Hang Zhao1, Alex Pui-Wai Lee2, Zheng Li1, Zhiqing Qiao1, Yiting Fan1, Dongaolei An1, Jianrong Xu1, Jun Pu1, Xuedong Shen1, Heng Ge1, Ben He3. 1. Department of Cardiology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. 2. Division of Cardiology, Department of Medicine and Therapeutics, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China. 3. Department of Cardiology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. Electronic address: heben@medmail.com.cn.
Abstract
BACKGROUND: Intramyocardial hemorrhage (IMH) and microvascular obstruction (MVO) are two major mechanisms of reperfusion injury of the left ventricle after acute ST-segment elevation myocardial infarction (STEMI). The aim of this study was to assess the impact of IMH and MVO on left ventricular (LV) cardiac mechanics using two-dimensional speckle-tracking echocardiography during the acute phase of STEMI and on LV functional recovery. METHODS: Eighty-one patients with STEMI who received primary reperfusion therapy were prospectively studied. Infarct segments were classified by cardiac magnetic resonance according to infarct transmurality and the presence or absence of IMH and/or MVO. Segmental systolic longitudinal strain, circumferential strain (CS), and radial strain were measured by two-dimensional speckle-tracking echocardiography. Adverse LV remodeling and major adverse cardiovascular events were assessed at 1 year. RESULTS: MVO without IMH was much less frequent in nontransmural infarct segments than in transmural infarct segments (6.0% vs 19.1%, P = .000), while IMH was present only in transmural infarct segments. In nontransmural infarct segments, MVO was not associated with any significant changes in strain (P > .5). In transmural infarct segments, there were no differences in all types of strain between segments without reperfusion injury and those with MVO alone (P > .20). IMH was evident in the midmyocardial layer within the infarct zone in 196 segments (46.1%). The presence of IMH in addition to MVO decreased CS significantly (P = .004), but not longitudinal and radial strain (P > .5). A receiver operating characteristic curve analysis with cross-validation by k-folding showed that the sensitivity and specificity of CS using a cutoff of >-11.66% to diagnose IMH were 78.00% and 79.45%, respectively (area under the curve = 0.86; P = .0001). At 1 year, patients with major adverse cardiovascular events and LV remodeling had significantly lower baseline measurements of all types of global strain (P < .05). CONCLUSIONS: In the acute phase of STEMI, reperfusion MVO and IMH injury have differential effects on cardiac mechanics. IMH preferentially affects CS, presumably related to its location in the midmyocardial layer.
BACKGROUND:Intramyocardial hemorrhage (IMH) and microvascular obstruction (MVO) are two major mechanisms of reperfusion injury of the left ventricle after acute ST-segment elevation myocardial infarction (STEMI). The aim of this study was to assess the impact of IMH and MVO on left ventricular (LV) cardiac mechanics using two-dimensional speckle-tracking echocardiography during the acute phase of STEMI and on LV functional recovery. METHODS: Eighty-one patients with STEMI who received primary reperfusion therapy were prospectively studied. Infarct segments were classified by cardiac magnetic resonance according to infarct transmurality and the presence or absence of IMH and/or MVO. Segmental systolic longitudinal strain, circumferential strain (CS), and radial strain were measured by two-dimensional speckle-tracking echocardiography. Adverse LV remodeling and major adverse cardiovascular events were assessed at 1 year. RESULTS:MVO without IMH was much less frequent in nontransmural infarct segments than in transmural infarct segments (6.0% vs 19.1%, P = .000), while IMH was present only in transmural infarct segments. In nontransmural infarct segments, MVO was not associated with any significant changes in strain (P > .5). In transmural infarct segments, there were no differences in all types of strain between segments without reperfusion injury and those with MVO alone (P > .20). IMH was evident in the midmyocardial layer within the infarct zone in 196 segments (46.1%). The presence of IMH in addition to MVO decreased CS significantly (P = .004), but not longitudinal and radial strain (P > .5). A receiver operating characteristic curve analysis with cross-validation by k-folding showed that the sensitivity and specificity of CS using a cutoff of >-11.66% to diagnose IMH were 78.00% and 79.45%, respectively (area under the curve = 0.86; P = .0001). At 1 year, patients with major adverse cardiovascular events and LV remodeling had significantly lower baseline measurements of all types of global strain (P < .05). CONCLUSIONS: In the acute phase of STEMI, reperfusion MVO and IMH injury have differential effects on cardiac mechanics. IMH preferentially affects CS, presumably related to its location in the midmyocardial layer.