August 2, 2018Open Access
Ver artículo completoLeft ventricular thrombus formation in myocardial infarction is associated with altered left ventricular blood flow energetics
Resultado clave
Myocardial infarction patients with left ventricular thrombus had a significantly higher relative drop in A-wave kinetic energy compared to those without thrombus (87% vs 78%, P=0.02).
Diseño del estudio
Tipo
Cohort (n=108)
PICO estructurado
Does 4D flow CMR-derived left ventricular blood flow kinetic energy differ between myocardial infarction patients with and without left ventricular thrombus?
P
Población
108 subjects, comprising 40 controls, 36 patients with myocardial infarction (MI) without left ventricular thrombus (LVT-), and 32 MI patients with left ventricular thrombus (LVT+).
I
Intervención
Four-dimensional (4D) flow cardiovascular magnetic resonance imaging (CMR) to assess left ventricular blood flow kinetic energy (KE).
C
Comparador
Comparison between MI patients with LV thrombus, MI patients without LV thrombus, and healthy controls.
O
Resultado
Left ventricular blood flow kinetic energy (KE) components, including relative drop in A-wave KE, proportion of in-plane KE, and time difference of peak E-wave KE.surrogate
4D flow CMR demonstrates that altered left ventricular blood flow energetics, specifically a relative drop in distal intra-ventricular A-wave kinetic energy, is strongly associated with the presence of left ventricular thrombus in patients with myocardial infarction.
Resultado numérico
Estimación del efecto: beta = 11.5
Tasa de eventos absoluta: 87% vs 78%
valor p: p=0.002
Resumen
Aims: The 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 results: This 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: KE=12 ρblood . Vvoxel . v2, 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). 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. Conclusion: Patients 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.