Rodrigo Bagur1, Karla Solo2, Saleh Alghofaili2, Luis Nombela-Franco2, Chun Shing Kwok2, Samual Hayman2, Reed A Siemieniuk2, Farid Foroutan2, Frederick A Spencer2, Per O Vandvik2, Tim G Schäufele2, Mamas A Mamas2. 1. From the Division of Cardiology, Department of Medicine, London Health Sciences Center (R.B., S.A., S.H.) and Department of Epidemiology and Biostatistics (R.B., K.S.), Schulich School of Medicine & Dentistry, Western University, London, Ontario, Canada; Keele Cardiovascular Research Group, Institute of Applied Clinical Science (R.B., C.S.K., M.A.M.), Keele University and Royal Stoke Hospital, Stoke-on-Trent, United Kingdom; Division of Cardiology, Hospital Clínico San Carlos, Madrid, Spain (L.N.-F.); Department of Medicine, University of Toronto, Ontario (R.A.S.); Department of Clinical Epidemiology & Biostatistics (F.F.) and Division of Cardiology, Department of Medicine (F.A.S.), McMaster University, Hamilton, Ontario, Canada; Department of Medicine, Innlandet Hospital Trust, Gjøvik, Norway; Institute for Health and Society, Faculty of Medicine, University of Oslo, Norway (P.O.V.); and Department of Cardiology, Robert-Bosch-Krankenhaus, Stuttgart, Germany (T.G.S.). rodrigobagur@yahoo.com. 2. From the Division of Cardiology, Department of Medicine, London Health Sciences Center (R.B., S.A., S.H.) and Department of Epidemiology and Biostatistics (R.B., K.S.), Schulich School of Medicine & Dentistry, Western University, London, Ontario, Canada; Keele Cardiovascular Research Group, Institute of Applied Clinical Science (R.B., C.S.K., M.A.M.), Keele University and Royal Stoke Hospital, Stoke-on-Trent, United Kingdom; Division of Cardiology, Hospital Clínico San Carlos, Madrid, Spain (L.N.-F.); Department of Medicine, University of Toronto, Ontario (R.A.S.); Department of Clinical Epidemiology & Biostatistics (F.F.) and Division of Cardiology, Department of Medicine (F.A.S.), McMaster University, Hamilton, Ontario, Canada; Department of Medicine, Innlandet Hospital Trust, Gjøvik, Norway; Institute for Health and Society, Faculty of Medicine, University of Oslo, Norway (P.O.V.); and Department of Cardiology, Robert-Bosch-Krankenhaus, Stuttgart, Germany (T.G.S.).
Abstract
BACKGROUND AND PURPOSE: Silent ischemic embolic lesions are common after transcatheter aortic valve implantation (TAVI). The use of embolic protection devices (EPD) may reduce the occurrence of these embolic lesions. Thus, a quantitative overview and credibility assessment of the literature was necessary to draw a robust message about EPD. Therefore, the aim of this meta-analysis was to study whether the use of EPD reduces silent ischemic and clinically evident cerebrovascular events associated with TAVI. METHODS: We conducted a comprehensive search to identify studies that evaluated patients undergoing TAVI with or without EPD. Random-effects meta-analyses were performed to estimate the effect of EPD compared with no-EPD during TAVI using aggregate data. RESULTS: Sixteen studies involving 1170 patients (865/305 with/without EPD) fulfilled the inclusion criteria. The EPD delivery success rate was reported in all studies and was achieved in 94.5% of patients. Meta-analyses evaluating EPD versus without EPD strategies could not confirm or exclude any differences in terms of clinically evident stroke (relative risk, 0.70; 95% confidence interval [CI], 0.38-1.29; P=0.26) or 30-day mortality (relative risk, 0.58; 95% CI, 0.20-1.64; P=0.30). There were no significant differences in new-single, multiple, or total number of lesions. The use of EPD was associated with a significantly smaller ischemic volume per lesion (standardized mean difference, -0.52; 95% CI, -0.85 to -0.20; P=0.002) and smaller total volume of lesions (standardized mean difference, -0.23; 95% CI, -0.42 to -0.03; P=0.02). Subgroup analysis by type of valve showed an overall trend toward significant reduction in new lesions per patient using EPD (standardized mean difference, -0.41; 95% CI, -0.82 to 0.00; P=0.05), driven by self-expanding devices. CONCLUSIONS: The use of EPD during TAVI may be associated with smaller volume of silent ischemic lesions and smaller total volume of silent ischemic lesions. However, EPD may not reduce the number of new-single, multiple, or total number of lesions. There was only very low quality of evidence showing no significant differences between patients undergoing TAVI with or without EPD with respect to clinically evident stroke and mortality.
BACKGROUND AND PURPOSE: Silent ischemic embolic lesions are common after transcatheter aortic valve implantation (TAVI). The use of embolic protection devices (EPD) may reduce the occurrence of these embolic lesions. Thus, a quantitative overview and credibility assessment of the literature was necessary to draw a robust message about EPD. Therefore, the aim of this meta-analysis was to study whether the use of EPD reduces silent ischemic and clinically evident cerebrovascular events associated with TAVI. METHODS: We conducted a comprehensive search to identify studies that evaluated patients undergoing TAVI with or without EPD. Random-effects meta-analyses were performed to estimate the effect of EPD compared with no-EPD during TAVI using aggregate data. RESULTS: Sixteen studies involving 1170 patients (865/305 with/without EPD) fulfilled the inclusion criteria. The EPD delivery success rate was reported in all studies and was achieved in 94.5% of patients. Meta-analyses evaluating EPD versus without EPD strategies could not confirm or exclude any differences in terms of clinically evident stroke (relative risk, 0.70; 95% confidence interval [CI], 0.38-1.29; P=0.26) or 30-day mortality (relative risk, 0.58; 95% CI, 0.20-1.64; P=0.30). There were no significant differences in new-single, multiple, or total number of lesions. The use of EPD was associated with a significantly smaller ischemic volume per lesion (standardized mean difference, -0.52; 95% CI, -0.85 to -0.20; P=0.002) and smaller total volume of lesions (standardized mean difference, -0.23; 95% CI, -0.42 to -0.03; P=0.02). Subgroup analysis by type of valve showed an overall trend toward significant reduction in new lesions per patient using EPD (standardized mean difference, -0.41; 95% CI, -0.82 to 0.00; P=0.05), driven by self-expanding devices. CONCLUSIONS: The use of EPD during TAVI may be associated with smaller volume of silent ischemic lesions and smaller total volume of silent ischemic lesions. However, EPD may not reduce the number of new-single, multiple, or total number of lesions. There was only very low quality of evidence showing no significant differences between patients undergoing TAVI with or without EPD with respect to clinically evident stroke and mortality.