AIMS: In this study we aimed to test the hypothesis that left ventricular (LV) afterload reduction in severe aortic valve stenosis (AS) by transcatheter aortic valve implantation (TAVI) acutely improves coronary haemodynamics. METHODS AND RESULTS: This was a prospective, pathophysiologic study in 40 patients with severe AS undergoing TAVI. Endpoints were determined invasively immediately before and after TAVI without altering coronary stenotic lesions if present. Myocardial hyperaemia was induced by intravenous adenosine. The primary study endpoints were coronary flow reserve (thermodilution-derived CFR), and fractional flow reserve (FFR). The secondary study endpoint was coronary collateral flow index (CFI) as obtained during a one-minute coronary balloon occlusion. CFR was 1.9±0.9 before TAVI and 2.0±1.0 after TAVI (p=0.72). FFR was 0.90±0.08 before TAVI and 0.93±0.08 after TAVI (p=0.0021). The TAVI-induced increase in FFR was related to a significant decrease in hyperaemic mean aortic pressure from 71±16 mmHg before TAVI to 67±15 mmHg after TAVI (p=0.0099). Hyperaemic CFI increased from 0.127±0.083 before to 0.146±0.090 after TAVI (p=0.0508). CONCLUSIONS: CFR appears not to be acutely affected by LV afterload reduction among patients with severe AS in response to TAVI. However, it acutely improves FFR; this occurs via lowering of mean aortic pressure. Hyperaemic coronary collateral flow index tends to augment in response to TAVI.
AIMS: In this study we aimed to test the hypothesis that left ventricular (LV) afterload reduction in severe aortic valve stenosis (AS) by transcatheter aortic valve implantation (TAVI) acutely improves coronary haemodynamics. METHODS AND RESULTS: This was a prospective, pathophysiologic study in 40 patients with severe AS undergoing TAVI. Endpoints were determined invasively immediately before and after TAVI without altering coronary stenotic lesions if present. Myocardial hyperaemia was induced by intravenous adenosine. The primary study endpoints were coronary flow reserve (thermodilution-derived CFR), and fractional flow reserve (FFR). The secondary study endpoint was coronary collateral flow index (CFI) as obtained during a one-minute coronary balloon occlusion. CFR was 1.9±0.9 before TAVI and 2.0±1.0 after TAVI (p=0.72). FFR was 0.90±0.08 before TAVI and 0.93±0.08 after TAVI (p=0.0021). The TAVI-induced increase in FFR was related to a significant decrease in hyperaemic mean aortic pressure from 71±16 mmHg before TAVI to 67±15 mmHg after TAVI (p=0.0099). Hyperaemic CFI increased from 0.127±0.083 before to 0.146±0.090 after TAVI (p=0.0508). CONCLUSIONS: CFR appears not to be acutely affected by LV afterload reduction among patients with severe AS in response to TAVI. However, it acutely improves FFR; this occurs via lowering of mean aortic pressure. Hyperaemic coronary collateral flow index tends to augment in response to TAVI.
Authors: Roberto Scarsini; Giovanni L De Maria; Giuseppe Di Gioia; Rafail A Kotronias; Cristina Aurigemma; Giuseppe Zimbardo; Francesco Burzotta; Antonio M Leone; Gabriele Pesarini; Carlo Trani; Filippo Crea; Rajesh K Kharbanda; Bernard De Bruyne; Emanuele Barbato; Adrian Banning; Flavio Ribichini Journal: J Cardiovasc Transl Res Date: 2019-05-22 Impact factor: 4.132
Authors: Muhammad Sabbah; Niels Thue Olsen; Mikko Minkkinen; Lene Holmvang; Hans-Henrik Tilsted; Frants Pedersen; Francis R Joshi; Kiril Ahtarovski; Rikke Sørensen; Jesper James Linde; Lars Søndergaard; Nico Pijls; Jacob Lønborg; Thomas Engstrøm Journal: J Am Heart Assoc Date: 2022-04-26 Impact factor: 6.106
Authors: Jo M Zelis; Pim A L Tonino; Nico H J Pijls; Bernard De Bruyne; Richard L Kirkeeide; K Lance Gould; Nils P Johnson Journal: J Interv Cardiol Date: 2020-07-22 Impact factor: 2.279