Tsunenari Soeda1, Takumi Higuma2, Naoki Abe2, Masahiro Yamada2, Hiroaki Yokoyama2, Shuji Shibutani2, Daniel S Ong1, Rocco Vergallo1, Yoshiyasu Minami1, Hang Lee3, Ken Okumura2, Ik-Kyung Jang4,5. 1. Cardiology Division, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. 2. Department of Cardiology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan. 3. Biostatistics Center, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. 4. Cardiology Division, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA ijang@mgh.harvard.edu. 5. Division of Cardiology, Kyung Hee University, Seoul, South Korea.
Abstract
AIMS: Myocardial no reflow after percutaneous coronary intervention (PCI) is associated with poor outcome. Patients with ST-segment elevation myocardial infarction (STEMI) caused by plaque rupture are at high risk for no reflow. However, specific morphologic characteristics associated with no reflow are unknown in this population. The aim of this study is to identify the morphological characteristics of culprit plaques associated with no reflow in patients with STEMI caused by plaque rupture using both optical coherence tomography (OCT) and intravascular ultrasound (IVUS). METHODS AND RESULTS: We enrolled 145 patients with STEMI who underwent both OCT and IVUS within 12 h of symptom onset. Among these patients, we excluded those with plaque erosion and calcified nodule and included 72 patients who had plaque rupture as an underlying mechanism for STEMI. Myocardial no reflow, defined as Thrombolysis in Myocardial Infarction flow grade 0-2 and/or myocardial blush grade 0-1 after PCI, was observed in 28 patients (38.9%). Onset to recanalization time was similar between the groups with and without no reflow. Receiver-operating curve analysis revealed OCT-derived lipid index > 3500 [area under curve (AUC) 0.77, P < 0.001] and IVUS-derived plaque burden > 81.5% (AUC 0.70, P = 0.002) were the best discriminators for myocardial no reflow. CONCLUSION: No reflow occurred in nearly 40% of patients with STEMI caused by plaque rupture. Large lipid index and plaque burden were critical morphological discriminators between no reflow and normal flow. Published on behalf of the European Society of Cardiology. All rights reserved.
AIMS: Myocardial no reflow after percutaneous coronary intervention (PCI) is associated with poor outcome. Patients with ST-segment elevation myocardial infarction (STEMI) caused by plaque rupture are at high risk for no reflow. However, specific morphologic characteristics associated with no reflow are unknown in this population. The aim of this study is to identify the morphological characteristics of culprit plaques associated with no reflow in patients with STEMI caused by plaque rupture using both optical coherence tomography (OCT) and intravascular ultrasound (IVUS). METHODS AND RESULTS: We enrolled 145 patients with STEMI who underwent both OCT and IVUS within 12 h of symptom onset. Among these patients, we excluded those with plaque erosion and calcified nodule and included 72 patients who had plaque rupture as an underlying mechanism for STEMI. Myocardial no reflow, defined as Thrombolysis in Myocardial Infarction flow grade 0-2 and/or myocardial blush grade 0-1 after PCI, was observed in 28 patients (38.9%). Onset to recanalization time was similar between the groups with and without no reflow. Receiver-operating curve analysis revealed OCT-derived lipid index > 3500 [area under curve (AUC) 0.77, P < 0.001] and IVUS-derived plaque burden > 81.5% (AUC 0.70, P = 0.002) were the best discriminators for myocardial no reflow. CONCLUSION: No reflow occurred in nearly 40% of patients with STEMI caused by plaque rupture. Large lipid index and plaque burden were critical morphological discriminators between no reflow and normal flow. Published on behalf of the European Society of Cardiology. All rights reserved.
Authors: Rafał Januszek; Zbigniew Siudak; Krzysztof P Malinowski; Roman Wojdyła; Piotr Mika; Wojciech Wańha; Tomasz Kameczura; Andrzej Surdacki; Wojciech Wojakowski; Jacek Legutko; Stanisław Bartuś Journal: J Clin Med Date: 2020-11-09 Impact factor: 4.241
Authors: Martin Reindl; Sebastian Johannes Reinstadler; Hans-Josef Feistritzer; Markus Theurl; Daniel Basic; Christopher Eigler; Magdalena Holzknecht; Johannes Mair; Agnes Mayr; Gert Klug; Bernhard Metzler Journal: J Am Heart Assoc Date: 2017-10-10 Impact factor: 5.501