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Echocardiography-quantified myocardial strain-a marker of global and regional infarct size that stratifies likelihood of left ventricular thrombus.

ABSTRACT: Myocardial strain provides a novel means of quantifying subtle alterations in contractile function; incremental utility post-MI is unknown.To test longitudinal-quantified by postprocessing routine echo-for assessment of MI size measured by cardiac magnetic resonance (CMR) and conventional methods, and assess regional and global strain (GLS) as markers of LV thrombus.The population comprised of patients with anterior ST-segment MI who underwent echo and CMR prospectively. Preexisting echoes were retrieved, re-analyzed for strain, and compared to conventional MI markers as well as CMR-evidenced MI, function, and thrombus.Seventy-four patients underwent echo and CMR 4 ± 1 weeks post-MI; 72% had abnormal GLS. CMR-quantified MI size was 2.5-fold larger and EF lower among patients with abnormal GLS, paralleling 2.6-3.1 fold differences in Q-wave size and CPK (all P ? .002). GLS correlated with CMR-quantified MI (r = .66), CPK (r = .52) and Q-wave area (r = .44; all P ? .001): Regional strain was lower in the base, mid, and apical LV among patients with CMR-defined transmural MI in each territory (P < .05) and correlated with cine-CMR regional EF (r = .53-.71; P < .001) and echo wall motion (r = .45-.71; P < .001). GLS and apical strain were ~2-fold lower among patients with LV thrombus (P ? .002): Apical strain yielded higher diagnostic performance for thrombus (AUC: 0.83 [0.72-0.93], P = .001) than wall motion (0.73 [0.58-0.88], P = .02), as did global strain (0.78 [0.65-0.90], P = .005) compared to LVEF (0.58 [0.45-0.72], P = .41).Echo-quantified longitudinal strain provides a marker of MI size and improves stratification for post-MI LV thrombus beyond conventional indices.

SUBMITTER: Kim J

PROVIDER: S-EPMC5985969 | biostudies-literature | 2017 Nov

REPOSITORIES: biostudies-literature

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Echocardiography-quantified myocardial strain-a marker of global and regional infarct size that stratifies likelihood of left ventricular thrombus.

Kim Jiwon J Rodriguez-Diego Sara S Srinivasan Aparna A Brown Rachel-Maria RM Pollie Meridith P MP Di Franco Antonino A Goldburg Samantha R SR Siden Jonathan Y JY Ratcliffe Mark B MB Levine Robert A RA Devereux Richard B RB Weinsaft Jonathan W JW

Echocardiography (Mount Kisco, N.Y.) 20170822 11

<h4>Background</h4>Myocardial strain provides a novel means of quantifying subtle alterations in contractile function; incremental utility post-MI is unknown.<h4>Objectives</h4>To test longitudinal-quantified by postprocessing routine echo-for assessment of MI size measured by cardiac magnetic resonance (CMR) and conventional methods, and assess regional and global strain (GLS) as markers of LV thrombus.<h4>Methods</h4>The population comprised of patients with anterior ST-segment MI who underwen ...[more]

PMID: 28833519

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Project description:BACKGROUND:Left ventricular systolic dysfunction (LVSD) occurs frequently after acute ST-segment elevation myocardial infarction (STEMI). The predisposing factors and underlying mechanism of post-infarct LVSD are not fully understood. The present study mainly investigated the correlation between glycaemic gap, a novel index of stress-induced hyperglycaemia (SIH), and post-infarct LVSD. METHODS:A total of 274 first STEMI patients were enrolled in this cross-sectional study. Transthoracic echocardiography was performed within 48 h after admission and at 6 months after discharge to obtain left ventricular ejection fraction (LVEF). The change in LVEF was calculated as LVEF at 6 months after discharge minus baseline LVEF. Additionally, post-infarct LVSD was defined as LVEF ? 50%. Most importantly, glycaemic gap was calculated as admission blood glucose (ABG) minus the estimated average glucose over the previous 3 months. RESULTS:In patients without diabetes mellitus (DM), multivariate linear regression analysis revealed that both glycaemic gap (Beta?=?- 1.214, 95% CI - 1.886 to - 0.541, p?<?0.001) and ABG (Beta?=?- 1.124, 95% CI - 1.795 to - 0.453, p?=?0.001) were associated with change in LVEF. In DM patients, only glycaemic gap was still associated with change in LVEF, although this association was not observed in univariate linear regression analysis. Regarding the association between SIH and post-infarct LVSD, multivariate logistic regression analysis revealed that both glycaemic gap (OR?=?1.490, 95% CI 1.043 to 2.129, p?=?0.028) and ABG (OR?=?1.600, 95% CI 1.148 to 2.229, p?=?0.005) were associated with an increased risk of having post-infarct LVSD in non-DM patients. However, after multivariate adjustment in DM patients, only glycaemic gap (OR?=?1.399, 95% CI 1.021 to 1.919, p?=?0.037) remained associated with an increased risk of having post-infarct LVSD. Furthermore, the predictive value of glycaemic gap for post-infarct LVSD was not inferior to ABG in non-DM patients (p?=?0.499), and only glycaemic gap, instead of ABG, could significantly predict post-infarct LVSD in DM patients (AUC?=?0.688, 95% CI 0.591 to 0.774, p?=?0.002). CONCLUSIONS:Glycaemic gap was strongly associated with a change in LVEF and an increased risk of having post-infarct LVSD in patients following STEMI. In STEMI patients with DM, glycaemic gap could provide more valuable information than ABG in identifying patients at high risk of developing post-infarct LVSD.

Project description:Left ventricular thrombus (LVT) is a serious complication of acute myocardial infarction (MI) and also non-ischemic cardiomyopathies. We performed a narrative literature review, manual-search of reference lists of included articles and relevant reviews. Our literature review indicates that the incidence of LVT following acute MI has decreased, probably due to improvement in patient care as a result of better and earlier reperfusion techniques. Predictors of LVT include anterior MI, involvement of left ventricular (LV) apex (regardless of the coronary territory affected), LV akinesis or dyskinesis, reduced LV ejection fraction (LVEF), severe diastolic dysfunction and large infarct size. LVT is associated with increased risk of systemic embolism, stroke, cardiovascular events and death, and there is evidence that anticoagulant therapy for at least 3 months can reduce the risk of these events. Cardiac magnetic resonance (CMR) has the highest diagnostic accuracy for LVT, followed by echocardiography with the use of echocardiographic contrast agents (ECAs). Although current guidelines suggest use of vitamin K antagonist (VKA) for a minimum of 3 to 6 months, there is growing evidence of the benefits of direct acting oral anticoagulants in treatment of LVT. Embolic events appear to occur even after resolution of LVT suggesting that anticoagulant therapy needs to be considered for a longer period in some cases. Recommendations for the use of triple therapy in the presence of the LVT are mostly based on extrapolation from outcome data in patients with atrial fibrillation (AF) and MI. We conclude that the presence of LVT is more likely in patients with anterior ST-segment elevation MI (STEMI) (involving the apex) and reduced ejection fraction (EF). LVT should be considered a marker of increased long-term thrombotic risk that may persist even after thrombus resolution. Ongoing clinical trials are expected to elucidate the best management strategies for patients with LVT.

Dataset Information

Echocardiography-quantified myocardial strain-a marker of global and regional infarct size that stratifies likelihood of left ventricular thrombus.

Publications

Echocardiography-quantified myocardial strain-a marker of global and regional infarct size that stratifies likelihood of left ventricular thrombus.

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