain; {Hospital Universitari ll d’Hebron, Universitat Autonoma de Barcelona, Barcelona, Spain; #Hospital Israelita Albert Einstein, São Paulo, Brazil; nstituto Dante Pazzanese de Cardiologia, São Paulo, Brazil; yyInstituto de Cardiologia do Rio Grande do Sul, Porto Alegre, Brazil; t. Michael’s Hospital, Toronto University, Toronto, Ontario, Canada; xxOttawa Heart Institute, University of Ottawa, Ottawa, tario, Canada; kkUniversity Heart Center, Transcatheter Valve Clinic, University Hospital Zurich, Zurich, Switzerland; and the Hospital Universitario Central de Asturias, Oviedo, Spain. Dr. Ribeiro is supported by a PhD research grant from CNPq, Conselho ABBR EV I A T I ON S