Lin Wang1, Guido Parodi2, Akiko Maehara3, Renato Valenti2, Angela Migliorini2, Ruben Vergara2, Nazario Carrabba2, Gary S Mintz4, David Antoniucci2. 1. Columbia University Medical Center, New York, NY, USA Cardiovascular Research Foundation, 111 East 59th Street, 12th Floor, New York, NY 10022, USA. 2. Division of Cardiology, Careggi Hospital, Florence, Italy. 3. Columbia University Medical Center, New York, NY, USA Cardiovascular Research Foundation, 111 East 59th Street, 12th Floor, New York, NY 10022, USA amaehara@crf.org. 4. Cardiovascular Research Foundation, 111 East 59th Street, 12th Floor, New York, NY 10022, USA.
Abstract
AIMS: The objective was to assess in vivo culprit lesion morphologies that caused ST-segment elevation myocardial infarction (STEMI) using optical coherence tomography (OCT). METHODS AND RESULTS: Culprit lesions in 80 patients presenting within 6 h of STEMI onset from the CompariSon of Manual Aspiration with Rheolytic Thrombectomy in patients undergoing primary PCI (SMART) trial were evaluated. Underlying morphology of 64 culprit lesions was identifiable by OCT and included 37 lesions with plaque rupture, 25 lesions without plaque rupture, and 2 lesions with calcified nodules. Patients with plaque rupture tended to be younger (64 ± 12 versus 70 ± 10 years, P = 0.08) and less often female (11 versus 40%, P = 0.007) compared with patients without plaque rupture. More thin-cap fibroatheromas were identified (60 versus 20%, P = 0.002); and residual thrombus was greater in the rupture than in the non-rupture group. OCT at 6 months showed more stent malapposition (65 versus 33%, P = 0.04) in the rupture compared with the non-rupture group. CONCLUSION: OCT analysis showed two dominant culprit lesion morphologies in STEMI: (i) lesions with plaque rupture with a large amount of thrombus or (ii) lesions without plaque rupture and a lesser amount of thrombus. Published on behalf of the European Society of Cardiology. All rights reserved.
RCT Entities:
AIMS: The objective was to assess in vivo culprit lesion morphologies that caused ST-segment elevation myocardial infarction (STEMI) using optical coherence tomography (OCT). METHODS AND RESULTS: Culprit lesions in 80 patients presenting within 6 h of STEMI onset from the CompariSon of Manual Aspiration with Rheolytic Thrombectomy in patients undergoing primary PCI (SMART) trial were evaluated. Underlying morphology of 64 culprit lesions was identifiable by OCT and included 37 lesions with plaque rupture, 25 lesions without plaque rupture, and 2 lesions with calcified nodules. Patients with plaque rupture tended to be younger (64 ± 12 versus 70 ± 10 years, P = 0.08) and less often female (11 versus 40%, P = 0.007) compared with patients without plaque rupture. More thin-cap fibroatheromas were identified (60 versus 20%, P = 0.002); and residual thrombus was greater in the rupture than in the non-rupture group. OCT at 6 months showed more stent malapposition (65 versus 33%, P = 0.04) in the rupture compared with the non-rupture group. CONCLUSION: OCT analysis showed two dominant culprit lesion morphologies in STEMI: (i) lesions with plaque rupture with a large amount of thrombus or (ii) lesions without plaque rupture and a lesser amount of thrombus. Published on behalf of the European Society of Cardiology. All rights reserved.
Authors: Sylvia Otto; Kristina Nitsche; Christian Jung; Aleh Kryvanos; Andrey Zhylka; Kerstin Heitkamp; Juan-Luis Gutiérrez-Chico; Björn Goebel; P Christian Schulze; Hans R Figulla; Tudor C Poerner Journal: BMC Cardiovasc Disord Date: 2017-04-26 Impact factor: 2.298
Authors: Timo P Kaivosoja; Shengnan Liu; Jouke Dijkstra; Heini Huhtala; Tej Sheth; Olli A Kajander Journal: PLoS One Date: 2018-12-17 Impact factor: 3.240