Abstract

AimsThe main aim of this study was to characterize changes in the left ventricular (LV) blood flow kinetic energy (KE) using four-dimensional (4D) flow cardiovascular magnetic resonance imaging (CMR) in patients with myocardial infarction (MI) with/without LV thrombus (LVT).Methods and resultsThis is a prospective cohort study of 108 subjects [controls = 40, MI patients without LVT (LVT− = 36), and MI patients with LVT (LVT+ = 32)]. All underwent CMR including whole-heart 4D flow. LV blood flow KE wall calculated using the formula: , where ρ = density, V = volume, v = velocity, and was indexed to LV end-diastolic volume. Patient with MI had significantly lower LV KE components than controls (P < 0.05). LVT+ and LVT− patients had comparable infarct size and apical regional wall motion score (P > 0.05). The relative drop in A-wave KE from mid-ventricle to apex and the proportion of in-plane KE were higher in patients with LVT+ compared with LVT− (87 ± 9% vs. 78 ± 14%, P = 0.02; 40 ± 5% vs. 36 ± 7%, P = 0.04, respectively). The time difference of peak E-wave KE demonstrated a significant rise between the two groups (LVT−: 38 ± 38 ms vs. LVT+: 62 ± 56 ms, P = 0.04). In logistic-regression, the relative drop in A-wave KE (beta = 11.5, P = 0.002) demonstrated the strongest association with LVT.ConclusionPatients with MI have reduced global LV flow KE. Additionally, MI patients with LVT have significantly reduced and delayed wash-in of the LV. The relative drop of distal intra-ventricular A-wave KE, which represents the distal late-diastolic wash-in of the LV, is most strongly associated with the presence of LVT.

Highlights

  • Left ventricular (LV) thrombus (LVT) remains a life-threatening complication of myocardial infarction (MI), being associated with a fivefold increased risk of systemic embolism.[1]

  • The risk for LVT is greater with anterior MI, low ejection fraction (EF), LV aneurysms, and apical akinesis or dyskinesis,[1,2] but LVT formation can be found in patients with smaller infarcts, inferior infarcts, and only mild to moderate LV systolic dysfunction.[3]

  • LV blood flow kinetic energy (KE) appears to be reduced in patients with heart failure,[13] and has the potential to provide new mechanistic insights into the pathophysiology of LVT formation in patients with ischaemic cardiomyopathy by detecting specific signatures of flow disturbance associated with LV flow stasis in LVT

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Summary

Introduction

Left ventricular (LV) thrombus (LVT) remains a life-threatening complication of myocardial infarction (MI), being associated with a fivefold increased risk of systemic embolism.[1]. Graphic studies have demonstrated that abnormal flow patterns are associated with LVT.[4,5,6] comprehensive insight into flow changes in post-MI patients with LVT is lacking, partly because tests capable of examining the complex 3D intra-cavity flow have not been available in the past. The development of four-dimensional (4D) flow cardiovascular magnetic resonance imaging (CMR) allows mapping and quantification of intra-cavity LV flow kinetic energy (KE).[7,8,9,10,11,12] LV blood flow KE appears to be reduced in patients with heart failure,[13] and has the potential to provide new mechanistic insights into the pathophysiology of LVT formation in patients with ischaemic cardiomyopathy by detecting specific signatures of flow disturbance associated with LV flow stasis in LVT

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